CO (carbon monoxide, CO) of pure product is colorless, odorless, non-irritating gas. Molecular weight 28.01, density 0.967g / L, freezing point -207 ℃, boiling point -190 ℃. Very low solubility in water, but soluble in ammonia. Air mixture explosion limit of 12.5% to 74%. After carbon monoxide into the body and the blood hemoglobin, and thus can not combine with oxygen to hemoglobin, causing the body tissue of oxygen, causing the body suffocation. Therefore, toxic carbon monoxide. Carbon monoxide is a colorless, odorless, tasteless gas, it is easy to ignore Erzhi poisoning. Common in the family room with poor ventilation conditions, the coal stove gas or liquefied petroleum gas production or industrial production of the gas pipeline leaks and carbon monoxide inhalation in the mines Erzhi poisoning.
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Mechanism and chemical properties of the physical properties of occupational exposure to carbon monoxide poisoning symptoms Introduction to clinical manifestations of acute poisoning delayed encephalopathy (delayed encephalopathy) hazard of carbon monoxide can be life-saving health effects of carbon monoxide pollution in Toxicology information on emergency treatment of emergency management information principles of medical diagnostic points sequelae poisoning prevention measures Monitoring chemical properties of the national standard electronic tragic accident the outermost layer of carbon has four electrons in the outermost layer of oxygen has 6 electrons, so the carbon into two single-electron p-orbital of oxygen and oxygen of the two single-electron pair bond, thus forming two keys, and then the oxygen lone electron pair into the empty carbon to form a track with P key, so oxygen and carbon is formed between the three keys. The electronic is: C::: O: CO (carbon monoxide) (CO) the physical properties of carbon monoxide
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In normal conditions, carbon monoxide is a colorless, odorless, tasteless, insoluble water, gas, melting point -199 ℃, boiling point -191.5 ℃. Standard conditions of gas density l.25g / L, and the air density (at standard conditions 1.293g / L) difference is small, which is prone to gas poisoning, one of the factors. It is neutral gas. Molecular Structure: carbon monoxide molecules as polar molecules, but because of the feedback electronics, molecular polarity is weak. Linear molecular shape. Chemical properties of carbon monoxide carbon monoxide molecules in the valence is +2, can be further oxidized to +4, so that a combustible and reducing carbon monoxide, carbon monoxide or oxygen in the air can be burned to produce carbon dioxide: 2CO + O2 = = == 2CO2 lit the flame burns with a blue and emit a lot of heat. So carbon monoxide can be used as fuel gas. Laboratory general use of concentrated sulfuric acid or oxalic acid catalyzed decomposition under heat and carbon dioxide with sodium hydroxide to remove carbon monoxide obtained, the specific reaction is as follows: 1.C2H2O4-Δ → CO2 ↑ + CO ↑ + H2O C2H2O4-concentrated H2SO4 → CO2 ↑ + CO ↑ + H2O2.2NaOH + CO2 = Na2CO3 + H2O carbon monoxide as a reducing agent in many metal oxides at high temperature can be reduced to elemental metal, so commonly used in metal smelting. Such as: the black copper oxide reduction in red copper and zinc will be reduced to metal zinc oxide: CO + CuO = Δ = Cu + CO2 CO + ZnO = Δ = Zn + CO2 can occur in the blast furnace in the multi-step reduction reaction: CO +3 Fe2O3 == heat == 2 Fe3O4 + CO2 Fe3O4 + CO == heat == 3FeO + CO2 FeO + CO == == Fe + CO2 Carbon monoxide high temperature reduction of iron oxide Fe2O3 +3 CO == == 2Fe + high temperature 3CO2 Note: The chemical stability of carbon monoxide carbon monoxide at room temperature, another important property: in the heat and pressure conditions, and some metal simple substance it can react to form molecular compounds. Such as Ni (CO) 4 (IV nickel carbonyl), Fe (CO) 5 (five carbonyl iron) and so on, these substances are not stable when heated decomposes into the corresponding metal and carbon monoxide, which is the purification of metals and obtained pure carbon monoxide One of the ways. However,
nike air force 1, these substances are highly toxic, and difficult to treat! Physical properties of the main ingredients: pure. Appearance: colorless, odorless, tasteless gas.
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Melting Point (℃): -199.1 Boiling Point (℃): -191.4 relative density (water = 1): 0.793 (liquid). Relative vapor density (air = 1): 0.967 Vapor Pressure (kPa): 309kPa/-180 ℃ heat of combustion (kJ / mol): Solubility: low solubility in water, but easily absorb ammonia. Stability: stable. INCOMPATIBILITY: Strong oxidizers, alkalis. Decomposition products: 400 ~ 700 ℃ between the decomposition of carbon and carbon dioxide. Hazardous characteristics: It is a flammable and explosive gases. Mixed with air can form explosive mixtures case of fire, high-heat combustion caused the explosion; and air mixture explosion matter limited to 12% to 75%. Other physical characteristics: self-ignition point 608.89 ℃. Formation mechanism of carbon monoxide is the most widely distributed in the atmosphere and the largest number of pollutants generated in the combustion process is also important pollutants. The main source of CO in the atmosphere is the combustion engine exhaust, followed by fossil fuel burning boilers. CO is generated during combustion of carbon fuels a kind of intermediate product, initially present in all carbon fuels will be the formation of CO. CO formation and destruction processes are under the control of chemical reaction kinetics mechanism is the process of hydrocarbon fuel combustion is one basic reaction, and its formation mechanism is: RH → R → RO2 → RCHO → RCO → CO where R is hydrocarbon radical group. RCO radical reactions, mainly through the decomposition of CO, oxidation of hydrocarbon groups can also be generated after R CO. CO combustion process than the rate of oxidation of CO into CO2 production rate is low, so the flames of hydrocarbons basic oxidation reaction CO: CO + H2O == == CO2 + H2 CO temperature is one of the products of incomplete combustion . If the combustion process well-organized, that with sufficient oxygen, fully mixed, sufficiently high temperatures and long residence time, will eventually burn CO intermediate is completed, generate CO2 or H2O. Therefore, controlling the emissions of CO formation is not an attempt to suppress it, but efforts to make the complete combustion. Studies have shown that hydrocarbon fuel and air premixed flame, due to the formation rate of CO very quickly, in the flame to the maximum CO concentration increased rapidly, the reaction mixture is usually higher than the maximum adiabatic combustion at a higher equilibrium value and then slowly ground down to balance the CO concentration values. Therefore, the exhaust from combustion equipment in the detection of CO levels lower than the maximum in the combustion chamber, but was larger than the equilibrium value under the exhaust. This shows that the CO chemical kinetic control of the generation and destruction. Laboratory production of carbon monoxide method: H2O + C = heat = CO + H2 CO2 + C = heat = 2CO HCOOH = concentrated H2SO4 / Δ = H2O + CO ↑ Introduction to occupational exposure to the material where the incomplete combustion of carbon, the CO can be produced gas. CO exposure in the industrial production of no less than 70 kinds of jobs, such as the metallurgical industry
CO
industry coking, iron making, blacksmiths, foundry and heat treatment of the production; chemical industry, ammonia, acetone, phosgene, methanol production; mine blasting, coal mine gas explosion; carbon graphite electrode manufacturing; internal combustion engine testing; and the production of metal carbonyl compounds such as nickel carbonyl [Ni (CO) 4], carbonyl iron [Fe (CO) 5] and other processes, or production of combustible gases containing CO (CO with water up to 40% gas, blast furnace and the furnace gas contains 30% of the gas containing 5% ~ 15%), are likely to contact with CO. Explosives or gunpowder explosion of gas containing CO by about 30% to 60%. Diesel, gasoline internal combustion engine exhaust gases containing CO is also about 1% to 8%. Carbon monoxide poisoning (carbon monoxide poisoning), also known as gas poisoning. After carbon monoxide into the body and the blood hemoglobin, the binding of CO and hemoglobin is far stronger than the binding of oxygen and hemoglobin, and thus make the oxygen combined with the sharp decline in the number of hemoglobin, causing the body tissue of oxygen, leading to the human body suffocation. Therefore, toxic carbon monoxide. Carbon monoxide is a colorless, odorless, tasteless gas, it is easy to ignore Erzhi poisoning. Common in the family room with poor ventilation conditions, the coal stove gas or liquefied petroleum gas production or industrial production of the gas pipeline leaks and carbon monoxide inhalation in the mines Erzhi poisoning. Symptoms of carbon monoxide poisoning symptoms in the following aspects: First, mild poisoning. Patients can be headache,
air force 1 high, dizziness, insomnia, blurred vision, tinnitus, nausea, vomiting, malaise, tachycardia, transient syncope. Blood carboxyhemoglobin levels of 10% -20%. Second, moderate poisoning. In addition to these symptoms have increased, the lips, nails, skin and mucous membranes appear cherry red, sweating, blood pressure first and then decreased, heart rate acceleration, arrhythmias, irritability, temporary separation of sensory and motor (that is still thinking, but not action) . Symptoms continue to increase, there may be drowsiness, coma. Carboxyhemoglobin in blood of about 30% -40%. The timely rescue, can quickly clear, generally no complications and sequelae. Third, severe poisoning. Patients quickly into a coma. The initial increase in limb muscle tone, or paroxysmal tonic spasm; advanced significantly reduce muscle tension, the patient pale or purple, blood pressure, dilated pupils, and finally due to respiratory paralysis and death. The rescue survivors may have serious complications and sequelae. Sequelae of carbon monoxide. In patients with severe poisoning, neurological weakness, tremor, paralysis, hemiplegia, hemianopia, aphasia, swallowing difficulties, mental retardation, toxic psychosis or a tonic to the brain. Some patients may occur secondary to encephalopathy. Clinical manifestations of acute poisoning with acute carbon monoxide poisoning is the largest number of morbidity and mortality of acute occupational poisoning. Many countries are also caused by accidental CO poisoning life
carbon monoxide poisoning
largest number of fatal poison. The occurrence of acute CO poisoning and exposure to CO concentration and duration. Workplace air CO of the maximum allowable concentration of 30mg/m3. Data shows that the concentration of inhaled CO in the air 240mg/m3 total of 3h, Hb in the COHb can be more than 10%; CO concentration of 292.5mg / m when the people can have a serious headache, dizziness and other symptoms, COHb can be increased to 25 %; CO concentration 117Omg/m3 when people can make inhalation more than 6Omin coma, COHb about as high as 60%. CO concentration 11700mg/m3, the minutes will enable people to death, COHb can be increased to 90%. With acute clinical symptoms and signs of cerebral hypoxia as the main performance. After exposure to CO, such as headache, dizziness, palpitations, nausea and other symptoms, the symptoms can be inhaled fresh air quickly disappeared in the case of general contact reaction. Mild poisoning be severe headache, dizziness, heart rate, blurred vision, weakness, nausea, vomiting, irritability, ataxia, mild to moderate disturbance of consciousness (such as confusion, hazy state), but no coma. Inhalation of toxic sites on the left of fresh air or oxygen for several hours, the symptoms gradually recovered. In addition to the above with moderate poisoning symptoms, facial flushing, sweating, rapid pulse, unconsciousness showed light to moderate coma. Promptly removed from the site and after poisoning gradually recover after emergency treatment, usually without significant complications or sequelae. Severe poisoning, a serious disturbance of consciousness, showing a deep coma or vegetative state. Common miosis, light reflex normal or slow, limb increased muscle tone, trismus, or paroxysmal tonic to the brain, and the cremaster reflex tendon reflex wall generally disappeared, the presence or slow tendon reflexes, and urine appeared incontinence. Cerebral edema continued to increase, the performance continued to be a deep coma, decerebrate rigidity continuous attack, pupillary light response and corneal reflex sluggish, body temperature of 39 ~ 40 ℃, fast and weak pulse, blood pressure, pale or cyanosis, cold extremities , tidal breathing occurs. Some patients with irregular fundus examination showed retinal artery spasm, venous filling, or see papilledema, increased intracranial pressure and prompted the formation of a hernia possible. However, many patients with fundus examination negative, and even CSF pressure is normal, and autopsy confirmed the final is still a serious brain edema. Treatment of patients with severe poisoning after waking from a coma in the process, often appear restless, consciousness cloudy, disorientation, or loss of far and near memory. Some patients recovered consciousness, can be found in cortical dysfunction such as apraxia (apraxia), loss of recognition (agnosia), failure to write (agraphia), aphasia (aphasia), or transient cortical blindness, deafness and other anomalies; also appear to mental retardation-based psychiatric symptoms. In addition, the short-term mild paralysis, Parkinson's syndrome, chorea, athetosis, or grand mal epilepsy Dengjun been reported. After an active salvage therapy, most patients with severe poisoning can fully recover. There were few vegetative state, manifested as loss of consciousness, eyes open,
nike air force 1 high, without a word, decerebrate rigidity, poor prognosis. In addition to the performance of cerebral hypoxia, the moderate and severe poisoning may also occur in other organs of hypoxic changes or complicated. Some patients with arrhythmias, myocardial damage or severe shock; pulmonary edema appears wet lung sounds, shortness of breath. About 1 / 5 of patients found that liver, often can be reduced after 2 weeks. Can occur due to stress ulcer upper gastrointestinal bleeding. Sometimes complicated by rhabdomyolysis (rhabdomyolysis) and fascia compartment syndrome (compartment syndrome) who, because there may be secondary to myoglobinuria with acute renal failure. Some patients with skin disorders of autonomic nervous nutrition, manifested as large limbs or trunk skin, small blisters or skin lesions similar to burns, or skin irritation into a film-like changes similar to erysipelas, after symptomatic treatment is not difficult to heal. Auditory vestibular damage can be expressed as deafness, tinnitus and eye shock; still 2% to 3% of patients with neurological damage, most commonly involved the lateral femoral cutaneous nerve, ulnar nerve, median nerve, tibial nerve, peroneal nerve , may be related to local compression after coma. Delayed encephalopathy (delayed encephalopathy) in some patients with acute CO poisoning, coma and regained consciousness, the consciousness returned to normal, but after 2 to 30 days more holiday period, and neuropsychiatric symptoms appear encephalopathy, known as delayed acute CO poisoning encephalopathy. Because of the performance of a Common clinical manifestations are the following: (1) psychiatric symptoms: sudden loss of orientation, expression indifferent, unresponsive, memory disorders, incontinence, life can not take care of themselves; or there visions, delusions, incoherent, behavioral disorders, performance such as acute psychosis of dementia stupor. (2) focal brain damage 1) extrapyramidal neurological damage: the Parkinson's syndrome more common in patients with tubular or gear limbs were like lead increased muscle tone, slow, walking out with the upper limbs with sports writing is too small or there disease, and resting tremor. A small number of patients might have chorea. 2) The cone system of nerve damage: the performance of one or both sides of the mild hemiplegia, upper extremity flexion rigidity, tendon hyperreflexia, ankle clonus positive, leads to one or both sides of the pathological reflex, motor aphasia may occur or false Palsy. 3) Other: cortical blindness, seizures, parietal lobe syndrome (agnosia, apraxia, agraphia, or miscalculation) has also been reported. 3. Low concentration of CO on the human body long-term exposure to low concentrations of CO can cause chronic poisoning, there is still controversy. Recent data suggest that long-term exposure to low concentrations of CO may cause both human health effects: (1) the nervous system: dizziness, headache, tinnitus, fatigue, sleep disorders, memory loss and other symptoms of cerebral wasting syndrome more See, neurological testing may be abnormal, more than from the CO can be restored after exposure. The persistent symptoms who tend to have multiple mild acute CO poisoning in history. (2) the cardiovascular system: ECG arrhythmia can occur, ST segment depression, QT interval prolongation, or right bundle branch block and other abnormalities. Occupational exposure to COHb in the saturation of more than 5%, you can see the serum lactate dehydrogenase (LDH), hydroxybutyrate dehydrogenase (HBD), creatine phosphokinase (CPK) increased the enzyme activity may increase related to myocardial damage. In addition, population survey found that about 20% to 25% of COHb in blood of smokers than 8% to 10%, the rate of sudden death were myocardial infarction is higher than non-smokers. In recent years, coronary artery of 63 patients found that the level of exposure to CO to COHb increased from 0.6% to 2% and 3.9%, its emergence time of myocardial infarction and angina in advance, on the exercise tolerance was significantly lower . These survey data, combined with animal studies, suggesting that low concentrations of CO in long-term effects, the cardiovascular system may be adversely affected. With the hemoglobin oxygen binding capacity of two times. 【Prevention】 in the production sites, should enhance natural ventilation, pipes and valves to prevent leakage. Conditions, the available CO automatic alarm. Mine blasting, should strictly abide by the rules, must be ventilated before entering the work 2Omin. Higher concentration of CO into the environment, the need to wear gas mask oxygen supply to operate. Winter heating season, should promote the knowledge of universal access to prevention, to prevent the life of the CO poisoning incidents. Cure of acute CO poisoning patients discharged from the families should be reminded to continue to observe the patient 2 months, where there is delayed encephalopathy symptoms, should be promptly reviewed and processed. 】 【Detoxification cause if inhaled small amounts of CO poisoning, should be plenty of fresh air, or inhalation of artificial respiration. Medical care can be injected through the blood of methylene blue for detoxification, because the CO and the combination of methylene blue stronger than carboxyhemoglobin, which is conducive to CO shift the release of methylene blue and hemoglobin returned to normal respiration. Carbon monoxide can be life-saving 60s of last century, people know that the body tissues by the toxins, ultraviolet radiation, hormones and drugs abuse, the heme oxygenase -1 (referred to as HO-1) would be the appropriate time against injury and infection, the when the body would naturally produce small amounts of carbon monoxide. However, when people think that carbon monoxide is a by-product of tissue metabolism. However, American scientists made in 1993, Solomon Snyder, carbon monoxide in the body plays a significant role. It has Nitric oxide administration to assist the function of internal organs, such as contraction of the large intestine, gastric emptying and so on. However, the researchers made a lot of effort, or did not check out the carbon monoxide in the exact role of the human body. beneficial to humans because of carbon monoxide Some scientists want it used for clinical treatment. However, carbon monoxide is a poisonous gas, the use of a little inappropriate, it will cause harm to humans. monoxide can be tightly bound to hemoglobin in red blood cells, the formation of carboxylation hemoglobin, the oxygen can not be carried to body. When about 20% of the body of hemoglobin into carboxylation hemoglobin, there will be nausea, vomiting and fainted in the situation; when about 40% of the body into carboxylation hemoglobin hemoglobin, it will takes away people's lives. Therefore, some scientists object to the introduction of carbon monoxide in human clinical therapy. but the U.S. 奥古斯丁乔 and Fritz Becky said, medicine should not be so quickly reject the therapeutic potential of carbon monoxide, carbon monoxide treatment is the best emergency methods. first half of 2001, Joe and Becky team led, in patients with trace of carbon monoxide inhalation can help prevent organ rejection. when they are conducting mouse heart transplantation, with something called HO-1 drugs will be closed the week mice transplanted with rejection reaction. But if the mice were placed contained traces of carbon monoxide in the air, you can survive. In other words, the trace of carbon monoxide inhalation in animals can be completed H0-1 can accomplish. This experiment also shows that the 20th century, people of 60 years found that HO-1 is not a metabolic waste of carbon monoxide, but the role of HO-1, the human body as a physiological defense reaction produced by the gas. 2001 In the end, David Pinsky, the United States experiments show that carbon monoxide on lung transplantation is also a great help. Lipinski change the genetic characteristics of some rats, so they lack the manufacture of HO-1 gene, and then let them and simulation of normal mice with lung transplantation. Lipinski with the clip cut off the blood supply to the rat left lung, an hour later let them regain mobility. Results The survival rate was 90% of the mice, and all changed genes The mice were killed have a blood clot in the lungs. In a further experiment, when Lipinski to the changed genes in mice breathing trace of carbon monoxide, only half of the mice died. At present, thousands of people each year of lung transplant 30% failure rate than other organ transplant failure rate is higher, for example, kidney transplant failure rate of only 10%. Therefore, medical scientists hope to the treatment of carbon monoxide introduced into the lung transplantation surgery. At present there are some doctors to carbon monoxide for clinical surgery, and achieved certain results. hazards of carbon monoxide (co) is a kind of blood,
air force one high, and nervous system are highly toxic pollutants., air carbon monoxide (co), through the respiratory system, blood enters the human body , and blood hemoglobin (hemoglobin, hb). Muscle myoglobin. Divalent iron with respiratory enzymes, forming reversible conjugates. The combination of carbon monoxide and hemoglobin not only reduces the ability of blood to carry oxygen, but also inhibited oxygen hemoglobin delay (o2hb) of the resolution and release, resulting in necrosis of the tissues from lack of oxygen, severe cases may endanger human life. Under normal circumstances, through the respiratory system of oxygen into the blood, with hemoglobin (hb), forming the oxygen hemoglobin (o2hb) is transported to the body's various organs and tissues involved in normal metabolic activity. Than if excessive concentrations of carbon monoxide in the air, a lot of blood carbon monoxide will enter the body. Of carbon monoxide into the blood, priority and hemoglobin (hb), forming carboxyhemoglobin (cohb), carbon monoxide binding with hemoglobin than oxygen binding with hemoglobin large 2 million to 3 times. Carboxyhemoglobin (cohb) the dissociation rate, but oxygen hemoglobin (o2hb 1 / 36 million. Harmful levels of carbon monoxide on the body depends largely on the concentration of carbon monoxide in the air with high concentrations of carbon monoxide in the air absorbed by the body length of time. Monoxide poisoning in the blood carboxyhemoglobin (cohb) the content and the concentration of carbon monoxide in the air is directly proportional to the severity of the poisoning and blood carboxyhemoglobin (cohb) content are directly related. In addition, the body's hemoglobin (hb) of the metabolic process can also produce carbon monoxide, endogenous formation of carboxyhemoglobin (cohb). normally the body, the general carboxyhemoglobin (cohb) accounted for only 0.4 to 1.0%, anemia in patients will be higher. heart and brain, and human life is most closely related tissues and organs, heart and brain responses of the body particularly sensitive to oxygen deficiency. Thus, carbon monoxide poisoning caused by the body tissue hypoxia on the heart and the most significant influence on the brain, the body within the blood carboxyhemoglobin (cohb) can reach more than 2%, causing the nervous system response, for example, for example, slow, and confusion. than if the carbon monoxide concentration of 30ppm, the blood carboxyhemoglobin (cohb) can be achieved 5%, can lead to visual and hearing impairment; when the blood hemoglobin and oxygen (cohb) more than 10%, the body will be severe poisoning symptoms, cases, for example, headache. dizziness. disgusting. chest tightness. weakness. Confusion and so on. monoxide poisoning can cause serious heart damage. When carboxyhemoglobin (cohb) more than 5%, the coronary blood flow increased significantly; cohb to 10%, 25% of coronary blood flow and myocardial oxygen uptake reduction in the number, resulting in some cells to oxidative enzyme system activities to stop. monoxide poisoning can also cause accumulation of lipids within the blood vessels increased, leading to atherosclerosis. arteriosclerosis patients more prone to carbon monoxide poisoning. 2.5% or even 1.7% carboxyhemoglobin (cohb), can make the onset of angina patients significantly shortened the time. As CO [in] the cumulative effect of muscle, even [in] Stop, after inhaling high concentrations of carbon monoxide, [in ] within a few days, the body will still feel the muscle weakness. monoxide poisoning on the most serious damage to the cerebral cortex, often resulting in softening of brain tissue. necrosis. U.S. health departments to carboxyhemoglobin (cohb) not more than 2% of the development in air carbon monoxide (co) limit of the standard basis. taking into account the elderly. Child safety in patients with cardiovascular diseases, environmental health authorities in China: the air of carbon monoxide (co) of the daily average concentration shall not exceed 1 mg / cubic meter (0.8 ppm); a determination of maximum allowable concentration of 3 mg / m (2.4ppm). cohb the body content of the normal level of 0.5%, the safety threshold of about 10%. When cohb content reaches 25% ~ 30% showed symptoms of poisoning,
nike air force one, after a few hours into a coma. When cohb content reached 70%, instantly killed. cohb in the blood content of 30% to 40%, the blood showed cherry red skin. nails. mucosa and lips show both the Department of . At the same time, there was even a headache. nausea. vomiting. palpitations and other symptoms, or even suddenly collapsed. depth of poisoning convulsions, cerebral and pulmonary edema, myocardial damage and other symptoms, such as not timely rescue, easily leads to death. monoxide pollution health effects of carbon monoxide (CO) is a coal, oil and other carbon material product of incomplete combustion, is a colorless, odorless, non-irritating poisonous gas, almost insoluble in water, easily in the air and other substances chemical reaction, it can be in the atmosphere for 2 to 3 years. such as local pollution is serious, there are certain hazards on human health. troposphere pollution sources in the background concentration of carbon monoxide is about 0.1 ~ 2ppm, such content on the human body harmless. As the world transport business, the continuous development of industrial and mining enterprises, coal and oil fuel consumption continues to grow, carbon monoxide emissions also increase. According to incomplete statistics, in 1970, the world total carbon monoxide emissions by up to 3.71 million tons. which accounts for vehicle exhaust discharge 237 million tons, accounting for about 64%, becoming increasingly serious urban air pollution sources. samovar stove heating and the use of, not only pollute the indoor air, but also increased the city's air pollution. some of the natural disasters such as volcanic eruptions, forest fires, earthquakes, mine explosions and disasters, can also cause carbon monoxide concentration increased in some areas. Smoking can also cause carbon monoxide pollution hazard. hazards and mechanisms of carbon monoxide in the air enter the body through blood circulation into the alveolar later, with blood hemoglobin (Hb), muscle myoglobin and ferrous iron containing enzymes of cell respiration reversibly combine to form. monoxide and hemoglobin oxygen affinity than the affinity of hemoglobin from 200 to 300 times as large, Thus, carbon monoxide intrusion body, will soon be combined into carboxyhemoglobin and hemoglobin (COHb), thereby preventing oxygen and hemoglobin into oxyhemoglobin (HbO2). but carboxyhemoglobin only oxyhemoglobin dissociation rate 1 / 3600, which extended the dissociation of carboxyhemoglobin time and increase the role of carbon monoxide poisoning. the severity of carbon monoxide poisoning, showing a clear dose - response relationship. The higher the concentration of carbon monoxide inhalation, oxygen saturation of hemoglobin (oxygen The percentage of total hemoglobin hemoglobin) is also higher, the shorter the time to reach saturation. can be seen from the inhalation of carbon monoxide concentration of 0.01%, over 8 hours later, oxygen saturation of hemoglobin is about 10%, no significant symptoms; but 0.5% inspired concentration of carbon monoxide, as long as 20 to 30 minutes, Carboxyhemoglobin can reach about 70%. poisoning will appear weak pulse, slow breathing, and finally failure death. This acute carbon monoxide poisoning accidents often occurred in the workshop and winter when home heating accidentally. prolonged exposure to low concentrations of carbon monoxide will cause chronic poisoning, there are two views: one that formed in the blood carboxyhemoglobin solution can be gradually from, as long as the disengagement, the role of carbon monoxide poisoning can be gradually eliminated, and therefore there is no chronic carbon monoxide poisoning; the other that exposure to low concentrations of carbon monoxide can cause chronic poisoning. In recent years, many animal experiments and epidemiological surveys have proved long-term exposure to low concentrations of carbon monoxide on health impact, mainly in: ① the impact on the cardiovascular system. SM Ayres et al found that when the blood oxygen saturation of hemoglobin of 8%, the venous oxygen tension reduction, which led to decreased myocardial oxygen consumption and promote some of the cells to cease their activities within the oxidase system. P. Aspen Troup and others also show that CO can induce lipid accumulation in large vessels increased in the class. When blood carbon hemoglobin up to 15% oxygen, can cause major vascular endothelium to increase the intake of cholesterol and promote cholesterol deposition, so that the original increased atherosclerosis, which affects cardiac muscle, the abnormal electrocardiogram. ② effects on the nervous system. The brain is the largest organ in the human body oxygen consumption, but also the most sensitive organ to hypoxia. Animal experiments showed that the brain's absorption of carbon monoxide was significantly higher than the heart, lung, liver, kidney and so on. monoxide into the body, the cerebral cortex and white ball hardest. hypoxic apnea can also cause cell respiration within, the occurrence of softening and necrosis, there narrow vision, hearing loss; light are also headache, dizziness, and decreased memory, neurasthenia syndrome, and both precordial needle-like sense of urgency and pain. ③ causing hypoxemia. appears red blood cells, hemoglobin and other compensatory increase in their symptoms and pathological changes induced by hypoxia similar. ④ impact on future generations. by smoking and non-smoking observation of pregnant women, fetuses of pregnant women smoke, there is a small birth weight and the tendency of mental retardation. monoxide control measures to develop and implement standards of hygiene. the United States, taking into account the case of labor intensity, provides access to 8-hour carbon monoxide standard 9ppm, exposure to 1 hour to 35ppm. China, the maximum allowable concentration of 30 mg / m 3. In addition, reforms to improve vehicle fuel and industrial production processes, so that the fuel is burnt; strengthen the management of winter heating, the room ventilation, heating stove installed in the exhaust ventilation equipment, etc., can to some extent, to prevent carbon monoxide poisoning. TOXICOLOGICAL INFORMATION Acute toxicity: LC50: Mouse 2300 ~ 5700mg/m3, guinea pigs 1000 ~ 3300mg/m3, Rabbit 4600 ~ 17200mg/m3, Cat 4600 ~ 45800mg/m3, dog 34400 ~ 45800mg / m3. sub-acute and chronic toxicity: rats inhaled 0.047 ~ 0.053mg / L, 4 ~ 8h / d,
air force one low, 30d, there slow growth, increased hemoglobin and red blood cell count, liver succinate dehydrogenase and cytochrome oxidase activity has been damaged. monkey inhalation 0.11mg / L, after 3 to 6 months induced myocardial injury. Metabolism: Carbon monoxide in the air inhaled through the alveoli into the blood circulation, and blood hemoglobin (Hb) and blood other than some iron-containing proteins (such as myoglobin, cytochrome divalent iron, etc.) form a reversible combination. More than 90% Hb together to form carbon monoxide and carboxyhemoglobin (HbCO), about 7% of the carbon monoxide combines with myoglobin into myoglobin oxygen, only a small amount of cytochrome combination. Experiments show that not accumulate in the body of carbon monoxide, carbon monoxide animal inhalation 200ppm for 1 month, stopped 24h after carbon monoxide poisoning has been completely discharged, the prototype of which 98.5% is excreted by the lungs, only l% oxidized into carbon dioxide in the body. monoxide absorption and elimination, depending on the partial pressure of carbon monoxide in the air and blood HbCO saturation (ie, the total Hb was combined with the percentage of carbon monoxide.) secondary contact time factors and lung ventilation; which are directly related to labor intensity. poisoning mechanism: is carbon monoxide and hemoglobin (Hb) induced by hypoxia in irreversible binding, is generally believed that the affinity of carbon monoxide and Hb and Hb oxygen affinity than the big 230 to 270 times, so the blood oxyhemoglobin (HbO2) forced out of oxygen, the formation of HbCO, and because the dissociation of HbCO 3600 times slower than HbO2, HbCO therefore more stable than HbO2. HbCO not of itself have the function of carrying oxygen, its existence also affect the HbO2 dissociation, so the role of tissue hypoxia by a double. eventually leading to tissue hypoxia and carbon dioxide retention, resulting in symptoms of poisoning. Hazard classification (GB5044-85): II-class (high hazard). Other harmful effects: the substance harm to the environment, with special attention to surface water, soil, air and water pollution. non-biodegradable: CO in the physical and chemical properties showed that the removal of CO in the atmosphere mainly through reaction with hydroxyl carbon monoxide, and its final product carbon dioxide. annual emissions in the atmosphere, the vast majority of CO reaction with the hydroxyl groups removed about 85%, the soil absorbs 10%, the rest spread to the stratosphere. In the annual emissions and removal process, there is a small small imbalance, causing the CO to increase 1% each year. This imbalance may be due to human activities cause emissions to increase. CO average concentration 100μg/m3, in the atmosphere is about 400 million tons of total CO ; carbon monoxide, the average life span is about 2 months. monoxide poisoning symptoms: (1) mild poisoning. may present with headache, dizziness, insomnia, blurred vision, tinnitus, nausea, vomiting, malaise, tachycardia, transient syncope. blood carboxyhemoglobin levels of 10% -20%. (2) moderate poisoning. In addition to the symptoms worsened, the lips, nails, skin and mucous membranes appear cherry red, sweating, blood pressure first and then decreased, heart rate accelerated , arrhythmias, irritability, temporary separation of sensory and motor (that is still thinking, but not action). the symptoms continue to increase, there may be drowsiness, coma. carboxyhemoglobin in blood of about 30% -40%. by the time rescue
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