In fact, both types of substances belong to the larger category of poisons. There is no absolute boundary between toxins and non-toxins.
There is a famous saying: "All substances are poisons, and no substance is not a poison; the only difference is their dosage".
In a sense, nature does not exist absolutely toxic or absolutely non-toxic substances,
such as, arsenic, mercury, snake venom, etc., we all know that the poison, if used in less than the dose of poisoning, can be used as a clinical treatment of certain diseases; and we rely on the survival of oxygen, if a high concentration of more than the normal need to enter the body into the body, will also occur oxygen poisoning.
And the ability of a poison to cause damage to the body is called toxicity.
We usually see the "high toxicity", "low toxicity" and so on actually refers to the toxicity of the poison. According to the WHO acute toxicity grading standards, the toxicity of poisons are graded as follows:
1, acute toxicity: toxicity grading 5; adult lethal dose, less than 0.05 g / kg body weight; 60 kg of adult lethal dose, 0.1 grams.
2. Highly toxic: Toxicity grade 4; adult lethal dose, 0.05-0.5 g/kg body weight; total lethal dose for 60 kg adult, 3 g.
3, moderately toxic: toxicity classification 3; adult lethal dose, 0.5-5 g/kg body weight; 60 kg adult lethal total, 30 g.
4, low toxicity: toxicity classification 2; adult lethal dose, 5-15 g/kg body weight; 60 kg adult lethal total, 250 g.
5. Microtoxicity: Toxicity classification 1; adult lethal dose, greater than 15 g/kg body weight; 60 kg adult lethal total, greater than 1,000 grams.
In forensic science, according to the identification of different purposes, the classification of poisons is not consistent,
such as in the analysis of symptoms of poisoning and pathological changes, often used according to the classification of toxicological effects;
In the chemical analysis of poisons, often used according to the classification of the chemical properties of poisons;
For the tracing of the source of poisons, the use of the body and its role in the organism, it is more used Mixed classification.
For detective work, the main use of the last classification - mixed classification:
1, according to the toxic effect of poison classification:
(1) corrosive poison. Refers to the body localized strong corrosive effect of poisons. Such as strong acids, strong alkalis and phenols, etc.
(2) Substance poison. Poisons that introduce pathological damage to organs and tissues after absorption. Such as arsenic, mercury heavy metal poison.
(3) Enzyme system poison. Inhibition of specific enzyme poisons. Such as organophosphorus pesticides, cyanide and so on.
(4) blood poisoning. Poisons that cause changes in the blood, such as carbon monoxide, nitrite and some snake venom.
(5) neurotoxicity. Poisons that cause central nervous disorders. Such as alcohols, anesthetics, tranquilizers and hypnotics, as well as strychnine, nicotinic acid, cocaine, amphetamines, etc.
2, according to the chemical nature of the poison classification:
(1) volatile poisons. Possible distillation or trace diffusion method of separation of poisons. Such as cyanide, alcohols, phenols, etc. .
(2) Non-volatile poisons. Poisons separated by organic solvent extraction. Such as barbiturates hypnotic drugs, alkaloids, morphine and so on.
(3) metal poisons. Using the method of destruction of organic matter to separate the poison. Such as arsenic, mercury, barium, chromium, zinc and so on.
(4) anionic poisons. The use of dialysis or ion exchange method of separation of poisons. Such as strong acids, strong bases, nitrites and so on.
(5) other poisons. Other toxicants must be separated according to their chemical properties using special methods. Such as arrow poisonous alkali, carbon monoxide, hydrogen sulfide and so on.
3, mixed classification. That is, according to the source of poison, use and toxic effects of comprehensive classification.
(1) corrosive poisons.
Including corrosive acids, alkalis, such as sulfuric acid, hydrochloric acid, nitric acid, phenol, sodium hydroxide, ammonia and ammonia hydroxide.
(2) Destructive poisons.
Toxins that can cause damage to the tissues of living organisms. Such as arsenic, mercury, barium, lead, chromium, magnesium, thallium and other heavy metal salts
(3) Functionally impaired poisons.
such as obstacles to cerebral spinal cord function of poisons, such as alcohol, methanol, hypnotic sedative tranquilizers, fenugreek alkaloids, atropine, isoniazid, opioids, cocaine, amphetamine, hallucinogens, etc.; obstacles to respiratory function of poisons, such as cyanide, nitrites and carbon monoxide, etc..
(4) Pesticides.
such as organophosphorus, carbamates, pyrethroids, organomercury, organochlorine, organofluorine, inorganic fluorine, chlorpyrifos, methomyl, chlorothalonil, chlorothalonil, chlorothalonil, chlorothalonil, bromomethane, zinc carbamate and so on.
5) Rodenticide.
Zinc Phosphide, Dichlorvos, Amtol, Sodium Dichlorvos, Rodenticide, etc. .
(6) Poisonous plants. Such as aconite plant, hookah, mandrake, oleander, poisonous mushrooms, mangosteen, red fennel, thunderbolt and so on.
(7) Poisonous animals. Such as snake venom, puffer fish, spotted fibers, toads, fish bile, bee venom, etc.
(8) Bacterial and mycotoxins. Such as salmonella, botulism, staphylococcus and other bacteria, as well as aflatoxin, moldy sugarcane, black spot disease sweet potatoes and other fungi
What are the more common poisonous flowers and fruits in daily life? What are the symptoms of poisoning?
There are many kinds of toxic plants, and their toxic components are very complex. Some toxic plants have a single toxic component, but some contain multiple toxic components (one of which can be the main one). In addition, there are many toxic plants contain toxic components are not yet fully understood. Classification of toxic components, toxic plants can be divided into:
(1) alkaloid-containing, alkaloids are a class of nitrogen-containing organic compounds.
There are many kinds of alkaloid-containing toxic plants, most of which are found in the family of Scrophulariaceae, Poppies, Antipathaceae, Rutaceae, Strychnos, Solanaceae, Ephedraceae and so on.
The common ones are atropine, strychnine, morphine, cocaine, aconitine, hookahine, and tretinoin.
(2) containing cardiac glycosides, cardiac glycosides have cardiac effects in small doses, larger doses can cause cardiac toxicity to arrest.
This kind of poisonous plants are mostly found in the Genusaceae, Oleanderaceae, Mushroomaceae, Weishauptaceae, Liliaceae and other certain species, such as oleander, Nelumbo nucifera, Fuchsia. Arrow poison also contains cardiac glycosides.
(3) cyanogenic glycosides, cyanogenic glycosides molecules containing cyanide, characterized by hydrolysis can generate hydrocyanic acid, this kind of toxic plants are mostly found in the Rosaceae and Leguminosae.
such as bitter almonds, bitter peach kernel, batch poi kernel, cassava and so on.
(4) saponin-containing, this kind of poisonous plants are mostly found in the legume family, Sapindaceae and Dioscoreaceae in some species, with hemolytic effect,
such as soap pods, wild yam, Shanglu, mouton and so on.
(5) Containing toxic proteins, mainly found in the seeds, have the effect of damaging liver and kidney parenchymal cells, causing degeneration and necrosis.
Such as the croton, castor beans, auricularia and mushrooms.
In addition, poisonous plants can also contain terpenes (such as horse mulberry), lactones (such as mangosteen), anthracene glycosides (such as aloe vera), phenols (such as white fruit) and other toxic ingredients.
And common chemical poisons are:
Carbon monoxide
Poisoning manifestations:
Acute CO poisoning is a systemic disease caused by inhalation of high concentrations of CO to central nervous system damage.
Acute CO poisoning has a rapid onset and short incubation period.
Mild and moderate poisoning is mainly manifested as headache, dizziness, palpitation, nausea, vomiting, weakness of limbs, blurred consciousness, or even coma, but the duration of coma is short, and after the rescue from the scene, it can be awakened quickly, and there is no obvious complication in general. The blood HbCO concentration is between 10% and 50%. Some patients showed EEG abnormalities.
Severe poisoning of the degree of consciousness to the degree of deep coma or decerebral cortical state. Often there is clenching of teeth, tonic generalized spasms, incontinence. Some patients can be complicated by cerebral edema, pulmonary edema, severe myocardial damage, shock, respiratory failure, upper gastrointestinal bleeding, skin blisters or patches of skin redness, muscle swelling and necrosis, liver and kidney damage. Blood HbCO concentration may be higher than 50%. Most patients have abnormal EEG.
The delayed onset encephalopathy of acute CO poisoning refers to the emergence of neuropsychiatric symptoms after the recovery of acute poisoning consciousness disorder, after 2-60 days of false healing period. The common clinical manifestations are as follows
a. Mental disorders: loss of orientation, significant decline in calculating power, memory loss, slow reaction, and inability to take care of themselves, and some of the patients may develop dementia syndrome.
Or hallucinations, illusions, incoherent speech, behavioral disorders, excitement and impulsivity, hitting and destroying things.
b. Extrapyramidal symptoms: the manifestation of dull face, increased muscle tone, slow movement, gait fragmentation, loss of accompanying movements of both upper limbs, small writing syndrome and resting tremor, the appearance of Parkinson's syndrome.
c. Conus nerve damage: manifested by mild hemiparesis, pseudobulbar palsy, positive pathological reflexes or urinary incontinence.
d. Focal dysfunction of the cerebral cortex: such as aphasia, blindness, dysgraphia, dyscalculia, etc., or secondary epilepsy.
Cranial CT may reveal areas of pathologic hypodensity in the brain. Electroencephalography may reveal moderate or high abnormalities.
Mild acute CO poisoning should be differentiated from cold, hypertension, food poisoning, etc. Moderate and severe poisoning should be differentiated from other causes such as diabetes mellitus, cerebrovascular accidents, sleeping pills, etc. Delayed onset encephalopathy needs to be differentiated from other disorders with similar symptoms.
Acute hydrogen sulfide poisoning
Hydrogen sulfide has a "rotten egg-like" odor, and produces strong irritation to the eyes and respiratory mucous membranes.
After absorption, hydrogen sulfide mainly affects the cellular oxidation process, resulting in tissue hypoxia
Poisoning manifestations:
Inhalation of hydrogen sulfide concentration and time according to the different clinical manifestations of the different severity.
The light is mainly irritation symptoms, manifested as tearing, eye stinging, runny, burning sensation in the throat, or accompanied by headache, dizziness, fatigue, nausea and other symptoms. The conjunctiva is congested, and the lungs may have dry rales, which can be recovered in a short period of time after being taken out of contact;
Moderate poisoning is characterized by worsening of mucous membrane irritation, coughing, tightness in the chest, blurred vision, conjunctival edema, and corneal ulceration; there are obvious symptoms of headache and dizziness, and mild impaired consciousness, and the lungs may smell dry or wet rhonchi.
An X-ray chest radiograph reveals enhanced lung texture or lamellar shadows;
Severe intoxication with coma, pulmonary edema, respiratory and circulatory failure,
Inhalation of very high concentrations (1000mg/m' or more), there can be a "lightning-type death". Severe poisoning can leave neurological and mental sequelae
Methylamine
Methylamine (CH3NH2) is a colorless gas at room temperature and pressure, with a specific gravity 1.07 times that of air.
Flammable, explosive, with a strong irritating ammonia-like odor. Alkalinity is stronger than ammonia. Generally pressurized into liquid storage or transportation.
Methylamine is mainly used as dyes, pesticides (such as methamidophos), pharmaceuticals (such as fenugreek, sulfanilamide), fuel additives, solvents, rocket propellant and so on.
During its transportation, production, use and pipeline maintenance, a large amount of monomethylamine leaks due to unauthorized operation, old equipment, overloaded transportation and other factors, resulting in poisoning occurs.
Methylamine can be absorbed through the respiratory tract, gastrointestinal tract and skin, and converted into dimethylamine or oxidized to formic acid in the body, which is similar to the toxic effect of methylamine on the human body and has a stronger effect.
Methylamine has a strong irritating and corrosive effect on the eyes, skin and respiratory mucosa, and has a sympathetic effect on the whole body.
Inhalation poisoning can appear cough, sputum, chest tightness, shortness of breath, cyanosis, severe patients can be seen laryngeal edema, pulmonary edema, and due to the detachment of the bronchial mucosa to cause asphyxia, pulmonary atelectasis, lung infections and so on.
A few severe patients due to the combination of subcutaneous emphysema, mediastinal emphysema, acute respiratory distress syndrome (ARDS), severe respiratory dysfunction, and the occurrence of brain, heart, liver, kidney and other multiple organ damage.
Skin burns Most patients with acute poisoning have varying degrees of chemical skin burns, mostly in the exposed parts of the skin, the burned skin is dark red, similar to strong alkali burns.
For patients with large skin burns, we should be alert to the percutaneous absorption of monomethylamine to aggravate systemic poisoning.
Eye burns may appear photophobia, tearing, eye pain, eyelid spasm, blurred vision.
Examination of the eyelids can be seen swelling, conjunctival congestion and edema, corneal clouding, corneal ulceration in severe cases, individual patients may appear blind.
Oral poisoning Oral administration of this product can cause burns in the mouth, throat, esophagus and stomach, which can be seen as nausea, vomiting, dry mouth, sore throat, dysphagia, epigastric pain, gastrointestinal bleeding.
Toxicity manifestations:
1. Irritation reaction Transient eye and upper respiratory tract irritation after exposure, no positive signs in the lungs, no abnormal findings on chest X-ray.
2. Mild intoxication Eye and upper respiratory tract irritation, conjunctival and pharyngeal congestion and edema; laryngeal edema with first- to second-degree inspiratory dyspnea; chest X-ray manifestations consistent with tracheo-bronchitis or peribronchitis.
3. Moderate intoxication One of the following:
laryngeal edema with third-degree inspiratory dyspnea;
chest X-ray findings consistent with acute bronchopneumonia or interstitial pulmonary edema.
Moderate toxic blood gas analysis is often associated with mild to moderate hypoxemia.
4. Severe poisoning:
asphyxia due to severe laryngeal edema or necrotic detachment of bronchial mucosa;
chest X-ray findings consistent with alveolar pulmonary edema;
acute respiratory distress syndrome
sudden death;
complication with severe pneumothorax, mediastinal emphysema, subcutaneous emphysema, or pulmonary atelectasis.
Severe poisoning blood gas analysis is often accompanied by severe hypoxemia.
Methanol
Methanol, also known as wood alcohol or wood alcohol, is a colorless, transparent liquid, highly volatile and flammable.
Acute poisoning is mainly characterized by central nervous system damage, eye damage and metabolic acidosis.
The vast majority of cases are caused by the accidental consumption of alcohol mixed with methanol, and a small number of cases are poisoned by respiratory inhalation and percutaneous absorption.
The lowest dose of oral poisoning is about o.lg/Kg, and the oral intake of O.3-1.g can be fatal.
The key points of judgment
1. Poisoning performance.
1. The incubation period is generally 2 to 24 hours, a few up to 2 to 3 days. Oral pure methanol poisoning shortest 40 minutes symptoms. Simultaneous intake of ethanol can prolong the incubation period
2. Central nervous system damage with headache, dizziness, fatigue, drowsiness and confusion. In severe cases, coma and seizure-like convulsions occur. A few patients may have psychiatric symptoms and extrapyramidal system damage.
3. Eye damage in front of the eyes, black shadow, snow feeling, flash feeling, blurred vision, eye pain, shyness, phantom vision. In severe cases, vision drops sharply, and even blindness. Ophthalmologic examination of most patients, pupil dilation, a few shrinkage, the fundus can be seen early optic papilla congestion and retinal edema, optic nerve damage in severe cases l ~ 2 months after the optic nerve atrophy. The visual field shows a central or paracentral dark spot change.
4. Metabolic acidosis is asymptomatic in mild cases, but in severe cases, dyspnea and Kussffiaul respiration may occur.
5. Digestive system damage oral poisoning nausea, vomiting and epigastric pain is more common, the proportion of complications of acute pancreatitis is higher, serious cases of liver damage
6. Respiratory system damage inhalation of poisoned people with eye and upper respiratory tract mucous membrane irritation symptoms.
7. Others may be accompanied by cardiac and renal damage in a few patients
2 Laboratory tests
l. Increased concentrations of methanol and formic acid in the blood
2. Metabolic acidosis is indicated by blood gas analysis or measurement of the carbon dioxide binding capacity of the blood.
3. In severe poisoning, blood leukocyte count and erythrocyte volume are increased, and there may be abnormalities in liver and kidney function. Individuals with myoglobinuria
4. Electrocardiogram shows ST-segment and T-wave changes, ventricular pre-systole.
5. CT examination of the brain in severe poisoning can be seen as hypodensity of white matter and basal ganglia, soft foci of pedunculated nucleus infarcts, etc.
Bitter almonds
Bitter almonds peeled and tipped, soaked in hot water for a day, cooked uncovered, can be eaten. Raw food or improper processing can lead to poisoning.
Bitter peach kernel, batch of kernel, flaxseed kernel, prune kernel, plum kernel, cherry kernel, apple kernel poisoning principle, diagnosis and treatment are the same as bitter almonds. A large number of raw sweet almonds can also be poisoned
[Toxicity OverviewBitter almonds contain about 3% amygdalin.
The bitter amygdalin belongs to cyanogenic glycosides, the oral LD50 of rats is 0.6 g / kg, under the action of the enzyme amygdalin, hydrolyzed to generate hydrocyanic acid and benzaldehyde, etc.
The bitter amygdalin is a cyanogenic glycoside.
Hydrocyanic acid can inhibit the activity of cytochrome oxidase, resulting in intracellular asphyxia, and first act in the medulla oblongata center, causing excitation, and then cause the medulla oblongata and the entire central nervous system inhibition, more than one due to respiratory center paralysis and death.
The amount of bitter almond poisoning, adults eat 4D ~ 6O grain. Children eat 10 to 20 grains of raw, lethal amount of about 60 grams.
Bitter peach kernel, the machine tool kernel lethal amount of 0.6 grams (about 1 grain) / kg, 2.5 ~ 4 grams (2 ~ 3 grains) / kg
Judgment points]
1. fast onset of the disease, most of them in the eating within 2 hours
2. mild poisoning digestive tract symptoms and red face, headache, dizziness, weakness, irritability, numbness of the lips and tongue, panic, chest tightness, etc., respiratory pain, and the symptoms of the digestive tract. The breath smells like bitter almonds
3. In severe poisoning, there are dilated pupils, loss of light reaction, impaired consciousness, paroxysmal convulsions, weak respiration, cyanosis, shock, etc., peripheral neuritis can occur, and most of them die of respiratory paralysis
Laboratory examination
1. identification of toxicants of gastric contents, which confirms the presence of cyanide
2. increased level of urinary thiocyanate Increased levels of thiocyanate in the urine
There is as yet no satisfactory definition of a poison. Strictly speaking, poisons are chemical substances that can impair the normal activities of life, cause functional or organic lesions and even death through chemical action after entering living organisms. Historical records show that poisoners were likely to succeed without being easily detected as long as they were careful.After the 17th century, some professional poisoners were usually employed by some wealthy people and occasionally by European royalty. Such major cases were generally difficult to detect.
The simplest and most commonly used poison was arsenic. This poison was used a long time ago. For example, in the novel "Water Margin", it is recorded that Pan Jinlian poisoned Wu Dalang, using arsenic (arsenic trioxide). Because arsenic poisoning, whether acute or chronic, is difficult to detect, even clinicians often misdiagnose arsenic poisoning as a variety of different diseases. Countless troubles can end in the blink of an eye under the effects of this horrible drug. And while no one has been able to determine the cause of death, it's different now.
In 1790, a chemist by the name of John Messger discovered that if a substance contained arsenic, a white layer of arsenic oxide appeared on a cool metal plate after the substance was heated and placed on top of the vapor. Although this layer of arsenic mirrors proved that the substance had been impregnated with arsenic, it could not tell whether arsenic had been absorbed in the body.
After 1806, this problem was solved by Dr. Valentin Rhodes. At that time he was working at the Forest Chemical Works, where he extracted the stomach contents of a corpse and boiled them in a pool, removing the remaining muscle tissue by filtration. He then treated this filtrate with nitric acid, which made it easier to form an arsenic mirror.
By far the greatest development in toxicology came in 1836. The chemist James Marcy invented a method of solving for the smallest doses of arsenic. This method was similar to that of Meggs. But instead of letting the vapor evaporate onto a metal plate, as in the past, most of the vapor was allowed to go into the air. The whole process is carried out in a U-shaped test tube. In the tube the vapors enter and exit only through a small orifice. The suspected substance is dropped on a zinc disk, which is then covered with a thin layer of sulphuric acid for the purpose of producing hydrogen. Any arsenic-containing gas heated through the tube and reaching the cooled portion of the tube would condense to form an arsenic mirror. The arsenic mirror reaction has been used up to the present day as well.
Arsenic, of course, is not just the only weapon used by poisoners; in addition there are traditional poisons such as phenylmethane and cyanide. To solve every type of poisoning case, modern analysts must constantly battle new poisons.