[edit]Mechanism of carbon monoxide generation
Carbon monoxide is the most widely distributed and largest number of pollutants in the atmosphere, but also one of the important pollutants generated in the combustion process. The main source of CO in the atmosphere is internal combustion engine exhaust, followed by the combustion of fossil fuels in boilers. CO is an intermediate product generated in the combustion process of carbon-containing fuels, initially all the carbon present in the fuel will form CO. The formation and destruction of CO are controlled by the chemical reaction kinetic mechanism, is one of the basic reactions in the combustion process of hydrocarbon fuels, it is generated by the following mechanism: RH → R → R → RO2 → RCHO → RCO → CO where R is a hydrocarbon free radical group. Reaction of the RCO group mainly through thermal decomposition to generate CO, but also can oxidize the hydrocarbon group R after the generation of CO. combustion process CO oxidation into CO2 rate is lower than the rate of CO generation, so the basic oxidation reaction of CO in the hydrocarbon flame: CO + H2O → CO2 + H2 CO is one of the products of incomplete combustion. If a well-organized combustion process is present, i.e., with sufficient oxygen, adequate mixing, sufficiently high temperatures, and long retention times, the intermediate product CO will eventually burn out to CO2 or H2O. therefore, controlling CO emissions is not an attempt to inhibit its formation, but rather an effort to make it burn completely. It has been shown that in premixed combustion flames of hydrocarbon fuels and air, due to the rapid rate of CO production, the CO concentration rises rapidly to a maximum in the flame zone, which is usually higher than the equilibrium value of the reaction mixture during adiabatic combustion, and then the CO concentration slowly decreases to the equilibrium value. As a result, the CO content detected in the exhaust of the combustion equipment is lower than the maximum value in the combustion chamber, but significantly greater than the equilibrium value in the exhaust state. This suggests that chemical reaction kinetics control the production and destruction of CO. Laboratory production of carbon monoxide: H2O+C=high temperature=CO+H2↑ CO2+C=high temperature=2CO HCOOH=concentrated H2SO4/Δ=H2O+CO↑
[edit]Occupational Exposure
CO gas can be produced from the incomplete combustion of any carbon-containing substance. No less than 70 kinds of operations in industrial production exposed to CO, such as metallurgical industry, coking, ironmaking, forging, casting and heat treatment production; chemical industry, ammonia, acetone, phosgene, methanol production; mine artillery, coal mine gas explosion accident; carbon graphite electrode manufacturing; internal combustion engine test; and the production of metal carbonyl compounds such as nickel carbonyl ［Ni(CO)4], carbonyl iron ［Fe(CO)5], etc. process, or the production and use of CO-containing substances, or production and use of CO-containing substances. and other processes, or the production and use of combustible gases containing CO (such as water gas containing CO up to 40%, blast furnace and furnace gas containing 30%, coal gas containing 5% to 15%), may be exposed to CO. explosives or gunpowder explosion of the gas containing CO about 30% to 60%. The use of diesel fuel, gasoline combustion engine exhaust gas also contains CO about 1% to 8%. Carbon monoxide poisoning (carbon monoxide poisoning), also known as gas poisoning. After carbon monoxide enters the body, it will be combined with hemoglobin in the blood, because the binding capacity of CO and hemoglobin is much stronger than that of oxygen and hemoglobin, which will make the number of hemoglobin that can be combined with oxygen decrease dramatically, thus causing the body tissues to suffer from hypoxia, and leading to death of asphyxia in the human body. Therefore, carbon monoxide is toxic. Carbon monoxide is a colorless, odorless, tasteless gas, so it is easy to ignore and cause poisoning. It is commonly found in poorly ventilated family rooms, gas produced by coal stoves or liquefied petroleum gas pipeline leakage or industrial production of gas and carbon monoxide inhalation in mines, resulting in poisoning. Carbon monoxide poisoning symptoms are manifested in the following aspects: First, mild poisoning . Patients may experience headache, dizziness, insomnia, blurred vision, tinnitus, nausea, vomiting, generalized weakness, tachycardia, transient fainting. The level of carboxyhemoglobin in blood reaches 10%-20%. The second is moderate poisoning. In addition to the aggravation of the above symptoms, cherry red color appears on the lips, nails, skin and mucous membranes, excessive sweating, blood pressure increases and then decreases, accelerated heart rate, arrhythmia, irritability, and momentary sensory and motor separation (i.e., there is still thinking, but no action). Symptoms continue to worsen and drowsiness and coma may occur. Blood carboxyhemoglobin is about 30%-40%. After timely resuscitation, can be relatively quickly awake, generally no complications and sequelae. Thirdly, heavy poisoning. The patient rapidly enters a comatose state. At the beginning of the limbs, muscle tone increases, or there are paroxysmal tonic spasms; in the late stage, muscle tone decreases significantly, the patient's face is pale or cyanotic, blood pressure decreases, pupils are dilated, and finally death is caused by respiratory paralysis. Those who survive resuscitation may have serious comorbidities and sequelae. Sequelae of carbon monoxide. Moderate and severe poisoning patients have neurasthenia, tremor paralysis, hemiparesis, hemianopsia, aphasia, dysphagia, mental retardation, toxic psychosis or de-cerebralization. Secondary encephalopathy can occur in some patients.
[edit]Clinical manifestations
1.Acute poisoning
Acute carbon monoxide poisoning is the acute occupational poisoning with the largest number of morbidity and mortality in China.CO is also the poison that causes the largest number of deaths in accidental life poisoning in many countries. The occurrence of acute CO poisoning is related to the concentration and time of exposure to CO. The maximum permissible concentration of CO in the air of workshop in China is 30mg/m3, and there are data proving that the concentration of CO in the inhaled air is 240mg/m3***3h, and the COHb in Hb can be more than 10%; when the concentration of CO reaches 292.5mg/m, it can make the person produce serious headache, dizziness and other symptoms, and the COHb can be increased to 25%; the concentration of CO reaches 117Omg/m3, and inhalation of more than 6Omin can make the person produce severe headache, dizziness and other symptoms; the concentration of CO reaches 117Omg/m3, and inhalation of more than 6Omin can cause the death of the accidental life poisoning. When the CO concentration reaches 117Omg/m3, inhalation for more than 6Omin can make a person to have coma, COHb is about as high as 60%.When the CO concentration reaches 11700mg/m3, it can make a person to die in a few minutes, and the COHb can be increased to 90%. Clinical signs and symptoms of acute cerebral hypoxia are the main manifestations. After exposure to CO, such as headache, dizziness, palpitations, nausea and other symptoms, in the inhalation of fresh air, the symptoms can be quickly disappeared, is a general contact reaction. Mildly poisoned persons have severe headache, dizziness, heartbeat, blurred vision, weakness of limbs, nausea, vomiting, irritability, unsteady gait, mild to moderate disturbance of consciousness (e.g., blurred consciousness, hazy state), but no coma. After leaving the place of poisoning and inhaling fresh air or oxygen for a few hours, the symptoms gradually recover completely. In addition to the above symptoms, moderately poisoned persons have flushed face, excessive sweating, rapid pulse and shallow to moderate coma. After timely removal from the place of poisoning and rescue, they can gradually recover, and generally have no obvious complications or sequelae. In severe poisoning, the consciousness disorder is serious, and it is deep coma or vegetative state. Commonly, the pupils are narrowed, the light reflex is normal or sluggish, the muscle tension of the limbs is increased, the teeth are closed, or there is paroxysmal de-cerebralization, the tendon wall reflex and the tibial reflex are generally disappeared, the tendon reflex exists or is sluggish, and urinary and fecal incontinence can occur. When cerebral edema continues to aggravate, there is persistent deep coma, consecutive episodes of deafferentation, pupillary reaction to light and corneal reflexes are sluggish, body temperature is elevated up to 39～40℃, pulse is fast and weak, blood pressure drops, face is pale or cyanotic, limbs are cold, and tidal respiration occurs. In some patients, fundus examination shows irregular spasm of retinal arteries, venous filling, or papilledema, suggesting increased intracranial pressure and the possibility of brain herniation. However, in many patients, fundus examination was negative, and even the cerebrospinal fluid examination pressure was normal, while pathologic autopsy still confirmed severe cerebral edema at the end. During the process of awakening from coma after treatment of severely poisoned patients, agitation, clouding of consciousness, disorientation, or loss of distant or near memory often occurs. After the recovery of consciousness in some patients, cortical dysfunction such as apraxia, agnosia, agraphia, aphasia, cortical blindness or transient deafness can be found; mental symptoms, mainly intellectual disability, can also occur. In addition, transient mild hemiparesis, Parkinson's syndrome, chorea, tardive dyskinesia, or grand mal seizures have been reported. After active rescue treatment, most patients with severe poisoning can still recover completely. A few patients with vegetative state, manifested by loss of consciousness, open eyes and speechlessness, and deafferentation, have a poor prognosis. In addition to the above manifestations of cerebral hypoxia, hypoxic changes or complications in other organs may occur in patients with severe poisoning. Some patients have cardiac arrhythmia, severe myocardial damage or shock; those with pulmonary edema have wet rales in the lungs and respiratory distress. Hepatomegaly is found in about 1/5 of patients and often shrinks after 2 weeks. Upper gastrointestinal bleeding may occur due to stress gastric ulcers. Occasionally, rhabdomyolysis and compartment syndrome may occur, and acute renal failure may occur as a result of myoglobinuria. Some patients have cutaneous autonomic trophic disorder, manifested as large or small blisters or skin lesions similar to burns on the skin of the limbs or trunk, or redness and swelling of the skin in patches similar to dengue-like changes, which is not difficult to be cured by symptomatic treatment. Hearing vestibular damage can be manifested as deafness, tinnitus and nystagmus; there are still 2% to 3% of patients with nerve damage, the most commonly involved are the lateral femoral cutaneous nerve, ulnar nerve, median nerve, tibial nerve, peroneal nerve, etc., which may be related to localized compression after coma.
2. Delayed encephalopathy (delayed encephalopathy)
Some patients with acute CO poisoning recovered from coma with normal consciousness, but after 2-30 days of false recovery, neuropsychiatric symptoms of encephalopathy appeared, which is called delayed encephalopathy of acute CO poisoning. Because of the "biphasic" clinical process, it is also called "acute CO poisoning neurological syndrome". The common clinical manifestations are as follows: (1) Psychiatric symptoms: sudden loss of orientation, apathy, slow reaction, memory impairment, incontinence, inability to take care of oneself; or hallucinations, illusions, incoherence, behavioral disorders, such as acute dementia and rigidity type psychosis. (2)Focal brain damage 1)Extrapyramidal nerve damage:Parkinson's syndrome is common, the patient's limbs are lead pipe or cogwheel-like increased muscle tone, slow movement, walking, loss of both upper limbs with the accompanying movement or the appearance of writing and static tremor. A few patients may have chorea. 2)Conus nerve damage:Mild hemiparesis on one or both sides, upper limb flexion and tonus, hyperreflexia, positive ankle clonus, eliciting pathological reflexes on one or both sides, motor aphasia or pseudobulbar palsy may also occur. 3) Others: Cortical blindness, epileptic seizures, parietal lobe syndrome (dyscognition, dysfunction, dysgraphia or dyscalculia) have also been reported. 3. Effects of low concentration of CO on human body Whether chronic poisoning can be caused by long-term exposure to low concentration of CO is still debated. In recent years, it is believed that long-term exposure to low concentrations of CO may cause two effects on human health: (1) Neurological: dizziness, headache, tinnitus, fatigue, sleep disorders, memory loss, and other symptoms of cerebral debility syndrome are more common, and neurobehavioral tests may reveal abnormalities, which can be recovered after separation from CO exposure. Those with persistent symptoms as described above often have a history of multiple mild acute CO poisoning. (2) Cardiovascular system:Electrocardiograms may show abnormalities such as arrhythmias, ST-segment decreases, prolonged QT intervals, or right bundle-branch conduction block. In occupationally exposed persons with COHb saturation of 5% or more, increases in serum lactate dehydrogenase (LDH), hydroxybutyrate dehydrogenase (HBD), and creatine phosphokinase (CPK) can be seen, and the increased activity of these enzymes may be related to myocardial damage. In addition, a population-based survey found that about 20% to 25% of smokers had blood COHb higher than 8% to 10%, and the sudden death rate of myocardial infarction in these people was higher than that of nonsmokers. In recent years, a study of 63 patients with coronary atherosclerosis found that after exposure to CO increased COHb levels from 0.6% to 2% and 3.9%, their time to myocardial infarction and angina pectoris was advanced and their tolerance to exercise was significantly reduced. These investigations, combined with experimental animal studies, suggest that the cardiovascular system is likely to be adversely affected under the prolonged action of low concentrations of CO. Its binding capacity to hemoglobin is two hundred times that of oxygen. Prevention In the production place, natural ventilation should be strengthened to prevent leakage of air from transportation pipelines and valves. When possible, use automatic CO alarms. After the mine is discharged, the operating procedures should be strictly observed, and the mine must be ventilated for 2Omin before entering the work. Entering the environment with high CO concentration, you should wear oxygen-supplied gas mask for operation. During the winter heating season, preventive knowledge should be publicized and popularized to prevent the occurrence of living CO poisoning accidents. For patients cured of acute CO poisoning, family members should be reminded to continue to pay attention to observing the patients for 2 months when they are discharged from the hospital, and if symptoms related to delayed encephalopathy appear, they should be reviewed and handled in a timely manner. Detoxification If inhalation of a small amount of CO causes poisoning, a large amount of fresh air should be inhaled or artificial respiration should be performed. Medically, detoxification can be carried out by injecting methylene blue into the bloodstream, as CO binds more firmly to methylene blue than carboxyhemoglobin, thus facilitating the shift of CO to methylene blue and the release of hemoglobin, and restoring normal respiratory action.
[edit]Carbon monoxide that can save lives
In the 1960s, it was known that when body tissues are attacked by toxins, ultraviolet radiation, hormones, and medications, heme oxygenase-1 (HO-1 for short) will fight off the corresponding injuries and infections in a timely manner, and at that time, a small amount of CO will be produced naturally in the body. At that time, however, carbon monoxide was thought to be a by-product of tissue metabolism. However, American scientist Solomon Sindel suggested in 1993 that carbon monoxide plays a meaningful role in the human body. It assists nitric oxide in the management of the body's internal organs, such as the contraction of the large intestine and the emptying of the stomach. However, after much effort, researchers have not been able to examine the exact role of carbon monoxide in the human body. Because of the benefits of carbon monoxide, some scientists want to use it in clinical trials. However, carbon monoxide is a toxic gas that can be harmful to humans if used improperly. Carbon monoxide binds tightly to hemoglobin in red blood cells, forming carboxyhemoglobin, which prevents oxygen from being carried throughout the body. When about 20% of the hemoglobin in the human body turns into carboxyhemoglobin, nausea, vomiting and fainting can occur; when about 40% of the hemoglobin in the human body turns into carboxyhemoglobin, it can kill people. For this reason, some scientists have opposed the introduction of carbon monoxide into the clinical treatment of humans. However, according to Augustin Joe and Fritz Becky of the United States, the medical profession should not be so quick to reject the therapeutic potential of carbon monoxide, which is the best method of treatment in emergency situations. In the first half of 2001, a team of researchers led by Joe and Becchi showed that inhaling minute amounts of carbon monoxide in patients could help prevent organ rejection. When they performed heart transplants in rats, they sealed the HO-1 with a chemical called porphyrin, and the rats showed rejection of the transplant within a week. However, if the rats were exposed to air containing traces of carbon monoxide, they survived. In other words, inhaling trace amounts of carbon monoxide into an animal can accomplish what H0-1 can do. This experiment also shows that carbon monoxide, which was discovered in the 1960s during the study of HO-1, is not a metabolic waste product, but a gas produced by the body as a physiological defense reaction under the action of HO-1. At the end of 2001, David Pinsky's experiments in the United States showed that carbon monoxide is also very helpful for lung transplantation. Pinsky genetically altered some rats so that they lacked the gene that makes HO-1, and then subjected them to simulated lung transplants with normal rats. Pinsky cut off the blood flow to the rats' left lungs with clamps and restored the flow an hour later. As a result, the normal rats had a 90% survival rate, while all the genetically altered rats died from blood clots generated in their lungs. In further experiments, when Pinsky breathed tiny amounts of carbon monoxide into the genetically altered rats, only half of them died. Currently, thousands of lung transplants are performed each year, with a failure rate of 30 percent, which is higher than the failure rate of other organ transplants, such as kidney transplants, which have a failure rate of only 10 percent. Pharmacists are therefore hoping to introduce the therapeutic effects of carbon monoxide into lung transplants. Some doctors are now using carbon monoxide in clinical procedures, with some success.