The magnitude of the toxicity of a substance is often expressed and divided by the semi-lethal dose of a warm-blooded animal. The animal can be tested to achieve the minimum dose of 50% of the animal's body weight per kilogram of death, said semi-lethal dose, its symbol LD50, unit mg / kg body weight, the specific division is as follows: Toxicity classification highly toxic, moderate toxicity Low toxicity, actual toxicity, non-toxic and semi-lethal dose LD50 (mg/kg body weight) ≤1 1～50 50～500 500～5000 5000～15000 >15000 Most inorganic cyanide is highly toxic, highly toxic, very small amount of cyanide (A few milligrams per kilogram of body weight will cause humans and animals to die in a short period of time. Water with a low concentration of cyanide (<0.05mg/L) will also cause fish and other aquatic organisms to die and cause crops. Production reductions. Cases of acute poisoning of fish, livestock and people to cyanide-contaminated water have been reported both at home and abroad. These incidents are caused by the discharge of large amounts of cyanide into water bodies in the short term. Therefore, in industrial production, it must be strict. Control the use and emissions of cyanide, especially with a comprehensive wastewater treatment facility to reduce the amount of cyanide emissions.

Not only simple cyanide will pollute the environment, causing poisoning of people, animals and even death, even low-toxic cyanide double salts like iron cyanate and ferrocyanate, if discharged into surface water, after sun exposure and other conditions The complex can also be decomposed to release a significant amount of free cyanide, resulting in poisoning death of aquatic organisms. Generally speaking, the environmental pollution of cyanide mainly refers to the pollution of rivers (surface water) and drinking water (groundwater) caused by the discharge of cyanide-containing wastewater. Since cyanide exists in the atmosphere for only ten minutes, Generally, it does not cause atmospheric pollution. The cyanide-containing waste residue can be stored and stored because it must be disposed of, and the pollution generated is still water pollution. 2.1 Cyanide toxicity to humans and its prevention and treatment measures Cyanide is more harmful to warm-blooded animals and humans. It is characterized by high toxicity and quick action. The action of hydrogen cyanide is extremely rapid. In the air with a very low concentration of hydrogen cyanide (0.005mg/L), people only have headaches, discomfort, and arrhythmia for a short time; the concentration of hydrogen cyanide is high (0.1mg/ In the air of L), people will die immediately or die quickly. When cyanide is moderately concentrated, people will develop initial symptoms within 2 to 3 minutes. In most cases, they die within 1 hour, sometimes only after 24 hours, and hydrogen cyanide is inhaled. The toxicity is shown in Table 2-1, Table 2-2, and Table 2-3. It is also irritating to the skin and absorbed through the skin. At high temperatures, especially when mixed with irritating gases to dilate blood vessels in the skin, it is more dangerous because it absorbs HCN easily. Table 2-1 Inhalation toxicity of hydrogen cyanide on humans (mg/L) Exposure time Damage concentration Semi-lethal concentration Lethal concentration 3 seconds - 15 15 seconds 1.5 to 2.0 2.5 to 2.75 3.0 to 3.5 30 seconds 0.5 1.0 to 1.5 2.5 ~ 2.5 1 minute 0.4～0.5 0.7 1.5 2 minutes 0.25～0.3 0.5 0.7 5 minutes 0.15* 0.2～0.3 0.4～0.5 15 minutes 0.1 0.15～0.20* 0.3 *The original data is obviously wrong, the author has revised it with reference to relevant information. Table 2-2 Hydrogen cyanide on human inhalation toxicity Effect of hydrogen cyanide concentration in air mg/L ppm 0～3 270 Rapid death 0.12～0.15 110～135 Acute death within or short of 0.5～1 hour Time to death 0.05 ~ 0.06 45 ~ 54 Inhalation 0.1 ~ 1 hour without obstacles 0.02 ~ 0.04 18 ~ 36 Inhalation for 6 hours without obstacles such as long-term inhalation, there are obstacles Table 2-3 people's response to low concentrations of HCN in air (estimated HCN concentration (ppm) Reaction 5~18 headache, dizziness 5-13 fatigue, headache, weakness, hand and foot tremor and pain, nausea 4.2 to 12.4 (mean 8.3) headache, weakness, smell, taste change, throat irritation , nausea, vomiting, rapid breathing 2-8 (average 5) thyroid enlargement, increased hematuria SCN-content, but still lower than smokers 0-7 (mean 4.9) No observed effect 0.1-0.9 No effect observed 0.23 average Leukocyte, cytochromeoxygenase, peroxidase, and succinyl dehydrogenase activities were slightly reduced after 5 and 4 years of exposure. The lethal dose of cyanide to the human body From the clinical data of poisoned patients, the tolerance of each person is very different. The small one can kill 0.5mg/kg body weight, and the older one can reach 3.5mg/kg body weight. According to one data, the average lethal dose of sodium cyanide is 150mg, potassium cyanide 200mg, hydrogen cyanide about 100mg. Another information shows that the lethal dose of sodium cyanide is 100mg, potassium cyanide is 120mg, or once. The average lethal dose of hydrogen acid and cyanide is 50-60 mg. In short, a small amount of cyanide will kill people. See Table 2-4. Table 2-4 Hydrogen cyanide cyanide sodium cyanide to human toxic agent name poisoning pathway lethal dose (mg / L) hydrogen cyanide (hydrocyanic acid) oral 50 ~ 100 potassium cyanide oral 200 ~ 250 potassium cyanide Oral 150 ~ 250 natural water body will not have cyanide, but some plants contain a small amount of cyanide in the form of glycocalyx such as cherry, plum, peach, apricot, medlar, medlar, apple and other nuts contain this Cyanide. It is not uncommon for people to suffer from inadvertent eating of such nuts. In particular, there are many cases of poisoning caused by children suffering from bitter apricots. In addition, there is a kind of cassava in the south of China, which is aliased to sweet potato, its epidermis, endothelium and potato. There are different amounts of cyanogenic glycosides in the heart of the potato, especially the endothelium. If it is not treated with water before consumption, it can cause poisoning. In the south, cotton beans are also produced, which also contain cyanogenic glycosides. Poultry can also be poisoned by poultry. Introduction, bitter almonds served 40 to 60 capsules, children with 10 to 12 capsules can be poisoned or killed, eating 3 to 6 untreated cassava can cause serious poisoning. The humus in the soil is also a complex organic compound. A certain amount of nitrogen compounds can form cyanogen and phenol under the action of soil microbes, and decrease with the depth of the soil, resulting in a CN-content of 0.003 to 0.13 mg/ Kg. Despite the large cyanide poison, except for the **, most of the poisoning causes the death to not be caused by the accidental consumption of solid cyanide or cyanide solution, but by inhalation of hydrogen cyanide gas, which is different from livestock. The reason is that on the one hand, due to the strict management of solid and liquid sodium cyanide, on the other hand, cyanide, with its characteristic odor, prevents people from eating, and does not allow the skin to come into contact with it for a long time. Even if it is hydrocyanic acid poisoning, it has its own specific conditions and has great limitations**. In short, there are very few deaths due to cyanide poisoning, but due to work reasons, there are relatively many people with slow ** poisoning.

2.1.1 Cyanide Hazards, Symptoms and Signs Symptoms and signs are different due to differences in the quality and path of cyanide. The response of humans to different concentrations of cyanide in the air is shown in Table 2-1, Table 2-2, and Table 2-3. Almost all reported cases or findings can occur in systems including neurological digestion and respiration, with similar neurasthenia. Syndromes and muscle soreness, limited activity and skin irritation also have symptoms that eventually lead to disability and death. Under the chronic action of cyanide, due to insufficient oxygen supply to the tissue, it can cause a series of reflexive changes, such as increased red blood cell hemoglobin metabolism, elevated blood glucose to improve blood oxygenation, accelerated energy metabolism recovery, due to increased SCN-in vivo. It can also cause blood pressure to drop, inhibit thyroid iodine function, interfere with the organic binding process of iodine , interfere with the synthesis of thyroid hormones, and increase the discharge of iodine from the kidneys, reduce the iodine reserves in the body, resulting in hypothyroidism, resulting in brain The anterior pituitary gland metabolically enhances the secretion of thyrotropin. This leads to hyperplasia of thyroid tissue. In addition, the occurrence of cyanide chronic poisoning and the body. The whole nutritional status is also related, such as vitamin B12 deficiency, protein malnutrition, especially the lack of sulfur-containing amino acids can make the body for CN-detoxification of S2O3, S and -SH reduce these factors can make the intake of CN-toxicity Increased, resulting in a series of symptoms and signs of chronic poisoning. 1. The nervous system can cause headache, dizziness, distraction, forgetfulness, weakness, sleep disturbance, vision loss due to CN-induced myelin sheath phenomenon and degeneration of brain tissue necrosis and vacuolar degeneration. There are multicolored vision, skin sensation abnormalities, sexual dysfunction, tropical neuropathy, and diffuse neurodegenerative diseases. Due to optic atrophy, neurological deafness and affecting bone marrow sensory nerves cause ataxia, such as tobacco amblyopia and other diseases. 2. Respiratory and digestive system cough, shortness of breath, suffocation. The sense of smell and taste changes, nausea, vomiting, heartburn and chest and abdomen have oppression. Isocyanates can cause allergic asthma. Most of these symptoms disappear after rest, and severe gastritis and hepatosplenomegaly occur. 3. Cardiovascular system tachycardia or bradycardia, palpitations, precordial pain, decreased vascular tone and slowing blood circulation, low heart sounds, blood pressure are generally reduced, and some people may have ECG changes. 4. Muscles and skin are mainly motility muscles, mostly starting from the sides of the lower back. There are muscle soreness, rigidity, stiffness, inflexibility, and limited activity. The skin often has rashes (plaques, blood rashes, rashes) or ulcers and itchy. V. Carcinogenicity, Teratogenicity, Mutagenicity The “three-way” response is inconclusive. Recent animal experiments have shown that long-term oral intake of trace amounts of KCN has an effect on mouse reproduction, and the mortality of the offspring of the animal (first and second generation) High, the number of pregnancies decreased significantly, and stillbirths increased. Organic cyanogens such as acrylonitrile have been shown to cause degeneration and mutagenic effects on animals, and have not been confirmed by humans, so it is still not easy to infer humans. 2.1.2 Human body's absorption, metabolism and excretion of cyanide There are three main ways to enter cyanide into the human body. One is to inhale hydrogen cyanide gas or cyanide-containing dust from the respiratory tract, and the other is to enter the stomach through the mouth. The mucous membranes and the gastrointestinal tract are absorbed. Third, the damaged skin contacts the cyanide directly into the blood. When the moist skin is in contact with high concentrations of cyanide, it also absorbs cyanide and causes poisoning. After the non-lethal dose of cyanide enters the human body, it can be gradually detoxified in the body. The mechanism is that the sulfur released by β-mercaptopyruvate under the action of the cleavage enzyme can be accepted by the sulfite produced by metabolism in the body. Thiosulfate, thiosulfate and cyanide are catalyzed by thiocyanate to produce non-toxic thiocyanate, which is discharged from the kidney (urine) to the body, which is the main detoxification pathway for cyanide in the body. About 90% of the thiocyanate is discharged through this route. The strength of detoxification is related to the amount of sulfur supplied in the body. The speed of detoxification is determined by the amount of thiocyanate-producing enzyme in the tissue. The sensitivity of humans to cyanide is also related to the content of thiocyanate-producing enzymes in the body. People with less thiocyanate-forming enzymes are sensitive to cyanide, and the individual differences are large. Vivo cyanide ion can be combined with cysteine to form 2-imino-thiazolidine-4-carboxylic acid, from the kidney; hydroxocobalamin with cyanide ion and generated vitamin cyanocobalamin, also from the kidney; cyanide ion may be Oxidation to cyanate, hydrolysis to produce carbon dioxide and ammonia exhaled by the lungs; cyanide ion oxidation to form formic acid, part of which is involved in single carbon metabolism, and another part is excreted by the kidney; hydrogen cyanide can also exhale part of it directly from the respiratory tract. The detoxification of cyanide in the body is limited. If the intake of cyanide exceeds the load of understanding poison, the concentration of poisoning will cause poisoning or even death. The detoxification and excretion pathway of cyanide in the body is shown in Figure 2-1. A small amount of cyanide enters the human body through the digestive tract for a long time, which will cause chronic toxicity. The subthreshold concentration obtained by animal test is 0.005mg/kg. According to the epidemiological investigation, some residents are contaminated with cyanide due to long-term drinking (including CN-0.14mg). /L) Groundwater, with decreased basal metabolism, pale edema, lack of energy, headache, dizziness, palpitations, unresponsiveness, etc. This may be due to cell degeneration in the nervous system, which occurs in these residents.

The rate has risen significantly, probably due to the long-term accumulation of thiocyanate in the body. Because thiocyanate can interfere with the synthesis of thyroxine, affecting the function of the thyroid, leading to metabolic hypertrophy of the thyroid, which also indicates that thiocyanate itself is also toxic to humans. The main route of cyanide │ Secondary route │ 1. Direct excretion a.HCN excretion from absorption │ b.CN-Excretion from secretion │ 2. Oxidation a ─→HCOOH-→Excretion reduction│ │↑ │ ↓│ │ Single carbon compound metabolic pool (transferase enzyme) │ │ ↑ │ ↓ │ + H2O │ b ─ → HCNO─ → CO + NH3─ → excretion │ │ B12a │ 3. metal binding: ──── → B12 │ │ │ H Excretion │ Cystine │ ↑ │ 4. Condensation: ───→ HOOC-C-NH │ Thiocyanate-producing enzyme │ │ C-NH-→Excretion │ and reduced sulphur ↓ H2C-S SCN-←──── CN- 2 - imino-thiazolidine - 4-hydroxy acid thiocyanate oxidase Figure 2-1 Cyanide detoxification and excretion pathways in vivo 2.1.3 Toxicological effects of cyanide and factors affecting poisoning Cyanide toxicity and its chemistry Whether the structure can rapidly release cyanide ions in the body, such as potassium cyanide, sodium cyanide, acrylonitrile, etc. can rapidly precipitate cyanide ions in the body, so the toxicity is high, it is easy to cause acute poisoning, and nitrile and Dinitrileamine, cyanate ester, isocyanate does not precipitate cyanide in the body, does not have the unique cyanide Toxicity, only local irritation symptoms. Cyanides after being substituted with a halogen in addition to significant toxicity further comprises eye, respiratory tract irritation, such as cyanogen chloride, cyanogen bromide, bromophenyl acetonitrile. In addition to anti-toxic treatment according to cyanide after poisoning, it is also necessary to treat the symptoms of eye and upper respiratory tract irritation and pulmonary edema caused by it. The protective mask has limited protective effect on cyanogen chloride, and the protection time is also short. The key to cyanide-induced poisoning is that cyanide ion [CN-] binds to the cell's iron-containing cell pigment oxidase. Iron-containing cell pigment oxidase is an enzyme necessary for cellular uptake and utilization of oxygen. When combined with cyanide, the cell will Loss of the ability to ingest and utilize oxygen, resulting in cellular hypoxia and asphyxia, leading to respiratory center inhibition and death. We know that under normal physiological conditions, the cell oxidative oxidase contains divalent iron pigment [Fe2+], and the divalent iron pigment becomes trivalent iron (Fe3+) when combined with oxygen, and the ferric sputum is sent to the tissue. After the cells are used by the cells, they can be reduced to ferrous iron, but when the cyanide ions entering the human body increase, the cyanide ions combine with the ferric iron, and because of its strong affinity, the ferrous oxidase is inhibited from ferric iron. Reduction and oxidation of ferrous iron, so that tissue cells can not get enough oxygen in time to form internal asphyxiation, this process is expressed as: iron cell pigment oxidase + cyanide → cyanide iron-containing cell oxidase cyanide ion and Sulfur, cobalt, and glucuronic acid in the human body can also bind, and these combinations are all reversible, and the degree of binding depends on the concentration of cyanide ions in the human body. Cyanide ion combines with sulfur to form a low-toxic thiocyanate, which combines with cobalt salt to form a low-toxic cyanide-cobaltate, which combines with glucuronic acid in the liver to form a slightly toxic nitrile compound, which produces low-toxic substances. The reaction actually plays a natural protective role for iron-containing cell pigment oxidase, buffering the degree of poisoning. It can be seen that after cyanide invades the human body, whether it can cause poisoning depends on the speed of invading the human body and the detoxification and excretion rate in the body. The small amount slowly collects and does not exceed the detoxification and excretion rate in the human body. It will not cause poisoning. For example, in a period of time, when the amount of entering the group slightly exceeds the detoxification effect and excretion of all consumed amount, some iron-containing cell pigment oxidase will reversibly combine with cyanide ions, as long as the contact with cyanide is quickly separated. The concentration of cyanide in the human body is gradually reduced with detoxification and excretion, and the iron-containing cell pigment oxidase can be decomposed from the iron-containing cytochrome oxidase, and can be self-healed even without medical treatment. If the dose into the body exceeds the human body's understanding of the toxic effects and the amount of excretion can be consumed, more serious poisoning will occur. In addition to the contact with cyanide, emergency treatment must be carried out. 2.1.4 Clinical manifestations of cyanide poisoning 1. Units with acute poisoning production and cyanide use are more common in acute poisoning. High-dose poisoning patients do not have any aura symptoms, sudden coma and respiratory heartbeat stop. If the lethal dose is poisoned and cannot be rescued in time, the condition can last for 1 hour and finally die with respiratory failure. In general, the following symptoms appear in the poisoned patients: 1) Oral, mouth has a bitter taste and burning sensation, followed by a tight feeling and numbness in the throat, increased mouth sputum and nausea inhalation poisoning early throat burning sensation, itching Tears, eye pain. 2) Mental care, ambiguity, headache, dizziness, and often feel that the jaw movement is not working, there is a feeling of rigidity.

3) Difficulty breathing and rapid. 4) Exhaled gas and vomit have bitter almond flavor. 5) In the early stage of poisoning, the increase of the tension of the vasomotor nerve causes the reflexed heart rhythm to slow down and the blood pressure to rise, and then the paralysis effect occurs, the blood pressure drops and the heartbeat is weak, and the heart rhythm is irregular. 6) Loss of consciousness, violent convulsions, incontinence, followed by paralysis, body sweating, eyeballs protruding, pupil dilation, mouth vomiting bloody foam, skin flushing, severe breathing difficulties, and finally, respiratory heartbeat stopped. The above performance can be divided into four phases: prodromal phase → dyspnea period → convulsion period → paralysis period. 2. Chronic poisoning Chronic poisoning is caused by a small amount of long-term exposure, or mild acute poisoning occurs repeatedly, causing some reactions in the human body. The main manifestations are: headache, dizziness, insomnia, memory and loss of attention, Loss of appetite, nausea and abdominal pain, constipation, frequent urination, pressure in the anterior region, low blood pressure, difficulty in breathing, sore muscles or tingling in the body, mental deterioration, mental retardation, thyroid enlargement, sexual dysfunction, skin contact It can produce rashes, pimples and herpes. Cyanide poisoning should be differentiated from organophosphorus pesticides and carbon monoxide poisoning to prevent misdiagnosis and mistreatment. See Table 2-5 for details. Table 2-5 Cyanide and other toxic poisoning differential diagnosis table category cyanide organophosphorus pesticide carbon monoxide identification project contact history has odor bitter almond flavor fruit flavor or special smell tasteless poisoning symptoms severe poisoning has four toxic base-like, nicotinic The toxic and convulsive period of the poisoning table and the central nervous system symptoms, the skin is reddish or the skin mucous membrane is pale red. The blood is detected in the blood. The cholinesterase activity in the blood is in the blood. Acid-lowering albumin increases salt increase* Anti-poisoning agent for high-hemoglobin red egg to resolve cholinergic drug reactivation There is no specific treatment for white forming agent thiol (enzyme regenerative agent) and other therapeutic drugs, with sodium sulfate and other therapeutic effects The treatment site is effective: 24 hours of normal non-smokers in the urine SCN-<2mg / L; smokers <14mg / L. 2.2 Rescue and treatment of patients with cyanide poisoning 2.2.1 Acute treatment method 1. For acute acute poisoning of cyanide, it is necessary to promptly carry out first aid, and must not miss the rescue opportunity. If the rescue personnel enter the poisoned area, they must wear protective equipment. Prevent self-poisoning. 1) Leave the environment of the dyeing area to avoid exposure to poisonous substances. Persons who inhale cyanide poisoning from the respiratory tract should immediately wear a gas mask to lift the poisoned person to the upper wind direction for rescue. Of liquid cyanide poisoning, exposure should immediately remove clothing, footwear poisoning prevent further absorption of ingested or swallowed cyanide poisoning caused by a gastrointestinal emetic immediately with 0.2% potassium permanganate or peroxide Hydrogen or 5% sodium thiosulfate gastric lavage. 2) Immediately give emergency medicine according to the severity of poisoning of the poisoned person, whether breathing or heartbeat is stopped, and give first aid accordingly. For example, if the person who breathes or stops the heartbeat is subjected to artificial respiration and external cardiac compression, inhale 1 to 2 nitrous acid. Amyl ester or intramuscular injection of anti-cyanide first-aid injection, experimental studies have shown that when the concentration of cyanide in blood reaches a certain concentration, the central nervous system, especially the respiratory center, is more sensitive to cyanide than the circulatory system, and the breathing stops first. The cyanide can be automatically recovered after the blood concentration is lowered. As long as the high hemoglobin is rapidly formed during the rescue, the concentration of cyanide in the blood is lowered, and the effect of the first aid can be displayed. 3) Give respiratory stimulants and cardiac resuscitation drugs, conditional pressure oxygen can increase the anti-drug first aid effect, but oxygen should not be used simultaneously with isopropyl pentoxide, if the blood pressure is not lower than 80mmHg after the use of isoamyl nitrite If the condition needs to be reusable, if the blood pressure has been lower than 80mmHg, it should be stopped. 2. Treatment of poisoning If the symptoms of the poisoned person have been relieved after the rescue, the anti-drug treatment should be carried out according to the actual situation. The determination of the cyanide ion concentration in the blood or the determination of the content of methemoglobin in the blood is very helpful for the treatment. When the symptoms of poisoning are still serious and the concentration of methemoglobin in the blood is low, the nitrite should be given intravenously and then sodium thiosulfate should be added to enhance the anti-toxic effect. When using sodium nitrite, the blood pressure should not be lower than 80mmHg. Intravenous injection of sodium thiosulfate into the anti-cyanide first-aid injection makes the anti-toxic effect better. Pay attention to the skin color change of the poisoned person during the treatment. For the use of the denatured hemoglobin forming agent, the edetate-dicobalt (B For the treatment of cobalt diamine tetraacetate, the usage and dosage of the most commonly used therapeutic agents are shown in Table 2-6. Table 2-6 Common Methods for Several Cyanide-Reducing Agents Name Concentration % Dose g/Human Mechanism Sodium Thiosulfate 25 12.5 Sulphur Solution Sodium Nitrite 3 0.3 Denatured Hemoglobin Forming Agent 4-DMAP 2.5～10.0 0.2～0.25 Denatured Hemoglobin Formation Agent edetate dicobalt 3 0.3 ~ 0.6 directly combined with cyanide III. Symptomatic treatment 1) The mechanism of oxygen therapy for cyanide poisoning patients Although the mechanism is not very clear, but observed from animal experiments, such as giving overdose to poisoned animals Oxygen absorption can improve the effect of cyanide treatment drugs, increase the body's tolerance, promote cyanide oxidation, improve secondary hypoxia, prevent respiratory and circulatory failure, and prevent oxygen deficiency caused by oxygen inhalation. 2) Maintaining the respiratory cycle function, it is necessary to treat the symptoms with respiratory stimulants, resuscitation drugs and booster drugs. If the blood pressure drop caused by the excess of the denatured hemoglobin forming agent is used, ephedrine can be given to raise blood pressure. 3) For respiratory and ocular mucosal irritation caused by cyanogen chloride poisoning, in addition to symptomatic treatment, anti-cyanide treatment drugs should be given. Especially for severe cyanogen chloride poisoning, we must not neglect to prevent and treat pulmonary edema. The first-aid treatment for cyanide poisoning is more complicated and varied than other cyanide poisoning treatment. 2.2.2 Measures to prevent cyanide poisoning 1. The production process should be carried out by mechanized, airtight, automated and continuous equipment, and have good ventilation facilities, especially the dead air circulation or poor circulation in the workshop. 2. The production process must have a complete set of safe operating procedures, and a special person is responsible for checking the implementation of the safety operation procedures, the use of safety equipment and protective equipment. 3. When working in a place with high or medium concentration of cyanide, you must wear effective protective equipment. At the same time, you must have someone to take care of it. If necessary, take anti-Cyanide prevention tablets for half an hour before you can maintain it for 5 hours. 4. Cyanide-containing wastewater must be treated and discharged, and the drainage must be separated from the acidic wastewater to avoid causing hydrogen cyanide gas to escape and poisoning people. 5. Each production workshop must be equipped with an acute poisoning first aid kit, equipped with anti-cyanide preventive tablets, anti-cyanide first aid needles or isoamyl nitrite. The operator should try to ensure that everyone will be rescued on the spot and that the person is responsible for the duty every day. 6. No smoking, drinking or eating in the production workshop. Wash your hands before meals. After work, take a bath and change clothes. 7. Regular preventive medical examinations. 8. Anyone suffering from chronic diseases such as kidney, respiratory tract, skin, thyroid, and mental depression and olfactory dysfunction should not be engaged in cyanide work. IX. For places and places where the above preventive measures are not effective and must be entered temporarily and work for a certain period of time, if the risk is high, anti-Cyanide prevention tablets should be taken in advance. X. For parking and overhaul, for those containers that may accumulate hydrogen cyanide gas, first ventilate and determine the content of hydrogen cyanide. When the content of hydrogen cyanide is less than 0.3mg/M3, it can enter. In particular, cyanide-containing liquids and slurries, when parking, the carbon dioxide in the air neutralizes the alkali in the water, so that the pH of the liquid gradually decreases, and the generated hydrogen cyanide continuously escapes into the gas phase, and the concentration thereof is high. If ventilation and venting measures are not taken, the person entering the site will be stunned and dying within tens of seconds to minutes. This is a precedent in our country. Table 2-6 Toxicity of certain cyanide to animals Cyanide species Animal species Toxic dosage of lethal dose (mg/L) Hydrogen cyanide frog subcutaneous 60 (hydrocyanate) White subcutaneous 5.3~10 Guinea pig subcutaneous 0.1 Rabbit oral 4 Cat Subcutaneous 1.1 potassium cyanide frog skin 149 pigeon muscle

4 mice subcutaneous 3 to 10 rats orally 10 to 15 dogs orally 1.6 to 5.3 rabbit muscle 3.0 sodium cyanide frog skin 60 to 65 white mice subcutaneous 10 rabbit muscle 5 dog muscle 3 2.3 cyanide toxicity to livestock HH of higher animals Symptoms of acute poisoning have something in common, that is, the initial breathing excitement, after paralysis, lateral flank, coma, suffocation, suffocation, respiratory paralysis, and finally death. For dogs, cats and monkeys, there is regular regular vomiting. According to the literature, the lethal dose of cyanide in cattle is 0.39~0.92g, the sheep is 0.04~0.10g, the horse is 0.39g, the dog is 0.03~0.04g, and the toxic dose of sheep is 1.05mg/ Kg body weight. The lethal concentration of hydrogen cyanide on cattle was 103 mg/L. Dogs are 0.35mg/L, cats are 0.12 mg/L, mice are 0.044 mg/L, rats are 0.12 mg/L, rabbits are 0.35 mg/L, and pigeons are 0.125-0.150 mg/L. For dogs, cats, monkeys The concentration of inhaled poisoning is also similar to the concentration of human poisoning. Table 2-6 shows the cyanide poisoning situation in some animals. There are fewer examples of livestock poisoning or death from inhalation of hydrogen cyanide gas. This is mainly due to the fact that during normal production, the amount of hydrogen cyanide escaping from the liquid phase is extremely small, and hydrogen cyanide dissipates quickly in the air, generally not A high concentration of hydrogen cyanide will be formed in some areas, and livestock will generally not enter the vicinity of the place where hydrogen cyanide is produced or used. Livestock are poisoned by ingestion of cyanide-containing wastewater, and there are relatively many deaths. The main reason is that cyanide-containing wastewater forms water in running, flowing, dripping, leaking or flowing into low-lying areas, and cattle, sheep, etc. This water causes poisoning and death. In normal production, the cyanide-containing wastewater discharged is treated because the cyanide-containing wastewater is low and will not cause poisoning to livestock. Only when the treatment facilities are not well managed, the design is unreasonable or there is no medicine can the drainage be made. Serious cyanide over-standard causes livestock poisoning. Large cattle such as cattle have the habit of eating salt and drinking salt water, while the cyanide-containing wastewater in the gold industry contains about 0.4-5 kg/m3 of salt after being treated by the alkali chloride method. If the cyanide treatment is not enough, the cattle may cause a large amount of drinking. Poisoning or death, so the tailings pond should be carefully guarded or fenced around it to prevent livestock from entering. In short, the cyanide plant should strictly enforce environmental regulations. The cyanide-containing wastewater and waste slag should be placed in the treatment setting, and should not be arbitrarily discharged, dumped in other places, and pipelines containing cyanide wastewater and waste slurry should be inspected to prevent breakage. The resulting leakage, in case of leakage, can be bleached to destroy cyanide (except for wastewater). 2.4 The toxicity of cyanide to aquatic organisms 2.4.1 The effect of cyanide on animals in water Cyanide is very toxic to aquatic organisms. When the concentration of cyanide ion is 0.04~0.1mg/L, it can kill fish, even In the water with a cyanide ion concentration of 0.009 mg/L, the ability of the squid to swim against the water is reduced by about 50%. The toxicity of cyanide to fish is related to the environment. This is because the toxicity of cyanide is mainly caused by the formation of hydrocyanic acid. Therefore, the change of pH can affect the toxicity, that is, the toxicity of cyanide under alkaline conditions. It is weak, and when the pH is lower than 6, the toxicity is increased. In addition, the concentration of dissolved oxygen in water can also affect the toxicity of cyanide. For example, in water with a cyanide concentration of 0.105-0.155 mg/L, the survival time of rainbow trout will increase with the increase of dissolved oxygen from 10% to 100%, the concentration of dissolved oxygen is large, and the survival time of fish is long. The presence of different metal ions also affects the toxicity of cyanide. For example, when zinc or cadmium ions are present, they act synergistically with cyanide ions, thereby enhancing toxicity, and when copper ions are present in nickel ions, Cyanide ions form stable complex ions, which can reduce their toxicity. See Table 2-7, Table 2-8, and Table 2-9 for details. It can be seen that the toxicity of simple cyanide is much greater than the toxicity of complex cyanide. In addition, the toxicity of inorganic cyanide is much greater than that of organic nitrile. Table 2-7 Toxicity of cyanide to carp when complexed with various metal ions (20 °C) The average tolerance (measured in mg/L of cyanide ion) in complex cyanide 24 hours 48 hours 96 hours sodium 0.25 0.24 0.23 zinc 0.20 0.19 0.18 cadmium 0.23 0.21 0.17 nickel 2.5 0.95 copper 2.2 2.0 1.5 Note: The mg/L of cyanide ion in Table 2-7 refers to the total cyanide concentration. Table 2-10 describes the acute poisoning concentrations of cyanide for various fish species. Table 2-8 Effect of cyanide on fish in electroplating wastewater Cyanide type concentration test Biological effect mg/liter means sodium cyanide 0.3 CN- squid, squid have no effect on potassium cyanide within 24 hours 0.04~1.2 CN- Goldfish 3 to 4 days of death, cyanogen chloride 0.08 CN- fish life and death critical point potassium ferricyanide 984 CN- squid, goldfish not dead potassium ferricyanide 848 CN- squid, goldfish do not die Table 2-9 Acrylonitrile wastewater main toxicity Toxic test

In order to prevent cyanide poisoning, the total cyanide concentration in the fishery water body shall not exceed 0.005 mg/L. It can be seen that the cyanide-containing wastewater must be treated in strict accordance with the regulations to meet the discharge standards stipulated by the national environmental protection department. For reservoirs or fish ponds or nature reserves downstream of the discharge port, the cyanide-containing wastewater should be treated in depth according to the requirements of the environmental protection department. To make the drainage reach the corresponding water quality standards. Table 2-10 Acute toxicity of cyanide to fishes Observation of fish species Total cyanide concentration (mg/L) Safety concentration of white peony 0.32 Lethal concentration of carp and grass carp 0.15～0.2 Minimum lethal concentration of carp 0.2 Ababa semi-lethal concentration 0.39 White Minimum lethal concentration of fish (4 days) 0.06 Minimum lethal concentration of carp (4 days) 0.2 Death of river otter (5-6 days) 0.05 Rainbow poisoning (3 days of turning) 0.07 Survival of big mullet (4 days) 0.40 Cyanide In addition to being highly toxic to fish, it is also very toxic to other aquatic organisms. According to the data, at 20 ° C and pH 6.1 to 8.7, the impact of cyanide on large leeches is: cyanide concentration 2.0 ~2.5mg / L, 24-28 hours of poisoning; cyanide concentration of 1.5 ~ 2.0mg / L, 12 ~ 120 hours of poisoning; 0.2mg / L of 120% after 1 hour of death; 0.05mg / L of no What is the bad influence. According to other data, the maximum allowable concentration of plankton and crustaceans is 0.01mg/L, and the maximum allowable concentration of cyanide in aquatic animals with greater resistance is 0.1mg/L. There is also information that when the cyanide concentration is 3.4mg / L, 48 hours of water mites are killed. Microorganisms in water can destroy low concentrations of cyanide, making it a non-toxic simple substance, but it consumes some dissolved oxygen in the water. This is the basic principle of cyanide-containing wastewater, so it can be treated with activated sludge. High, it will have a toxic effect on bacteria, thus affecting the biochemical treatment process of wastewater. According to research, when the cyanide concentration is greater than 1mg/L, it will affect the processing capacity of activated sludge. The concentration of cyanide-containing wastewater passing through the biofilter should not exceed 2 mg/L. The presence of cyanide in water will reduce dissolved oxygen in the water, reduce biochemical oxygen demand, and reduce digestion, which will also cause a series of water quality problems. In a domestic mine, the lack of chlorine gas causes the concentration of cyanide in the external drainage to exceed the standard, and reaches 50mg/L when the water is high. After the drainage enters a stream, the water volume is about one-thirtieth of that of the stream. All the water creatures in the creek are dead. The green moss growing on the pebbles in the water all flakes and dies. The pebbles are reddish, while the creek receives the upper part of the cyanide-containing wastewater. Fish, frogs and underarms often grow. Swimming, all kinds of water and plants grow vigorously, forming a sharp contrast. 2.4.2 The effect of cyanide on plants is described in the literature. Cyanide can cause carcinogenesis of laver, which can enlarge a part of somatic cells of laver. Or the cell division is abnormal, from a general single layer arrangement to a multi-layer arrangement, in severe cases, chestnut spots or curls appear on the leaves. When the concentration of cyanide in irrigation water is below 1mg/L, the growth of wheat and rice is normal. When the concentration is below 0.5mg/L, the growth of crops is stimulated. The yield is increased. When the concentration is 10mg/L, the rice begins to suffer. The yield was 78% of the control, and the damage of wheat was not obvious. When the concentration was 50mg/L, both wheat and rice were obviously affected, but the damage of rice was more serious. The yield was only 34.7% of the control and 63% of the control of wheat. When the cyanide content was 1 mg/L, the growth and development of rice began to be affected. When the concentration was 10 mg/L, the growth of rice was obviously inhibited, and the yield was 50% lower than that of the control. When 50 mg/L, most of the damage was caused by death, and a few remained. The plant is no longer strong. Irrigation of wheat rice with low cyanide-containing sewage (<0.5mg/L), the fruit contains very low cyanide, generally in the range of dozens of PPb. In the land with serious pollution of cyanide-containing wastewater, the yield of fruit trees is reduced, and the amount of results is reduced.但低浓度的含氰废水对大田作物的影响较小，甚至还有农民用氰化厂尾矿库排水浇地使粮食增产的情况。除了氰化物能转变为氮肥外，废水中少量的铜、锌等元素也有利于作物的生长。 2.5 氰化物衍生物的毒性氰化物的各种衍生物即氰、氯化氰、氰酸盐、硫氰酸盐也都有毒，但毒性各不相同。其中氰的毒性与氰化氢相似，在这里不再赘述，氯化氰的毒性与氰化氢相近，硫氰酸盐的毒性较小，下面分别介绍。 2.5.1 氯化氰、溴化氰的毒氯化氰是一种刺激性极强的气体，因其作用与光气及氰化氢相似，第二次世界大战期间法国曾用作毒气，氯化氰对人和动物的呼吸道和支气管有强烈刺激，能引起肺水肿而致死。对人来说，在极低的浓度下，就能刺激眼、咽喉而催泪、咳喇，并且在0.05mg/L(20PPM)的浓度下1分钟也忍耐不了。如果长时间吸入比这更低浓度的气体时，能引起轻度的结膜炎、嗓音嘶哑而且还能引起消化器官的障碍

.在120mg/m3条件下，接触30分钟后即死亡。氯化氰进入人体内约有30%迅速变为氰化氢，与血红蛋白和谷胱甘肽反应，可释放出氰离子。氯化氰作用见表2-11。溴化氰也与氯化氰一样极毒，曾作为第一次世界大战期间澳大利亚军队的毒气。

黄金氰化厂大多数用氯气处理含氰废水，时常发生氯化氰气体逸出的事故，使操作者眼、鼻、咽喉受到很大刺激，并引起各种疾病，因此，必须采取必要的措施，确保良好的操作环境。 表2-11 氯化氰的作用效果动物类别氯化氰浓度作用时间作用情况mg/L PPM 小鼠0.2 80 5分没有损伤而能忍耐0.3 120 3.5分立即致死1.0 400 3分立即致死狗0.05 20 20分没损伤而能忍耐0.12 48 6小时立即死亡0.3 120 8分重症后可恢复0.8 320 7.5分立即死亡猫<0.1 <40 ─ 敏感度各有不同0.1 40 18分9天后死亡0.3 120 3～3.5分立即致死1.0 400 瞬时立即致死山羊2.5 1000 3分70小时后死亡家兔3.0 1200 2分立即致死2.5.2 氰酸及其盐类的毒性氰酸和异氰酸的无机盐比较稳定，游离酸中两者呈动态平衡同时存在，且极不稳定，即使在0℃下也会聚合为三聚物，三聚物受热时解离出氰酸。 氰酸强烈刺激皮肤、粘膜、呼吸道，并且在有催泪性、发疱性的气体下，有类似氰化氢的毒性。 异氰酸常与氰酸共存，因此性质类似。三聚异氰酸不溶于水及有机溶剂，具有与氰化氢同样的毒性。

O HO─C≡N─→H─N=C─O─→HN─CC=NH (氰酸) (异氰酸) │ │ ↓ ↓ OO OH O │ ‖ CCC │ NH NNH─NN─H (三聚异氰酸) │ │ │ │ HO─CC─OH CCNO=N=O │ H (三聚氰酸) (异三聚氰酸) 三聚氰酸因其被加热时在未熔前就分解为氰酸，故作为氰酸的原料生产除草剂等。其毒性尚不清楚，但其氯化物即氯化三聚氰酸刺激性强，在动物试验中呈现相当强的毒性。与氰酸及其聚合物相比，氰酸盐的毒性都很小。 LD50(mg/kg) 小鼠大鼠口服550～620 200～1270 腹腔或皮下注射300～310 300 氰酸盐是氰酸中的氢原子被碱金属离子取代后的产物，氰酸的结构是在氢氰酸(HCN)中引入一个氧原子;因此对人畜、鱼类的毒性很小，氰酸盐在排水中流失时，碱性条件下稳定，酸性条件下即被分解，此时，生成碳酸盐和氨，未检测出氰离子。 2.5.3硫氰酸及其盐类的毒性硫氰酸毒性小，比其它酸在酯类中的溶解度大，因此对细菌的作用强，在胃酸中单纯盐酸杀菌性不够，而因痕量的硫氰酸则确保其杀菌效果，微量的硫氰酸广泛地存在于动植物中，在唾液中为0.017～0.217mg/L，在尿中为0～0.006mg/L。 无机硫氰酸盐与氰酸盐不同，其毒性小危险性也小，它在机体中分解可生成硫氰酸但并不生成氰离子，因硫氰酸有强烈地使蛋白质膨润的性质，可使细菌膨润而抑制其生长，所以从前在含嗽水中添加它来作为杀菌剂，但在动物试验中不论采用何种给药方法，一次投给0.5g/kg的时候，则有腹泻、呕吐、角弓紧张、痉孪、强直性局部麻痹，带有蛋白尿的肾障碍之后出现过敏症，如反复少量投药时，在甲状腺中蓄积而阻碍碘的蓄积作用，造成甲状腺疾病，此外，长期服用时，可降低血压，但作用机理不明，对人体的中毒作用表现最明显的是粘膜过度剥离皮肤发红，皮炎，生理变态，肾障碍等，硫氰酸盐与氰化物的毒性之比较见表2-12。硫氰酸盐在水中对鱼类的允许浓度与其它盐类之比较见表2-13。 表2-12 无机氰化物和硫氰酸盐的毒性比较化合物名称化合物分子式毒性(mg/kg体重) 无机氰化物NaCN 兔(经皮)MLD2.5 KCN 大鼠MLD2.5 狗口服MLD1.6 无机硫氰化物NH4SCN 小鼠LD50 720±113 NaSCN 大鼠LD50 764 KSCN 大鼠LD50 854 表2-13 硫氰酸盐对鱼类的允许浓度(PPM)与其它盐类的比较化合物名称Nellist实验Gollmac实验无机氰化物0.3 1.0 NH4SCN 200 200 (NH4)2SO4 262 500 NH4Cl 194 500 由表2-13可见，硫氰酸铵的毒性与硫酸铵、氯化铵相当。 近几年，国外报导，硫氰酸盐在水中可被某种重金属离子如镍所分解，产生氰化物，而且硫氰酸盐在人体中的积累会防碍人体甲状腺激素的合成，引起甲状腺机能不足症，故外排水中硫氰酸盐含量高时，也应考虑处理措施。尤其是不能做饮用水。 异硫氰酸与硫氰酸同时经游离态存在时不能分离开，故其毒性也较小，但由于它刺激皮肤、粘膜、特别是眼睛，所以要十分注意。 前苏联饮用水标准中，SCN-与氰化物浓度均为0.1mg/L。 2.5.4 乙腈的毒性乙腈具有醚的香味，毒性小，在乙腈饱和的空气中大鼠停留4小时以上不致死，但对小鼠15分钟就可致死。这种明显的差别与大鼠和小鼠的甲状腺活动差别有关，因此用含甲状腺素的甲状腺制剂可以对乙腈解毒，有关乙腈的致死浓度，从动物实验结果提出，工作场所空气中最高允许浓度为3mg/L(70mg/kg体重)。乙腈经口服的致死量LD50对大鼠为3.8g/kg，对小鼠为0.2g/kg，对家兔、猫则居于其间，对家兔的皮下注射最低致死量为130mg/kg。 总之，含氰废水对环境的污染并不仅仅是氰化物的污染，氰酸盐?硫氰酸盐、重金属等均存在于废水中，其协同作用对生物、植物产生的危害比单独氰化物时更大些。

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