chemical warfare agents toxicology and treatment pdf

Chemical Warfare Agents Toxicology And Treatment Pdf

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They are divided into two classes of G and V agents.

Facts About Nerve Agents

CWAs include five primary categories: nerve agents, asphyxiants, blistering agents, toxic industrial chemicals and blood agents. The French military used tear gas and acetone-based compounds for crowd control; chlorine gas was placed in capsules and released at the Battle of Ypres in , and was used as an alternative weapon after the German military exhausted materials for explosive weapons and began to investigate and use CWAs.

Later, other agents such as phosgene and cyanide were considered for military use, because these chemicals had more toxic pulmonary effects. Nerve agents developed in the s and s were stockpiled during the Cold War. More recently, nerve agents have been used in the Iran—Iraq War in the s, the Japanese terrorist attacks by the Aum Shinrikyo cult in and attacks in Syria in The creation of the Chemical Weapons Ban in by the Organization for the Prohibition of Chemical Weapons stifled the development, use and stockpiling of these materials for military use across nations.

Effective treatment of all patients exposed to CWAs requires use of appropriate personal protective equipment PPE and early patient decontamination by first responders. PPE may vary depending on the exposure. Early decontamination by first responders with appropriate PPE is essential in the care of patients and emergency personnel with chemical exposure. Patients should be decontaminated prior to being placed in an ambulance and prior to arrival in a healthcare facility to minimize exposure and risks to health care workers.

Initial decontamination includes removal of all articles of clothing and storage in sealed containers to decrease persistent exposure and aerosolization of the chemical. Additionally, all patients should be washed thoroughly with water and diluted bleach. Eye wash stations should be used for extensive eye irrigation to remove exposure.

Detoxification agents may be considered in assisting with chemical weapon decontamination. For example, hypochlorite solution may be added to decontaminate from mustard gas exposure. Maintained by the military, M skin decontamination kits and Reactive Skin Decontamination Lotion RSDL are also available during exposures; studies have demonstrated superior decontamination with RSDL in animal models exposed to soman, a chemical agent.

Nerve agents include two primary categories of chemical agents: G-agents and V-agents. Developed first, G-agents are sarin, cyclosarin, tabun and soman.

Nerve agents have a chemical structure similar to organophosphates which allows them to covalently bind acetylcholinesterase to deactivate the enzyme. The primary mechanism of action for nerve agents is blockage of acetylcholinesterase at the neuromuscular junction of muscarinic and nicotinic receptors. Acetylcholinesterase is the primary degrading enzyme of acetylcholine. The result of nerve agent blockade is increased acetylcholine availability at the neuromuscular junction.

Nerve agents may also have effects at glutamate receptors and direct neurotoxic effects. Clinical symptoms of nerve agent poisoning are a direct result of muscarinic and nicotinic nerve stimulation.

Most importantly, nerve agents cause the more life-threatening clinical symptoms: bradycardia, bronchospasm and bronchorrhea. Seizures are common in patients who have been exposed to nerve agents. Nerve agents also demonstrate clinical latency periods. Latency depends on the route of exposure. Inhalational exposures generally have near immediate symptom onset. The pharmacology of nerve agents is key to understanding treatment options.

Nerve agents phosphoylate acetylcholinesterase to inactivate the enzyme. The acetylcholinesterase-nerve agent complex will undergo a process called aging, in which the nerve agent permanently binds to the enzyme, rendering acetylcholinesterase completely inactivated. Treatment for nerve agent poisoning is a multimodal therapy with three primary components: 1 atropine; 2 a benzodiazepine; and 3 an oxime.

Atropine is a competitive antagonist to the acetylcholine receptor that produces anticholinergic effects. It helps treat the clinical symptoms associated with nerve agent poisoning but has no direct effect on the nerve agent.

An atropine infusion can also be started and should be titrated to respiratory effects e. Early intubation and ventilator use is essential to caring for patients with nerve agent poisoning and may be necessary until additional therapies are given.

Benzodiazepines are included in the autoinjectors and treatment regimens to manage seizures. Oximes are nucleophiles that bind the phosphoryl component of nerve agents, consequently releasing the nerve agent from acetylcholinesterase. Pralidoxime is a common oxime used to treat organophosphate poisoning, but has limited effectiveness in nerve agent poisoning.

Several studies have compared the effectiveness of various oximes. In both in vitro and in vivo animal models, for soman, cyclosarin and VX exposures, HI-6 is a superior treatment compared to other oximes.

Other studies have demonstrated that the optimal regimen includes HI-6, procyclidine and keppra. Another promising therapy is organophosphate hydrolyzing enzymes OPHEs. OPHEs are enzymes that directly hydrolyze nerve agent—acetylcholinesterase complexes. However, these molecules currently have limited catalytic capacity and biologic stability. Further research is required to optimize their development for human use. Finally, pyridostigmine has been used by the military as prophylaxis for nerve agent poisoning in high risk areas, most notably for potential soman exposure.

Pyridostigmine is a carbamate which reversibly inactivates acetylcholinesterase. Therefore, prophylactic pyridostigmine temporarily occupies acetylcholinesterase binding sites, preventing nerve agent binding.

Prophylactic dosing is 30 mg every eight hours by mouth. However, the key limitation to pyridostigmine is its inability to cross the blood-brain barrier, leaving central acetylcholinesterase susceptible to nerve agents. Nitrogen mustard and sulfur mustard, more commonly known as mustard gas, were developed and used as chemical weapons during World War I.

Today, nitrogen mustard derived compounds are used as chemotherapy for leukemia and lymphoma. Mustard gas is an alkylating agent that crosslinks DNA and blocks cellular replication.

Although not technically a gas agent, exposure occurs via inhalation when the liquid evaporates or is aerosolized. Although mustard gas is generally not a fatal chemical agent, it causes both acute and chronic medical injury to those exposed to it. Depending on the exposure dose, patients may have only an erythematous rash low dose or large, painful blisters that may become necrotic high dose.

Skin blistering can result in long-term skin hypopigmentation, permanent scarring and increases the risk of infection. Patients should be treated at a dedicated burn center for wound care and fluid management. Initial symptoms of eye injury secondary to mustard gas exposure including pain, photophobia, scleral injection and lacrimation. Corneal ulceration can result if significant high-dose exposure occurs. For eye injury and exposure, supportive care, including initial eye decontamination with water, darkened glasses for photophobia management and avoiding eye bandaging are all recommended.

Lung damage from mustard gas exposure also results in both acute and chronic lung injury; however, long-term, lung-associated sequelae of mustard gas exposure are severe and debilitating. In the acute phase, lung injury from mustard gas includes pulmonary edema and pulmonary hemorrhage.

Late sequelae include chronic obstructive pulmonary disease COPD , asthma and bronchiolitis obliterans BOOP , which are caused by the fibrotic changes that occur. Some patients with mustard gas exposure will suffer from neutropenia or pancytopenia. Supportive measures are generally indicated for acute lung injury secondary to mustard gas exposure.

Patients may require supplemental oxygen, intubation and mechanical ventilation. Due to its antioxidant and radical scavenger properties, research studies in both animal and human models suggest that NAC is an effective treatment. In both the acute and long-term treatment phases, NAC helped decrease respiratory symptoms associated with mustard gas inhalation. Additionally, NAC alone or combined with clarithromycin improved pulmonary function in patients with BOOP secondary to mustard gas exposure.

Common chemical asphyxiants include carbon monoxide, chlorine, phosgene and hydrogen sulfide gases. Both of these gases exert their toxic effects on the respiratory system. Chlorine is an asphyxiant gas used in various industries including polyurethane and polychloroethene PVC production, chemical solvent production and water sterilization.

Its toxic effects are primarily localized to the upper airways and occur immediately after exposure. Chlorine gas can also cause skin and eye irritation. In addition to decontamination, some studies have trialed the use of nebulized sodium bicarbonate; results suggested improved lung function based on lab studies but overall no improved survival. Phosgene is also an asphyxiant gas used in the pesticide and plastics industries.

Phosgene has direct toxic effects on the lungs and exposure results in fatal pulmonary edema and acute respiratory distress syndrome ARDS.

Pulmonary edema is often delayed up to 24 hours and carries high mortality. Treatment options in addition to general supportive care, IV diuretics and mechanical ventilation are limited and have only been evaluated in animal models. They include IV corticosteroids, nebulized N-acetylcysteine, and nebulized bronchodilators. Cyanide, or hydrogen cyanide, is a weak acid that blocks cytochrome C oxidase and shuts down mitochondrial respiration.

Exposure to cyanide can occur via ingestion, skin absorption and inhalation. Patients with cyanide poisoning present in severe distress with tachycardia, cyanosis and hypotension. The most notable and life-threatening lab abnormality is severe metabolic acidosis. Seizures are common and cardiac arrest may occur. There are several antidotes currently available for treatment of cyanide poisoning. Due to the risk of large-scale poisonings that require immediate treatment, much research is working towards finding antidotes that can be administered intramuscularly IM in the field by first responders and have immediate treatment effects.

The Lily kit, also known as Nithiodote, contains three essential medications: amyl nitrite, sodium nitrite and sodium thiosulfate. Most often, sodium nitrite is administered at a dose of mg IV, which causes methemoglobinemia. Cyanide has a higher binding affinity for methemoglobin compared to the oxidative phosphorylation enzymes, and helps restore cellular respiration.

The risk associated with nitrite administration is the formation of methemoglobin, which has no oxygen carrying capacity. In patients exposed to house fires, who may already suffer from hypoxia due to smoke inhalation or lung injury, administration of nitrite therapy carries significant risk. Sodium thiosulfate acts to increase enzymatic activity of rhodanase, an enzyme that metabolizes thiocyanate by products.

Hydroxocobalamin is a newer therapy for cyanide intoxication. Although first developed and tested in , hydroxocobalamin was not approved for use in the United States until Hydroxocobalamin has a strong binding capacity for cyanide and forms cyanocobalamin or vitamin B

Handbook of Toxicology of Chemical Warfare Agents

CWAs include five primary categories: nerve agents, asphyxiants, blistering agents, toxic industrial chemicals and blood agents. The French military used tear gas and acetone-based compounds for crowd control; chlorine gas was placed in capsules and released at the Battle of Ypres in , and was used as an alternative weapon after the German military exhausted materials for explosive weapons and began to investigate and use CWAs. Later, other agents such as phosgene and cyanide were considered for military use, because these chemicals had more toxic pulmonary effects. Nerve agents developed in the s and s were stockpiled during the Cold War. More recently, nerve agents have been used in the Iran—Iraq War in the s, the Japanese terrorist attacks by the Aum Shinrikyo cult in and attacks in Syria in The creation of the Chemical Weapons Ban in by the Organization for the Prohibition of Chemical Weapons stifled the development, use and stockpiling of these materials for military use across nations. Effective treatment of all patients exposed to CWAs requires use of appropriate personal protective equipment PPE and early patient decontamination by first responders.

Advances in toxicology and medical treatment of chemical warfare nerve agents

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E-mail: horstthiermann bundeswehr. The treatment of nerve agent poisoning is still a major challenge for medical services. The high toxicity of these agents calls for specific methods for self-protection, e. Patients are at risk due to the fast onset of life threatening cholinergic crisis.

Note to reader: This fact sheet is intended to provide general awareness and education on specific chemical agents. For information on preparedness and response e. Nerve agents are chemicals that affect the nervous system. The health effects are similar to those produced by some pesticides.

A Review of Chemical Warfare Agents and Treatment Options

Wiley Online Library Sample Chapter. Chemical Warfare Agents: Toxicology and Treatment, Second Edition provides a detailed summary of chemical warfare agents, their physico-chemical properties, dispersion and fate in the environment, tooxicology and management of their effects on humans. It also discusses decontamination and protective equipment.

Fact Sheets and Publications

Handbook of Toxicology of Chemical Warfare Agents, Second Edition covers every aspect of deadly toxic chemicals used in conflicts, warfare and terrorism. Including findings from experimental as well as clinical studies, this essential reference offers in-depth coverage of individual toxicants, target organ toxicity, major incidents, toxic effects in humans, animals and wildlife, biosensors and biomarkers, on-site and laboratory analytical methods, decontamination and detoxification procedures, and countermeasures. Expanding on the ground-breaking first edition, Handbook of Toxicology of Chemical Warfare Agents has been completely updated, presenting the most recent advances in field. Brand new chapters include a case study of the Iran-Iraq war, an overview of chemical weapons of mass destruction, explosives, Ricin, the human respiratory system, alternative testing methods, brain injuries, and more. Toxicologists, defense scientists, homeland and governmental security, and risk assessment specialists. Ramesh C. He is recipient of Murray State University's distinguished researcher award of the year, and Outstanding research award of the year

И не похоже, что… - Что? - Бринкерхофф даже подпрыгнул. Мидж смотрела на цифры, не веря своим глазам. - Этот файл, тот, что загрузили вчера вечером… - Ну. - Шифр еще не вскрыт.


Chemical Warfare Agents, Second Edition has been totally revised since the successful first edition and expanded to about three times the length, with many.


Classification of CW Agents

 Рассказывай. Немедленно. Но Дэвид знал, что никогда ей этого не откроет. Секрет выражения без воска был ему слишком дорог. Он уходил корнями в давние времена. В эпоху Возрождения скульпторы, оставляя изъяны при обработке дорогого мрамора, заделывали их с помощью сеrа, то есть воска.

От ее слов повеяло ледяным холодом: - Джабба, я выполняю свои должностные обязанности. И не хочу, чтобы на меня кричали, когда я это делаю. Когда я спрашиваю, почему многомиллиардное здание погрузилось во тьму, я рассчитываю на профессиональный ответ. - Да, мэм. - Я хочу услышать только да или. Возможно ли, что проблема шифровалки каким-то образом связана с вирусом. - Мидж… я уже говорил… - Да или нет: мог в ТРАНСТЕКСТ проникнуть вирус.

Фонд электронных границ усилил свое влияние, доверие к Фонтейну в конгрессе резко упало, и, что еще хуже, агентство перестало быть анонимным. Внезапно домохозяйки штата Миннесота начали жаловаться компаниям Америка онлайн и Вундеркинд, что АНБ, возможно, читает их электронную почту, - хотя агентству, конечно, не было дела до рецептов приготовления сладкого картофеля. Провал Стратмора дорого стоил агентству, и Мидж чувствовала свою вину - не потому, что могла бы предвидеть неудачу коммандера, а потому, что эти действия были предприняты за спиной директора Фонтейна, а Мидж платили именно за то, чтобы она эту спину прикрывала. Директор старался в такие дела не вмешиваться, и это делало его уязвимым, а Мидж постоянно нервничала по этому поводу.

Задача дешифровщиков состояла в том, чтобы, изучив его, получить оригинальный, или так называемый открытый, текст. АНБ пригласило Беккера, потому что имелось подозрение, что оригинал был написан на мандаринском диалекте китайского языка, и ему предстояло переводить иероглифы по мере их дешифровки. В течение двух часов Беккер переводил бесконечный поток китайских иероглифов.

 - Нам нужно число. Сьюзан еще раз перечитала послание Танкадо. Главная разница между элементами… разница между… нужно найти число… - Подождите! - сказала .

Его безумная поездка вот-вот закончится.

Стратмор не скрывал недовольства. - Он ничего не спрашивал про ТРАНСТЕКСТ. - Нет. Но если он посмотрит на монитор и увидит в окне отсчета значение семнадцать часов, то, будьте уверены, не промолчит. Стратмор задумался.

Затем наступила тишина. Мгновение спустя, словно в дешевом фильме ужасов, свет в ванной начал медленно гаснуть. Затем ярко вспыхнул и выключился. Сьюзан Флетчер оказалась в полной темноте. Сьюзан Флетчер нетерпеливо мерила шагами туалетную комнату шифровалки и медленно считала от одного до пятидесяти.

 Работайте, - поторопил Фонтейн. На ВР последняя стена стала уже тоньше яичной скорлупы. Джабба поднял брови.

4 comments

Rolarawohl

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Galzumenic

Among the Weapons of Mass Destruction, chemical warfare CW is probably one of the most brutal created by mankind in comparison with biological and nuclear warfare.

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Ewan L.

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Haizea G.

Organophosphorus compounds as chemical warfare agents: a review.

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