Toxic Lethal War Poisons

Description

The use of toxins of war dates from World War. There is evidence that such practices were used and before its outbreak. In recent years signed several conventions which prohibit the use of chemicals in case of war. The last of these conventions was signed in Paris in 1993. Recently, it talks about the possibility of terrorist attacks using chemicals against civilians, something that already happened resulting in the Tokyo train station killing 12 people and injuring more than 5000.

War toxins can be classified into several categories. Generally, they are divided into two main groups, the non-lethal and lethal.

Lethal toxins - kills or causes serious pathological conditions that can not be solved except through the application of complex and long-term therapeutic measures. For survival, the victim remains, most likely, with sequels, more or less serious. At low concentrations, can cause only incapacitating effects. In this category are general toxins such as cyanide neurotoxicele and derivatives, and sufocantele vezicantele.

Disabling toxins (lethal) - are chemical substances that cause temporary physical or mental incapacity. The psychological effect depressant or stimulant substances include central nervous system. The physical effect include iritantele ( tear , smoke, sternutatorii) colinergicele parkinsonian effect (oxotremorina) hipertensivele (guanethidine), paralizantele (decametoniu) and emetizantele (apomorphine).

Lethal toxins

1. Sufocantele
Chemical agents that cause respiratory disorders can lead to pulmonary edema acute lesion. They include a wide range of substances among which phosgene, difosgenul, methyl isocyanate, ammonia , nitrogen oxide, per-fluoro-isobutilen (PFIB). It should be noted that none of the respirator filter cartridge filter PFIB’s not, so that use insulating breathing apparatus, positive pressure mask, is mandatory.
The products mentioned are either gases or volatile liquids. Phosgene, for example, is an extremely dangerous toxic considering that smell can be detected only at a concentration of 22 mg / m 3 . At this concentration, signs of irritation, respiratory and eye, occurs in less than a minute. Being heavier than air remains at floor level. Sufocantele adsorb in different materials for a long period of time remaining in the space.

Effects on the body - where a person remains an hour in a room with 50 mg phosgene / m 3 is observed serious injuries epithelium bronchialcapillary and the alveolar and lung interstitium and secretion of surfactant is impaired. Increased membrane permeability will lead to acute toxic pulmonary edema. For survival, the above-mentioned lesions lead to the appearance of pulmonary fibrosis . A concentration of 300 mg / m 3 is lethal in about 30 minutes.

Symptoms - irritation of the eyes and airways, with a feeling of tightness or chest pain . If the person leaves immediately toxic environment, these symptoms disappear quickly. If the person remains in the toxic environment, the initial period, characterized by irritative symptoms lasting about 2-8 hours (depending on the concentration of toxic). In the phase of clinically silent and 2 hours before the appearance of acute pulmonary edema are present radiological changes. Hilurile general appearance of pulmonary opacities essentially of bulk especially in central areas of the lungs.
The onset of pulmonary edema is masked by tachypnea and a locked chest, followed by dyspnea , anxiety , irritating cough, expectoration of yellow-or hemoptoica, nausea, vomiting, epigastric . Intoxicated person may have a face congested, even cyanotic, with shock , hypocapniaand alkalosis respiratory. May occur hematuria or install anuria. The patient became unconscious with a predominant picture of respiratory failure acute. Death is usually due to respiratory failure or heart failure .
2. Neurotoxicele
Organophosphorous substances are related to products used as pesticides . Sarin gas used in the terrorist attack in Tokyo, part of this group of toxins.

Can be classified into:
- Fugitive (Agent G, cyanic acid esters);
- Persistent (V agent);
- Semipersistente (Soman).

These products are presented in liquid form at ambient temperature. Vapors that increase the amount of time with increasing temperature and lead poisoning by percutaneous and respiratory. Neurotoxicele are substances that adsorb and can be absorbed. Can traverse most materials such as wood, textiles, paint, skin. Contaminated materials are sources of poisoning in a sustainable period. These substances easily cross the gloves of latex , the butyl rubber is more durable and offer a form of protection. Neurotoxicele are easily hydrolyzed with concentrated alkaline solution and water (Javel water).

Effects on the Body - inhibits enzymes essential for the functioning of the nervous system - plasma butyrylcholinesterase and acetylcholinesterase red blood cells and tissue.
Acetylcholine is no longer hydrolyze but accumulates in the cholinergic muscarinic and nicotinic receptors. This accumulation causes a hyperactivity in the autonomic ganglia, parasympathetic nerve endings of the neuromuscular junction and at synapses of the central nervous system .
Neurotoxicelor toxicity is extreme. A drop of 0.5 to 10 mg of VX on the skin of the victim leading to death. Lethal toxic concentration for 50% of people who inhale the gas Soman to die (CTL 50) is 25-100 mg / m 3 of air inspired per minute at a respiratory rate of 15 liters per minute.

Symptoms - depends on the dose and route of toxic penetration.
I. In the case of massive inhalation or exposure to Agent G (VX in contact with small amounts) – poisoning is severe and is associated with:
- Paralysis of the respiratory center;
- Neuromuscular blocking the plate, leading to a chest muscle paralysis, flaccid;
- bronchospasm severely
- Abundant secretions that can flood the upper airway;
- Loss of consciousness;
- Convulsions that can occur in minutes, as a form of intense and prolonged, irreversible damage induced by the CNS ;
- Activity of cholinesterase plasma and red blood cells is reduced by 70-80%.
Poisoning can be saved if breathing is assisted early. Otherwise, death may occur even in the first minutes.

II. Brief exposure to neurotoxic fumes – clinical signs limited to:
- miosis , frontal headache ;
- rhinorrhea , hypersalivation abundance, dyspnea marked cough;
- Tearing.
Erythrocyte cholinesterase activity at this stage is still normal.

III. Cutaneous or gastrointestinal absorption and prolonged exposure to vapors – associated clinical signs are:
- sialoree , nausea, vomiting, epigastric pain;
- Chest pressure, bronhoree , dyspnoea, cough;
- sweating , pallor or cyanosis ;
- bradycardia (occasionally tachycardia );
- Tearing;
- miosis (unless there was direct contact between toxic and eye);
- Emission of urine;
- Muscle weakness, fasciculations, trembling until the appearance of paralysis ;
- coma , convulsions , respiratory failure .

3. Vezicantele
The components of this group shows a general toxicity, their mode of action is different from one substance to another. It causes the appearance of debilitating skin lesions “flictene” acutely toxic and cause pulmonary edema.

I. Yperite - considered the most dangerous lethal vesicant agents as there is no antidote or effective course of treatment. These agents were often used during the First World War and is believed to have been used during the Gulf War in 1991.
These agents have a penetrating power and fast (5-6 minutes) in all common materials such as clothing, wood, paint, skin. They persist in soil and chemical stability. Are poorly soluble in water which, when brought into contact, forming hydrochloric acid and tiodglicol or triethanolamine. Their harmfulness increases with increasing ambient temperature.

Effects on the body - are highly alkaline products that react on contact with proteins and nucleic acids, altering especially rapidly dividing cells (keratinocytes, mucosal epithelial cells and parenchymal). It works chemotherapy and the resulting cell necrosis induced inflammatory response. Their toxicity is lower than organofosforielor, but their effect on medium and long term is not neglected. Mortality during the First World War was estimated at 2%.

Symptoms - installs faster or slower depending on the amount of substance inhaled or in contact with skin.
- The eye - if mild poisoning victim and will have tears stinging sensation accompanied by itching and burning. If poisoning is severe, clinical signs usually develop within 1-2 hours and is characterized by intense pain, photophobia , blepharospasm . There is a conjunctivitis and eyelid blistering level. Blindness can occur from secondary infections and corneal damage. Between the iris and pupil can develop a severe injury that will reduce the movements of the latter, predisposing to the occurrence of glaucoma .
- In the skin - skin barrier penetration is made in less than three minutes and is painless. Initially there is an intense erythema with itching, painful, then form flictene fragile wall, with content that has a tendency to clotting. Breaking flictenelor lead to bleeding lesions that progress tonecrosis in the epidermis and dermis.
- The respiratory system - nasal congestion and epistaxis , followed by irritation and burning sensation in the throat associated with lower respiratory tract congestion. Cough, initially dry, rapidly becomes productive with purulent sputum. Bronchi become obstructed with secretions and fragments of necrotic epithelium. Death occurs by mechanical asphyxia, pulmonary edema and acute lesional hemorrhagicbronchopneumonia after superinfection, sepsis with leukopenia and atelectasis secondary.
- The digestive system - easy cholinergic effect of causing moderate gastrointestinal symptoms (nausea, vomiting, bloody diarrhea).
In general, regardless of the route of penetration, toxic causes symptoms similar to that caused by radiation, with severe immunosuppression. Appear vomiting, abdominal pain, oligoanurie epithelium destruction due to renal tubular necrosis ranging, stimulatingthe central nervous system followed by a depression of his seizures , impaired consciousness, abnormal heart rhythms , anemia, trombocitipenie and leucopenia reaching the marrow aplasia .
The major risks in the short and medium term are infectious, the medium and long term addresses forming organs and the long term areteratogenic and carcinogenic .
II. Lewisites - is derived by substitution of hydrogen organic arsenic. Vesicant effect combines with the toxic effect of arsenic. It was used and mixed with neurotoxicele Yperit potentate’s causing toxic effect of the latter.

Effects on the Body - inhibits enzymes of the thiol (SH), in particular hexokinase and pyruvate dehydrogenase.

Symptoms - is similar to that caused by Yperit but appears much earlier. It is characterized by nasal irritation and a burning sensation in eyes, skin and respiratory system.
III. Of phosgene oxime (CX) - is a white powder, soluble in water and organic solvents.

Effects on the Body - CX vapors are very irritating to the eye causing severe corneal damage even at low concentrations, can affect the respiratory mucosa causing acute toxic pulmonary edema.

Symptoms - burning sensation in the eye with the appearance of conjunctivitis . At develop a skin rash accompanied by localized swelling and the appearance of blisters and areas of necrosis. It is very irritating to the upper airway, pulmonary edema being able to develop as a result of inhalation or percutaneous exposure. Inflammatory and hemorrhagic reactions appear localized to the gastrointestinal tract.
IV. Mycotoxins - their use has been reported in conflicts in Cambodia and the war in Afghanistan (red or yellow rain). It presents as a crystalline powder of different colors (yellow, red, white). Penetrates the human body via skin and mucosa, and their toxicity is lower than the organophosphorus derivatives.

Effects on the Body - mycotoxins structure gives them a strong inhibitory action in the synthesis of nucleic acids and proteins . clotting factorsare affected, which causes bleeding . Similar Yperit’s have a radiomimetic leading to abnormal mitosis and chromosomal alterations.cytotoxicity especially their effect on cells that divide quickly, such as skin and the lymphoid, leading to leucocitopenie, thrombocytopenia and anemia.

Symptoms - chronology of appearance of clinical manifestations depend on the route of entry of toxic in the body, percutaneous or respiratory failure. epidermal necrolysis syndrome hemorrhagic dominate the picture.
Toxic intracellular V. General - this category includes derivatives of cyanide, arsenic and hydrogen fluorocarbons.

Effects on the Body - derivatives of cyanide-inhibited cytochrome oxidazele of mitochondria and prevent the use of oxygen leading to intracellular accumulation of lactic acid and the development of metabolic acidosis . Bulbar paralysis senior centers, which are most sensitive to anoxia, leading to respiratory arrest followed by cardiovascular collapse. Mortality depends on the speed of its strength and dosage admministrarii. A dose can be fatal if absorbed quickly or slowly absorbed atoxica giving you enough time to transform into liver-derived non-toxic.
Arsenic Hydrogen is a strong reducer that fits in the erythrocyte . Inhalation of high concentrations leads to immediate and massive intravascular hemolysis onset several hours after exposure. Whatever the doorway, fluoroacetatii disrupt glicoreglarea by combining them with acetyl-coenzyme A, finally being blocked gamma aminobutyric acid synthesis central ( GABA ).

Symptoms - in case of cyanide derivatives – in case of survival, the initial phase of excitation is followed by a phase of depression with decreased blood pressure , AV block, coma, respiratory center depression and the occurrence of metabolic acidosis . In case of survival in the absence of early resuscitation maneuvers, the victim will be left with serious neurological sequelae. If symptoms depends on the concentration of hydrogen inhaled arsenic. You notice that is rapid succession anemia (Hgb <5 g / dl), pigmented skin intense circulatory failure and anuria later due to a kidney tubulopathy and hepatocyte lysis.
A few hours after exposure to fluorocarbon victim appear nausea, vomiting, epigastric pain, sialoree, due to central respiratory failure, metabolic acidosis, impaired thermoregulation (central case), neuromuscular Epileptic spasms, nystagmus , hypotension , cardiac rhythm disturbances (arrhythmias, myocardial excitability disorders, flutter , fibrillation ). Death occurs within 24-48 hours after exposure
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