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carbon monoxide


Carbon monoxide (carbon monoxide, CO) Pure product is colorless, odorless, non-irritating gas. Molecular weight 28.01, density 1.250g/l, the freezing point of -207 ℃, the boiling point of -190 ° C. Very low solubility in water, but soluble in ammonia. Air mixture explosion limit of 12.5% ​​to 74%. Carbon monoxide enters the body and the hemoglobin in the blood, thereby enabling the hemoglobin can not combine with oxygen, causing body tissue hypoxia, resulting in the death of human asphyxia. Thus carbon monoxide is toxic. Carbon monoxide is a colorless, odorless, tasteless gas, it is easy to ignore Erzhi poisoning. Common in the family room ventilation, coal stove gas or liquefied petroleum gas pipeline leak or industrial production, gas and carbon monoxide in the mine inhalation Erzhi poisoning.


This gas is used to the execution of the Greeks and Romans in ancient times, in the 11th century, a Spanish doctor who first described this gas. Preparation of carbon monoxide is the French chemist de Lassone (1776). He had carbon monoxide by heating zinc oxide and carbon system. However, due to the combustion of the carbon monoxide and hydrogen is similar to the blue flame, de Lassone mistakenly believe that he obtained is hydrogen. In 1800 the British chemist William Cruikshank carbon monoxide is a compound composed of carbon and oxygen.
is the first thorough study of the French physiologist Claude Bernard of carbon monoxide toxicity. In 1846, he let the dog to inhalation of this gas and found the dog's blood become more than should be bright red blood in any artery. We now know that the blood into a "cherry red" is the symptoms of carbon monoxide poisoning.
carbon monoxide in the blood to become very red features, and some meat merchants of fresh meat treated with carbon monoxide, can make the raw meat is not oxidized color, and can even be kept for 28 days under 10 ° C temperature as the new slaughtered meat, and therefore objectionable. Consumer Federation of America that even if such processing is not harmful, will cover the meat is not fresh, even if the meat is about to rot state, consumers are unaware of.


electronic structure

carbon in the outermost layer of the outermost of four electrons and oxygen has six electrons, so that carbon two single-electron into two single-electron pair of the oxygen p orbit of oxygen bonding, so that the formation of two keys, then oxygen lone electron pair into the empty carbon p orbital in the formation of a distribution key, so that oxygen and carbon the formation of the three keys. Electronic: C ::: O:
molecular structure: carbon monoxide molecule is a polar molecule, but due to the presence of feedback π bond, the polarity of the molecules is weak. The molecular shape is linear.

carbon monoxide structure

carbon monoxide (carbon monoxide) (CO)

carbon monoxide

physical properties in normal conditions, carbon monoxide is a colorless, odorless, tasteless, insoluble in water, gas, melting point -207 ° C, the boiling point of -191.5 ° C. Standard conditions of gas density is 1.25g/L, and density of air (standard conditions under 1.293g/L) the difference is small, which is also prone to one of the factors of gas poisoning. It


neutral gas.

chemical properties and chemical properties: flammability and reducing toxicity
The valence of carbon in the carbon monoxide molecule is +2, can be further oxidized to +4, so that carbon monoxide flammability and reducing carbon monoxide burning in air or oxygen to produce carbon dioxide:
2CO + O2 == lit == 2CO2
burning issue blue flame to release a lot of heat. Carbon monoxide can be used as fuel gas.
Laboratory of the general use of concentrated sulfuric acid catalysis or heating oxalic acid decomposition and carbon monoxide with sodium hydroxide to get rid of carbon dioxide in the system, the specific reaction is as follows:
1.C2H2O4 = heat = of CO2? + CO? + H2O
C2H2O4 = Concentrated of H2SO4 = of CO2? + CO? + H2O
2NaOH + CO2 = Na2CO3 + H2O
able to when the carbon monoxide as a reducing agent, high temperature or heating metal oxide reduced to metal simple substance, and therefore commonly used in metal smelting. Such as: black copper oxide is reduced to red copper, zinc oxide is reduced to metallic zinc:
Special Note: unless it is prepared under strict protection of Ni (CO) 4, otherwise may not use reduction by CO of NiO because the reaction to generate highly toxic Ni (CO) 4
NiO +5 CO = Δ = Ni (CO) 4 + CO2
CO + CuO = Δ = Cu + CO2
CO + ZnO == Zn + CO2
in the blast furnace can occur in multi-step reaction:
CO +3 Fe2O3 == high temperature == 2 Fe3O4 + CO2
Fe3O4 + CO == high temperature == 3FeO + CO2
FeO + CO == high temperature == Fe + CO2
CO Hematite Reduction of Fe2O3 +3 CO == high temperature == 2Fe +3 of CO2
Note: The carbon monoxide at room temperature, chemically stable, but still be able to participate in the reaction, but pay particular attention to the simple solution of potassium permanganate reaction with carbon monoxide.
common room temperature CO oxidation reaction is as follows
CO + PdCl2 + H2O = CO2 + Pd +2 HCl
5CO + I2O5 → I2 + 5CO2
carbon monoxide, there is an important properties:
in the heat and pressure conditions, it can, and some single mass of metal react to form molecules. Of Ni (of CO) 4 (four carbonyl-based nickel), Fe (of CO) 5 (five carbonyl-based iron) and so on, these substances are not stable, when heated immediately decompose into the corresponding metal and carbon monoxide, the purification of metal and the system have pure carbon monoxide One of the ways. However, these substances are highly toxic, and treatment is extremely difficult!
under certain conditions, CO and powder NaOH reaction generates sodium formate, CO as formic acid anhydride.
NaOH + of CO == HCOONa (473K 1.01X10 ^ 3 kPa)
toxicity. CO with hemoglobin, the hemoglobin can not combine with oxygen to cause human poisoning.

physicochemical constants

The main ingredients: pure.
CAS No. :630 -08-0
InChI: InChI = 1/CO/c1-2
Appearance and properties: colorless, odorless, tasteless gas.

carbon monoxide detector

Melting point (° C): -199.1
boiling point (° C): -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): 283.0 kJ · mol
Solubility: solubility in water, but easily absorbed by the ammonia.
Stability: stable.
INCOMPATIBILITY: Strong oxidizers, bases.
decomposition products: from 400 to 700 ℃ decomposed into carbon and carbon dioxide.
hazardous characteristics: a flammable and explosive gases. Mixed with air can form explosive mixtures in case of fire, high-heat combustion caused the explosion; explosion limit of 12% to 75% with air mixed material.
other physical properties: spontaneous combustion point of 608.89 ° C

generation mechanism

Carbon monoxide is distributed in the atmosphere the most extensive and largest number of pollutants, combustion generated pollutants. The main source of atmospheric CO combustion engine exhaust, followed by the burning of fossil fuels in the boiler.
CO is an intermediate product generated in the process of combustion of carbon fuels, originally exist in all the carbon in the fuel will form CO CO formation and destruction processes are affected by the chemical reaction mechanisms of control, is one of the basic reactions of hydrocarbon fuel combustion process, its mechanism of formation:
RH → R → RO2 → RCHO → RCO → CO
type in R is a hydrocarbon radicals. Reaction of RCO radicals by thermal decomposition CO, can also be oxidized hydrocarbon group R generated of CO Combustion process, CO oxidation than CO, the rate of CO2 formation rate, so the CO oxidation reaction in the flame of hydrocarbons:
CO + H2O == high temperature == CO2 + H2
CO is a product of incomplete combustion. Combustion process if the organization is good, that is, with sufficient oxygen, adequate mixing, a high enough temperature and long residence time, the intermediate product CO would eventually burning is completed, generate CO2 or H2O. Therefore, control of CO emissions is not an attempt to inhibit its formation, but efforts to complete combustion.
show that the hydrocarbon fuel and air premixed combustion flame, CO production rate quickly rose rapidly to the maximum CO concentration in the flame zone, the maximum value is usually higher than the reaction mixture in the adiabatic burning when the equilibrium value, then the CO concentration slowly drops to the equilibrium value. Therefore, from the exhaust of combustion equipment to detect the CO content than the maximum in the combustion chamber is low, but significantly greater than the exhaust state equilibrium value. This indicates that the chemical kinetic control of CO production and destruction.
carbon monoxide laboratory system of law:
H2O + C = high-temperature = of CO + H2
CO2 + C = high-temperature = 2CO
HCOOH = Concentrated of H2SO4/Δ = H2O, + CO ↑

occupational exposure


where the carbonaceous material of incomplete combustion can produce CO gas. No less than 70 kinds of contacts in the industrial production of CO operations, such as metallurgical industry

carbon monoxide

coking, iron making, blacksmiths, foundry and heat treatment in the industry production; the chemical industry in the synthetic ammonia , phosgene, acetone, methanol production; mine blasting, coal mine gas explosion; carbon-graphite electrode manufacturing; internal combustion engine test; and production metal carbonyl objects such as carbonyl-based nickel [of Ni (of CO) 4], Carbonyl iron [of Fe (of CO) 5] process, or production of combustible gases containing CO, (such as water gas containing CO by 40%, with 30% in the blast furnace and the furnace gas, gas containing 5% ~ 15%), all that may come into contact with CO Explosives or gunpowder to explode, the gas containing CO about 30% to 60%. The use of diesel, gasoline internal combustion engine exhaust containing CO about 1% to 8%.

carbon monoxide poisoning

(carbon monoxide poisoning), also known as gas poisoning.
carbon monoxide enters the body and blood hemoglobin combination of CO with hemoglobin binding capacity is far stronger than the oxygen and hemoglobin binding capacity, thus drastically reduced the amount of hemoglobin can combine with oxygen, causing the body tissue hypoxia, resulting in the death of human asphyxia. Thus carbon monoxide is toxic. Carbon monoxide is a colorless, odorless, tasteless gas, it is easy to ignore Erzhi poisoning. Common in the family room ventilation, coal stove gas or liquefied petroleum gas pipeline leak or industrial production, gas and carbon monoxide in the mine inhalation Erzhi poisoning.

poisoning symptoms

carbon monoxide poisoning symptoms in the following areas:
First, the mild poisoning. They may present with headache, dizziness, insomnia, blurred vision, tinnitus, nausea, vomiting, malaise, tachycardia, short syncope. Blood carboxyhemoglobin content of 10% -20%.
The second is moderate poisoning. In addition to the above symptoms, lips, nails, skin and mucous membranes to reduce cherry red, sweating, blood pressure increased, heart rate, arrhythmia, irritability, temporary nature of sensory and motor separation (ie, still thinking, but not action) . The symptoms continued to increase, drowsiness, coma. Carboxyhemoglobin in the blood of about 30% -40%. Timely rescue, the faster a clear, generally no complications and sequelae.
Third, severe poisoning. Patients quickly into a coma. Early limb muscle tension increases, or paroxysmal tonic spasm; late muscle tone significantly lower in patients with pale or bruising, blood pressure, dilated pupils, and finally respiratory paralysis and death. The rescue of survivors may have serious complications and sequelae.
sequelae of carbon monoxide.
in severe poisoning patients with neurasthenia, paralysis agitans, hemiplegia, hemianopia, aphasia, swallowing difficulties, intellectual impairment, toxic psychosis, or tonic to the brain. Some patients may occur secondary encephalopathy.

clinical manifestations

acute poisoning with acute carbon monoxide poisoning is acute occupational poisoning of our incidence and deaths. CO in many countries caused by the accidents of life poisoning

carbon monoxide poisoning

the largest number of fatal poison. The occurrence of acute CO poisoning and exposure to the CO concentration and time. The maximum allowable concentration of CO in our workshop in the air to 30mg/m3. Data demonstrate that in the air inhaled CO concentration 240mg/m3 total of 3h, Hb in COHb of more than 10%; CO concentration up to 292.5mg/m, can produce severe headaches, dizziness and other symptoms, levels of COHb can be increased to 25 %; CO concentration of 117Omg/m3 inhalation coma more than 6Omin make people about high levels of COHb to 60%. CO concentration of 11700mg/m3 allows people to lethal levels of COHb can be increased to 90% within a few minutes.
acute cerebral ischemia in the clinical symptoms and signs as the main performance. Exposure to CO, such as headache, dizziness, palpitations, nausea and other symptoms, the symptoms after the inhalation of fresh air can quickly disappear, is a general contact reaction.mild poisoning
severe headache, dizziness, heart rate, blurred vision, weakness, nausea, vomiting, irritability, unsteady gait, mild to moderate disturbance of consciousness (such as confusion, dim state), but no coma. Leave the poisoned place to breathe fresh air or oxygen for several hours, the symptoms gradually recovered completely. Moderate poisoning, in addition to the above symptoms, flushing, sweating, rapid pulse, disturbance of consciousness manifested as light to moderate coma. Timely shift to the place from poisoning and can be gradually restored after the rescue, in general no significant complications or sequelae.
severe poisoning, serious disturbance of consciousness, was a deep coma or vegetative state. Common miosis, normal light reflex or slow, limbs, increased muscle tone, trismus, or paroxysmal decerebrate rigidity, tendon wall reflex and cremaster reflex generally disappears, tendon reflexes or slow, and may appear toilet incontinence. Cerebral edema continues to grow, the performance continued to be a deep coma, continuous brain tonic seizures, pupillary reactions and corneal reflex sluggish, fever up to 39 to 40 ℃, the fast but weak pulse, blood pressure, pale or cyanosis, cold extremities, , tidal breathing. Some patients with fundus examination showed irregular spasm of retinal artery, vein filling, or see papilledema prompted increased intracranial pressure and herniation. But many patients fundus examination was negative, even the normal pressure of the cerebrospinal fluid examination, and pathologic anatomy of the end proved to have severe brain edema.
severe poisoning patients through the process of treatment from the coma, and often appear restless, cloudy consciousness, disorientation, or loss of recent memory. Consciousness recovery in some patients, can be found in the cortical dysfunction such as apraxia (apraxia), agnosia (agnosia), agraphia (agraphia), aphasia (aphasia), cortical blindness or deafness had abnormal; also appear to mental retardation based psychiatric symptoms. In addition, short-lived and mild paralysis, parkinsonism, chorea, hand, foot and Xu hyperactivity disorder or epilepsy grand mal Dengjun was reported. After an active life-saving treatment, the majority of patients with severe poisoning can still be fully restored. The small number of patients with vegetative state, showing loss of consciousness, eyes open, without a word, and decerebrate rigidity, and poor prognosis.
In addition to the performance of the above-mentioned cerebral hypoxia, severe poisoning can also occur in other organs of hypoxic changes or concurrent. Arrhythmia in some patients, severe myocardial damage or shock; auscultation the lungs, pulmonary edema, difficulty in breathing. About 1/5 of the patients found that the liver, often can be reduced after two weeks. Gastrointestinal bleeding due to stress ulcer may appear on. Sometimes complicated by rhabdomyolysis (rhabdomyolysis), and compartment syndrome (compartment syndrome), may be secondary to myoglobinuria, acute renal failure. Some patients with skin's own neurotrophic disorders, large and small blisters or burn-like skin lesions, or skin into tablets swelling similar to erysipelas-like changes in the performance of the limbs or trunk skin, and by symptomatic treatment is not difficult to heal. Auditory vestibular damage can be manifested as deafness, tinnitus and eye shocks; there are 2% to 3% of patients with neurological damage, the most commonly involved the lateral femoral cutaneous nerve, the ulnar nerve, median nerve, tibial nerve, sural nerve, may be related to the partial pressure after the coma. of delayed encephalopathy

(delayed encephalopathy)

part of acute CO poisoning patients in the wake of the coma, consciousness returned to normal, but after 30 days of leave more of the neuropsychiatric symptoms of encephalopathy, known as delayed encephalopathy after acute CO poisoning. The clinical course showed biphasic "also called" acute CO poisoning of the nervous system after complications. Common clinical manifestations are the following:
(1) psychiatric symptoms: sudden onset of disorientation, apathy, unresponsive, memory impairment, incontinence, life can not take care of themselves; or visual hallucination, delusions, incoherent speech, abnormal behavior, performance, such as acute dementia, stupor type of mental illness.
(2) focal cerebral damage
1) extrapyramidal neurological damage: Parkinson's syndrome more common in the limbs of patients showed a lead tube or the gear-like increased muscle tone, slow, losing with with movement of the upper limbs when walking or writing is too small disease and resting tremor. The small number of patients the chorea.
2) of the cone system of nerve damage: the performance of one or both sides with mild hemiplegia, rigidity of the upper limb flexion, tendon hyperreflexia, ankle clonus positive, leads to one or both sides pathological reflex may also be motor aphasia, or pseudobulbar palsy.
3): cortical blindness, seizures, parietal lobe syndrome (agnosia, apraxia, agraphia or miscalculated) also has been reported.
3. low concentration of CO on the human body
Long-term exposure to low concentrations of CO can cause chronic poisoning, and so far is still controversial. In recent years, the data suggest that the long-term exposure to low concentrations of CO may cause two effects on human health:
(1) of the nervous system: dizziness, headache, tinnitus, fatigue, sleep disorders, memory loss and other symptoms of brain wasting syndrome is more common neurological behavior test may be abnormal, rather than from the CO contact can be restored. Refractory to the above symptoms, often many mild acute CO poisoning.
(2) the cardiovascular system: ECG may appear arrhythmia, ST segment depression, QT interval prolongation, or right bundle branch block and other abnormalities. Occupational exposure to COHb saturation more than 5%, you can see the serum lactate dehydrogenase (LDH), hydroxybutyrate dehydrogenase (HBD), creatine phosphokinase (CPK) increased the enzyme activity increased may associated with myocardial damage. In addition, population-based surveys, found that about 20% to 25% of smokers blood COHb higher than 8% to 10%, myocardial infarction, sudden death rate than non-smokers. In recent years, 63 patients with coronary artery disease found that after exposure to CO COHb level increased from 0.6% to 2% and 3.9%, myocardial infarction and angina in advance, markedly reduced exercise tolerance . These survey data, combined with the animal studies, suggesting that the cardiovascular system may be adversely affected in the long-term effects of low concentrations of CO,. Oxygen and hemoglobin binding capacity 200 times.
production sites should enhance natural ventilation to prevent the pipeline and valve leakage. Conditions, the available automatic CO alarm. Mine blasting, should strictly abide by the rules to enter the work must ventilation 2Omin before. Into the environment a higher concentration of CO required to wear oxygen respirators operation. Winter heating season, should promote the popularization of knowledge of prevention, to prevent the occurrence of life sexual CO poisoning. Cure of acute CO poisoning patients discharged from hospital should be reminded that family members continue to observe two of the patients, such as delayed encephalopathy symptoms, they should promptly review and action.
If you inhale a small number of CO caused by poisoning, absorbing large quantities of fresh air or give artificial respiration. Medical treatment by injection of methylene blue to blood detoxification, because the combination of CO with methylene blue is more solid than the carboxyhemoglobin, thus contributing to the CO turned to the methylene blue and the release of hemoglobin, and return to normal respiration.

can be life-saving carbon monoxide

in the 1960s, people know that the body tissues by toxins, ultraviolet radiation, hormones and drugs against the heme oxygenase -1 (referred to as HO-1) will against the corresponding injury and infection, then the body will naturally produce a small amount of carbon monoxide, but when people think that carbon monoxide is a by-product of tissue metabolism.
However, Solomon Snyder, U.S. scientists in 1993, carbon monoxide play a meaningful role in the body which assist the function of internal organs of the nitric oxide, such as colon contraction, stomach after emptying. However, the researchers made a lot of effort, or did not check out the exact role of carbon monoxide in the human body.
Carbon monoxide is beneficial to humans, some scientists want it used in the treatment, however, carbon monoxide is a poisonous gas, using slightly improper, it will cause harm to humans. carbon monoxide can be tightly bound to red blood cells hemoglobin to form the carboxylation hemoglobin, oxygen can not be carried to the body when the hemoglobin of about 20% of the human body into carboxylation hemoglobin, nausea, vomiting and fainted; hemoglobin change about 40% of the human body into carboxylation hemoglobin, will be taking a life, scientists opposed to the introduction of carbon monoxide on human clinical treatment. Augustin Joe and Fritz, Becky, said the pharmaceutical industry should not be so quickly rejected the carbon monoxide the therapeutic potential of carbon monoxide therapy is the best way to emergency situations.
In the first half of 2001, the research team led by Joe and Becky pointed out that the trace of carbon monoxide to help prevent organ rejection in patients with inhalation in rat heart transplantation, called "porphyrin "chemicals HO-1 closed, the mice within one week of reaction of rejection of transplanted mice contain trace amounts of carbon monoxide in the air, you can survive. In other words, the trace of carbon monoxide inhalation in animals complete the task can be completed in H0-1 This experiment also shows that carbon monoxide is not a metabolic waste found in the study HO-1 in the 1960s, but the role of HO-1, human physiological defense reaction produced by gases.
2001 year-end, the United States, David Pinsky, experiments show that carbon monoxide would also help in the lung transplant. Lipinski change the genetic characteristics of some of the mice, making them the lack of manufacturing HO- 1 gene, and then let them and normal mice with simulated lung transplant surgery. Lipinski clip truncated supply to the rat left lung blood flow, an hour later to allow them to resume the flow. the results of the survival rate of normal mice 90% of all changed genes in mice are die to produce a blood clot in the lung. In further experiments, Lipinski changed the genes of mice breathing small amounts of carbon monoxide, only half of the mice died. Currently, the annual thousands of people, lung transplants, a failure rate of 30%, higher than the rate of failure of other organ transplants such as kidney transplant failure rate of only 10% of medicine is introduced into the therapeutic effect of carbon monoxide lung transplantation surgery, there are some doctors carbon monoxide used in clinical surgery and achieved certain results.


carbon monoxide (co) is a highly toxic blood, and nervous system of pollutants, carbon monoxide (co) in the air through the respiratory system, into the human blood with the hemoglobin in the blood (of hemoglobin, hb). Myoglobin in the muscles. The respiratory enzymes containing divalent iron to form reversible conjugates.
carbon monoxide and hemoglobin combination not only reduces the ability of blood to carry oxygen, but also inhibit, delay the oxygen hemoglobin (o2hb,) the resolution and release, leading to body tissue due to hypoxia and necrosis, severe cases may endanger people's lives.
Under normal circumstances, after the respiratory oxygen into the blood, with hemoglobin (hb) combine to form oxygen hemoglobin (o2hb,) to be transported to various organs and tissues of the body, to participate in normal metabolic activity. Than if the concentration of carbon monoxide in the air is too high, a lot of carbon monoxide into the body of blood. Of carbon monoxide into the blood, priority combined with the hemoglobin (hb) to form carboxyhemoglobin (cohb), carbon monoxide and hemoglobin binding capacity is two hundred to three hundred times larger than the binding of oxygen and hemoglobin. Carboxyhemoglobin (cohb) dissociation rate, only the oxygen hemoglobin (o2hb of 1/36 of one hundred.
harmful levels of carbon monoxide on the body, mainly depends on the concentration of carbon monoxide in the air and absorbed by the body length of time of the high concentration of carbon monoxide in the air. Is proportional to the concentration of carbon monoxide content in the air of carbon monoxide poisoning in the blood carboxyhemoglobin (cohb), the relationship between the severity of poisoning in the blood carboxyhemoglobin (cohb), content has a direct relationship. In addition, body the metabolic process of hemoglobin (hb), can also produce carbon monoxide, carboxyhemoglobin (cohb) the formation of endogenous normal body, the general carboxyhemoglobin (cohb) accounted for only 0.4 to 1.0% in patients with anemia will be higher .
heart and the brain is most closely connected with human life organizations and organs, heart and brain of the body not getting enough oxygen reaction are particularly sensitive to carbon monoxide poisoning caused by the body tissue hypoxia, the heart and brain the impact most significantly, the human blood carboxyhemoglobin (cohb) can reach more than 2%, causing the nervous system response, for example, such as slowness of movement, confusion, than if the carbon monoxide concentration of 30ppm of carbon in the human blood can reach about 5% oxygen hemoglobin (cohb,), can lead to visual and hearing impairment; when blood carboxyhemoglobin (cohb) more than 10%, the body will be in serious symptoms of poisoning, cases such as, headache, vertigo, nausea chest tightness. weak. confusion.
carbon monoxide poisoning on the heart can cause serious injury. coronary blood flow increased significantly when more than 5% carboxyhemoglobin (cohb); cohb 10%, coronary blood flow increased 25%, myocardial uptake to reduce the amount of oxygen, resulting in some organizations intracellular oxidase system activity stops. carbon monoxide poisoning can also cause increased accumulation of lipids within the vascular, leading to atherosclerosis, arteriosclerosis, more prone to carbon monoxide poisoning 2.5%, or even the 1.7 percent carboxyhemoglobin (cohb), can make patients with angina pectoris attack time is greatly reduced.
due to the cumulative effect of carbon monoxide [in] the muscles, even [in] to stop inhalation of high concentrations of carbon monoxide, [within] a few days, the body will still feel muscle weakness. carbon monoxide poisoning on the brain cortex damage is most serious, often lead to the softening of brain tissue necrosis.
U.S. health carboxyhemoglobin (cohb) does not exceed 2% as the development of the air carbon monoxide (co) limits the standard basis taking into account the safety of the elderly. Children and cardiovascular disease, China under the environmental health department: the air of carbon monoxide (co), 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 content of normal levels of the human body is about 0.5%, the safety threshold of about 10%. when cohb content of 25% to 30%, showing symptoms of poisoning, after a few hours into a coma when cohb content of 70%, immediate death. the blood cohb content reaches 30% ~ 40%, the blood showed a cherry red skin. nails. mucosa and the lips are show the same time, headache, nausea, vomiting, palpitations and other symptoms, or even suddenly collapsed. depth of poisoning symptoms of convulsions, cerebral and pulmonary edema, myocardial damage to, such as not timely rescue, can easily lead to death.

carbon monoxide pollution on health


carbon monoxide (CO), coal, oil and other carbonaceous material is a product of incomplete combustion, is a colorless, odorless, non-irritating, toxic gases, hardly soluble in water, difficult to produce a chemical reaction with other substances in the air, it can be 2 to 3 years stay in the atmosphere. Serious, such as local pollution on human health hazards.

sources of pollution

tropospheric carbon monoxide background concentration of about 0.1 ~ 2ppm, this content is not harmful to humans. Transport undertakings in the world, industrial and mining enterprises and the continuous development of fuel such as coal and oil consumption continued to grow, and carbon monoxide emissions also increase. According to incomplete statistics, in 1970, the world's total carbon monoxide emissions by up to 371 million tons. Vehicle exhaust emissions account for 237 million tons, accounting for about 64%, worsening urban air pollution sources. Heating and samovar stove, use only pollute the indoor air, but also increased the city's air pollution. The number of natural disasters such as volcanic eruptions, forest fires, pit explosion, earthquake or other disaster event, will result in increased local concentration of carbon monoxide. Smoking can also cause carbon monoxide pollution hazards.

hazards and Mechanism

into the body of carbon monoxide in the air through the alveoli into the blood circulation and blood hemoglobin (Hb), myoglobin in muscle cells and containing divalent iron respiratory enzymes and the formation of The reversibility combination. Affinity of carbon monoxide and hemoglobin is 200 ~ 300 times larger than the affinity of oxygen and hemoglobin, carbon monoxide enters the body, will soon combine with hemoglobin to carboxyhemoglobin (levels of COHb), thereby preventing oxygen and hemoglobin as oxyhemoglobin (HbO2 ). The carboxyhemoglobin just oxyhemoglobin dissociation rate of 1/3600, thus prolonging the carboxyhemoglobin dissociation time and exacerbate the toxic effects of carbon monoxide. The severity of carbon monoxide poisoning, showing a significant dose - response relationship. The higher the inhalation of carbon monoxide concentration, carboxyhemoglobin saturation (percentage of total hemoglobin, carboxyhemoglobin) the higher the saturation time is shorter. Can be seen from the Figure, the inhaled concentration of 0.01% of carbon monoxide, 8 hours, carboxyhemoglobin saturation of about 10%, and no obvious symptoms of poisoning; but when inhaled concentration of 0.5% carbon monoxide, as long as 20 to 30 minutes Carboxyhemoglobin can reach about 70%. The poisoning occurs a weak pulse, slow breathing, and finally failure death. This acute carbon monoxide poisoning often occurs in a workshop accident and winter home heating accidentally.
prolonged exposure to low concentrations of carbon monoxide can cause chronic poisoning, there are two views: One is that the formation of carboxyhemoglobin in the blood can gradually dissociation, as long as the disengagement of the toxic effects of the carbon monoxide can be gradually eliminated, thus there is no chronic carbon monoxide poisoning; another that exposure to low concentrations of carbon monoxide can cause chronic poisoning. In recent years, many animal studies and epidemiological investigations have proved that long-term exposure to low concentrations of carbon monoxide is influential on health, mainly in: ① on the cardiovascular system. SM Ayers, who found that when blood carboxyhemoglobin saturation of 8%, the venous oxygen tension is reduced, causing the myocardial uptake of oxygen reduction and promote oxidase system in some cells to stop their activities. The P. Aspen Troup, and also prove that carbon monoxide can lead to large blood vessels in the class of lipid deposition increased. When the carboxyhemoglobin in the blood of 15%, can induce large intimal cholesterol intake to increase and promote cholesterol deposition, so that the original atherosclerosis increase, thus affecting the myocardium, so that ECG abnormal. ② impact on the nervous system. The brain is the largest organ of the human body oxygen, is also the most sensitive organ to hypoxia. Animal experiments showed that the brain tissue on the absorption capacity of carbon monoxide was significantly higher than the heart, lung, liver, and kidney. Carbon monoxide enters the body, the cerebral cortex and globus pallidus hardest hit. Hypoxia can also cause suffocation cellular respiration, the occurrence of softening and necrosis, and a narrow field of vision, hearing loss; light will also be headache, dizziness, memory and reduce neurasthenia syndrome, and both precordial sense of urgency and acupuncture The kind of pain. ③ caused by hypoxemia. Compensatory increase in red blood cells, hemoglobin and other symptoms similar to the pathological changes caused by hypoxia. ④ impact on future generations. Through the observation of smoking and non-smoking pregnant women, smoking to the fetus of pregnant women, small weight and mental retardation at birth tend to.

prevention measures

development and implementation of carbon monoxide health standards. The United States in regard to the labor intensity, the provisions of exposure to 8 hours the carbon monoxide standard for 9ppm contact with one hour for 35ppm. "Design of Industrial Enterprises Standard provides: air of residential areas the maximum time allowable concentration of 3 mg/m 3, the average daily maximum permissible concentration of 1 mg/m 3, the workshop continuous contact with an eight-hour maximum allowable concentration of 30 mg/m 3.If breathing is difficult, give oxygen.Medical treatment.
physical protection: wear anti-static overalls.
Hand Protection: Wear protective gloves general operations.Cut off the fire source. The proposed emergency personnel wearing self-Pressurized respirators to wear anti-static overalls.Extinguishing Media: Water spray, foam, carbon dioxide, dry powder. The operator must go through specialized training, and strictly abide by the rules. Away from fire, heat, workplace smoking. To prevent gas leakage into the workplace air. Handling Handle gently to prevent the breakage of cylinders and accessories.
storage precautions: Store in a cool, ventilated coffers. Keep away from fire and heat source. The storage temperature should not exceed 30 ℃. Explosion-proof lighting and ventilation facilities. The storage area should be equipped with spill response equipment.Rail transport to prohibit the slide release.Two.
7.The affinity of carbon monoxide and hemoglobin is about 300 times more than the affinity of oxygen and hemoglobin, carboxyhemoglobin off than oxyhemoglobin dissociation is about 3600 times slower, and the presence of carboxyhemoglobin also inhibit the oxyhemoglobin dissociation, by inhibition of oxygen release and delivery of the body caused by acute anoxemia.Especially in the cerebral cortex, white matter and globus pallidus is the most serious. After the first spasm in the pathological manifestations of cerebrovascular expansion, increased permeability, cerebral edema and varying degrees of focal softening necrosis, clinical increased intracranial pressure or herniation, and life-threatening. Cerebral ischemia and cerebral edema may be secondary to the cerebral circulation disorders, caused by thrombosis or ischemic softening, or a wide range of demyelinating disease, caused by acute carbon monoxide poisoning of the nervous system sequelae, limb paralysis, paralysis agitans, peripheral neuritis, The autonomic nervous system dysfunction, the onset of headache, mental disorders, and even epilepsy.[Cause]

boil is caused by what the?

infection and skin dirty, scratches, high ambient temperature or lower the body resistance to infection-related. Boils can occur in any follicles of the skin area, often to the head, face, neck, armpits and buttocks so often by the friction of the parts is more common.

(a) causes

boil the pathogenic bacteria Staphylococcus aureus based, Streptococcus, Staphylococcus epidermidis, are also caused by the disease. Local and systemic skin's resistance to infection is reduced mainly due to Benbingfasheng, so infants, malnutrition, diabetes is a good risk of this disease. Dirty skin, skin abrasions, high ambient temperatures often lead to local infection such as the direct cause.

(B) the pathogenesis

bacteria invade the hair follicle and their sebaceous glands and sweat glands, in hair follicles and surrounding tissue multiply rapidly, producing toxins, causing local tissue degeneration, necrosis, and the center of the formation of boils, the performance of local congestion, exudation, induration. Aggregation of neutrophils to the damaged body tissue cells and bacteria to be destroyed, and he gradually necrosis and dissolution, the formation of abscesses in the dermis. Due to Staphylococcus aureus, coagulase contain toxins, so the formation of pus bolt, protruding outward. Swelling and induration clinically visible in the center of a yellow-white pus plug. This is Staphylococcus aureus infected lesion characteristics. Ulceration after discharge pus, abscess gradually by the new fibrous tissue repair and healing.


boil the early symptoms?

1. redness, swelling, heat, pain summary, cylindrical cone.

2. inflammation to the development of nodules increases, the pain intensified.

3. A few days later nodules central necrosis, abscess formation, dissolution, soft induration, pain relief, the central pus head most of the self-rupture, discharge pus, inflammation subsided recovery.

4. furuncle usually no obvious symptoms, but if the blood flow occurred in the rich parts of the body resistance weakened, it can cause discomfort, chills, fever, headache and loss of appetite and other symptoms of toxemia.

5. Facial Boil such as intracranial infection, facial swelling and severe, may be associated with chills, fever, headache, sinus infections and other embolization.

boil because of location, severity of different clinical manifestations may vary.

local swelling and pain sclerosis: no systemic symptoms of early disease and more, only infection redness, swelling, pain, range of not more than 2cm in diameter, small nodules gradually enlarged, as papules bulge. A few days later lesions extended about 3 ~ 5cm, nodules gradually softened, the center was white, a slight touch of the fluctuations; then ulceration pus, and the emergence of yellow-white pus plug. Pus bolt off, pus shed, the inflammation subsides and healing. There is no pus boil bolt (the so-called headless boil), since the collapse a bit late, need to find ways to promote its pus discharge (Figure 2 ).

fever, swollen lymph nodes: furuncle serious infection, the local area of ​​the lymph nodes, tenderness, and may be associated with body heat, and sometimes lymph node abscess formation.

nose, upper lip and around (called "dangerous triangle") of the surface boil, add or pushed in touch, the bacteria via the angular vein, ophthalmic vein into the brain, causing intracranial suppurative infection. At this point may have fever, headache, vomiting, consciousness disorders.

early follicular redness, swelling, heat, pain, induration. After the white purulent center, there is volatility. May be associated with systemic fever, elevated white blood cell count and differential count.


boil ate?

therapeutic side:

1. composed of: a single head of garlic, honey, 9 grams. Usage: pound evenly wrap the affected area.

2. consists of: single head of garlic amount. Usage: Peel and slice into 2 to 3 mm, with the first affected area with warm salt water when dry wash, and then sticking garlic, and gently massage the 10 to 20 minutes, 2 or 3 times a day, 2 3 There is no more. Indications: Boil, folliculitis. Note: In severe cases, such as local irritation may reduce the massage time, a serious condition should be added to serve anti-inflammatory drugs.

3 . composed of: tea 2 grams of dried honeysuckle 1 gram. Usage: boiling water 6 minutes after each meal drink in a cup. Indications: Boil, exogenous heat.

4. composed of: fresh Malan first 100 grams, the amount of liquor. Usage: Add a little salt before blindly smashed wine Ban Cheng paste, coating the surface of the skin furuncle carbuncle. Indications: furuncle, carbuncle.

5. Composition: rosin 10 grams of white wine. Usage: rosin research to fine tune white wine into a paste, resisting heat, wrap the affected area after dissolution, for the degree of responsibility to cover all of the above and then covered with wax paper and tape securely, to enhance efficacy, can drop a few drops of wine, rosin to keep moist. Indications: furuncle, carbuncle, folliculitis.

6. smashed topical papaya leaves, swollen boil carbuncle treatment drug.

7. fresh peach leaf, plug smashed the lesion, treatment of nasal furuncle.

8. rhizome or fresh banana leaves smashed Jiao Zhi, coating the surface of the skin, cure carbuncles, boils, swelling.

9. almond powder with sesame oil paint, heat treatment boil.

10. Purple cane coal deposit of the skin, powder, paint the affected area or sesame oil dressing, boil carbuncle treatment, stomatitis , eczema.

11. raw taro add a little salt, smashed drunk wrap the affected area twice a day replacement, bones can cure pain, swelling of unknown drugs, pediatric head hot boil, finger boil.

12. raw loofah (or leaf), smashed juice, coated surface of the skin, soak sore treatment days, yellow water sores, heat boils, urticaria .

13. mung bean sugar kelp: seaweed 60 grams, shredded, green beans, 150 grams, with the soup, add brown sugar to taste food. There Sedative, diuretic, soft-kin, Phlegm, scattered gall tumor effect. For hypertension, beriberi edema, neck lymphadenopathy, simple goiter, prickly heat boils hot summer day in children poison, phlegm cough embolism.

14. yi melon soup: melon (not peeled) 500-600 g, yi 50-100 grams of soup. Can be flavored with sugar or salt, on behalf of the tea used, heat, hot weather, diuretic, dehumidification effect. Drugs for Rush boils, eczema athlete's foot, yellow urine deficient.

15. Daozhi raw turnip, vinegar and rub the affected area transfer, heat treatment boil.

16. green beans 30 grams of powder, each 10 grams, water delivery service, boils cure breast swelling and pain.

17. failure to adopt the open rose 3 - 5 朵 wash, add water, two pregnant, suffering from a cup of low heat, ice sugar 30 grams, made of rose soup, until the temperature dose, to cure blood stasis amenorrhea, boils Chung pain, traumatic swelling and pain.

18. boils and pus ulceration of the skin sore or eczema, rinse with water, tea, allow the wound clean and promote healing.

19. a white sweet potato, peeled and chopped, smashed, can also be added with the same amount of fresh Houttuynia smashed, spreads in the affected area, apply to the local heating that line replace (about two three hours long), and even apply a few days more, boils cure mastitis.

20. soybeans amount, turn on the water immersed soft, add a little alum were smashed drunk, external surface of the skin, swollen boils boil treatment.

21. adzuki beans with water until soft, mash with water or vinegar, or honey or egg amount, into a paste, external surface of the skin, cure mumps, hot boil.

22. Kapok 30 - 50 grams of sugar amount, fry a bowl with water and drink two bowls and a half. Favorable moisture, heat effect. For enteritis, urethritis, eczema, summer boil embolism.

23. fresh buckwheat leaves 60 grams, Shuijianbi day one; or fried yellow noodles with the vinegar into a paste, applied to the lesion, sooner or later be replaced. Governance sore, swollen boils, erysipelas, mastitis, and swelling of unknown drugs.

appropriate patients to eat what?

1, edible grapes plus zinc salt or zinc, other foods such as soy, sunflower seeds, wheat bran, yeast, brown sugar and so on.

2, Yi Shi taste light, the cold food, such as Malan head, purslane, melon, red and white radish, bitter gourd, sponge gourd, mung bean, red bean, lily, chrysanthemum brain and celery.

patients unfit to eat what?

not eat ginger, pepper and other spicy foods , as well as mustard, yellow croaker, shrimp, crab, chicken head, goose, Zhu Tourou so fat objects.

should avoid fried foods and meat, edible oil cans.

data only refer to the specific, please ask a doctor.


how to prevent boils?

boil is born of acute suppurative superficial skin disorders, widely available health, children, young people more common. "Surgical management case" that: "boil persons, birth processes, floating red rootless feet, swollen found in the skin, only the width of an inch, there is less pain, a few days later Microsoft, thin peel, the beginning of the blue water, the latter from breaking the pus out of. "The disease occurs in the summer and autumn, protruding roots shallow, swelling potential limitations, lift the red pain, mostly in the range of about 3cm, easily swollen, easy to collapse, Yi Lian. Early can be divided into a head, without the first two kinds of general light and easy to cure the symptoms, so the saying goes, "no boil the size of a pus like." ;;; ;;;;; ;;;;; ;;;;; But also due to the formation of improper treatment or care "mole cricket boils," or repeated seizures, lack of disunion. Multiple furunculosis ", is difficult to cure.


boil precautions before treatment?

attention to the skin clean, timely replacement of underwear and avoid skin injuries, especially in the summer, to bathe, wash your hair, hair, changing clothes, nails, children in particular should pay attention. With honeysuckle and wild chrysanthemum Jiantang tea. Boil the surrounding skin should be kept clean and coated with 70% alcohol to prevent infection spread to nearby hair follicles.

boil Chinese medicine treatment methods

total boil caused by the toxic heat treatment to detoxify the basic principles.

A Differential Treatment:

1. Heat toxin Accumulation card: lesion processes, such as cone, burning pain, or fever, thirst, tongue pink, yellow fur, rapid pulse. Detoxification. Flavors disinfection decoction.

2. Shushi heat Melancholia: seen in summer and autumn, the affected area, such as agglomeration cone, single or multiple, burning pain, chest tightness, anorexia, deficient urination, red tongue, greasy or yellowish, veins slippery. Qingshu dampness, detoxification swelling. Qingshu Decoction.

3. Is virtual evil love cards: distributed in the body, local color dark red, pus scarce, one after another, delayed healing, with fever, irritability, thirst, or fatigue, limb soft, red tongue thin yellow, rapid pulse. Righting detoxification. Liu Wei Di Huang Decoction.

Second, external treatment and other treatment:

1. The beginning of detoxification should be swelling, moderate to henbane, water reconcile, wrap the affected area. Or wishful golden powder for external application. Or green cream Waicha.

2. Pus, the clip bolt out the pus.

3. Unhealed after the collapse, sores can be a little ninety-one Dan to drugs or drug line twist into sores, topical berberine gauze.

4. Oral Meihuadianshe Dan, Niuhuangjiedu, Fang Feng Tong Sheng Wan, Liushen other medicine.

5. Unilateral prescription: Silver Flower 30g, licorice 10g, decoction, on behalf of the tea.

Western boil treatment

1. Local treatment, such as heat, physical therapy, 10% ichthyol coated ointment. Facial Boil should rest in bed should not squeeze or prick Boil, so as not to spread to the brain.

2. Swelling or have a large range of obvious symptoms, should give systemic antibiotics (third-generation cephalosporin antibiotics).

3. The formation of abscess, incision and drainage should be timely but should be avoided Boil the face cut.

(a) treatment

1. The principles of early treatment to promote inflammation subsided, after early drain purulent pus; timely elimination of systemic adverse reactions.

2. Local treatment

(1) Physical therapy: early, ultraviolet micro-irradiation, can promote local anti-inflammatory, to prevent proliferation. Swelling stage, the selection of FM, infrared and other heat, promote Boil liquid. 2 to 3 times / d, 20 ~ 30min / times.

(2) Drug eraser: 0.5% povidone-iodine scrub, the drug not only for skin irritation, and the role of long-lasting, no pigmentation. Can also be used erythromycin, tetracycline ointment.

(3) topical cream: local swelling and a small pustules, use ichthyol, wishful golden powder, Gyokuro powder and so on.

(4) incision and drainage: Boil into pus, nodules soften, a sense of volatility, you can make a small incision drainage or fire needle drainage. Taboo squeeze purulent lesions.

(5) to keep local clean and dry: adhere to local skin cleaning, daily showers are the best conditions. Young children with skin, topical lip after taking a bath in summer, to avoid the formation of multiple Boil.

3. Systemic treatment usually does not require systemic treatment of boils. But facial boils or accompanied by chills, fever, headache, general malaise, etc., should be given antibiotics. Clinical observations and experimental results show that the efficacy of penicillin, cephalothin, cefazolin and amikacin better effect.

(B) the prognosis

generally good prognosis after active treatment, without sequelae.


boil should be how?

1. Peripheral blood

(1) white blood cell count: fever, elevated WBC count may have.

(2) white blood cell count: white blood cell count was elevated often accompanied by increased neutrophils .

2. diabetes check

(1) fasting plasma glucose measurement: two fasting blood glucose were increased, should consider the possibility of diabetes.

(2) glycated serum protein: This clinical trial is not the impact of fluctuations in blood glucose higher than normal to help the diagnosis of diabetes.

(3) glycosylated hemoglobin: glycosylated hemoglobin and blood glucose were positively correlated, and the irreversible reaction. Diabetes is often higher than the normal 2 to 3 times.

3. bacteriologic

(1) bacterial culture: the multiple, repeated infections, abscesses can be extracted directly pus for bacterial culture, positive results will help the diagnosis of pathogens.

(2) drug susceptibility testing: bacterial culture in the pus, while line drug susceptibility testing can provide the scientific basis of clinical drug treatment.


boil diseases easily confused?

1. Multiple sweat gland abscesses are summer disease, more common in infants and young children and frail mother's head, forehead, etc .. Lesions of multiple subcutaneous abscesses. Surface tenderness, inflammation lighter. No pus bolt, left scars. Usually accompanied by a lot of prickly heat. Generally known as prickly heat poison. It was also known as pseudo furunculosis (Pseudofurunculosis).

2. Hidradenitis suppurativa common in young women, lesions of the skin induration. Subcutaneous abscess formation, followed by skin redness, swelling, heat, pain, ulceration scarring. Lesions occur in the armpits, groin, genital and perianal, umbilical, etc.

3. acne acne mild infection, red, swollen, painful, but the disease is small, the top a little bit like creamy.

4. sebaceous cysts sebaceous cyst infection are redness, swelling, pain, but the previous round has been painless mass over an extended period , the epidermis as usual.

5. carbuncle carbuncle with redness, swelling, pain, but there are several hair follicle infection, lesions larger than the boil.


hump-related diseases

juvenile osteochondrosis of vertebral osteoporosis youth sexual hump sore scoliosis ankylosing spondylitis vitamin D deficiency disease

more back symptoms

small blisters appear back back pain back spasms, back pain does not have subtle linen spine back pain sinus pain Road with sensory ataxia spinal nerve root damage spinal cord hemisection syndrome, spinal cord lesions of hemorrhagic infiltration of the spinal cord injury spinal cord infarction, cauda equina involvement across the spinal cord within the spinal cord gliosis in the spinal cord anterior horn of the spinal cord lesion cavity formed spinal thalamic tract compression

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