A chemical weapon is a specialized munition that uses chemicals formulated to inflict death or harm on humans. According to the Organisation for the Prohibition of Chemical Weapons, "the term chemical weapon may be applied to any toxic chemical or its precursor that can cause death, temporary incapacitation or sensory irritation through its chemical action. Munitions or other delivery devices designed to deliver chemical weapons, whether filled or unfilled, are considered weapons themselves."Chemical weapons are classified as weapons of mass destruction, though they are distinct from nuclear weapons, biological weapons, radiological weapons. All may be used in warfare and are known by the military acronym NBC. Weapons of mass destruction are distinct from conventional weapons, which are effective due to their explosive, kinetic, or incendiary potential. Chemical weapons can be dispersed in gas and solid forms, may afflict others than the intended targets. Nerve gas, tear gas and pepper spray are three modern examples of chemical weapons.
Lethal unitary chemical agents and munitions are volatile and they constitute a class of hazardous chemical weapons that have been stockpiled by many nations. Unitary agents do not require mixing with other agents; the most dangerous of these are nerve agents and vesicant agents, which include formulations of sulfur mustard such as H, HT, HD. They all become gaseous when released. Used during the First World War, the effects of so-called mustard gas, phosgene gas and others caused lung searing, blindness and maiming; the Nazi Germans during WW-II committed genocide against Jews but included other targeted populations in the Holocaust, a commercial hydrogen cyanide blood agent trade named Zyklon B discharged in large gas chambers was the preferred method to efficiently murder their victims in a continuing industrial fashion, this resulted in the largest death toll to chemical weapons in history. As of 2016, CS gas and pepper spray remain in common use for riot control. Under the Chemical Weapons Convention, there is a binding, worldwide ban on the production and use of chemical weapons and their precursors.
Notwithstanding, large stockpiles of chemical weapons continue to exist justified as a precaution against putative use by an aggressor. International law has prohibited the use of chemical weapons since 1899, under the Hague Convention: Article 23 of the Regulations Respecting the Laws and Customs of War on Land adopted by the First Hague Conference "especially" prohibited employing "poison and poisoned arms". A separate declaration stated that in any war between signatory powers, the parties would abstain from using projectiles "the object of, the diffusion of asphyxiating or deleterious gases"; the Washington Naval Treaty, signed February 6, 1922 known as the Five-Power Treaty, aimed at banning CW but did not succeed because France rejected it. The subsequent failure to include CW has contributed to the resultant increase in stockpiles; the Geneva Protocol known as the Protocol for the Prohibition of the Use in War of Asphyxiating, Poisonous or other Gases, of Bacteriological Methods of Warfare, is an International treaty prohibiting the use of chemical and biological weapons.
It was signed at Geneva June 17, 1925, entered into force on February 8, 1928. 133 nations are listed as state parties to the treaty. Ukraine is the newest signatory; this treaty states that chemical and biological weapons are "justly condemned by the general opinion of the civilised world". And while the treaty prohibits the use of chemical and biological weapons, it does not address the production, storage, or transfer of these weapons. Treaties that followed the Geneva Protocol did have been enacted; the 1993 Chemical Weapons Convention is the most recent arms control agreement with the force of International law. Its full name is the Convention on the Prohibition of the Development, Production and Use of Chemical Weapons and on their Destruction; that agreement outlaws the production and use of chemical weapons. It is administered by the Organisation for the Prohibition of Chemical Weapons, an independent organization based in The Hague; the OPCW administers the terms of the CWC to 192 signatories, which represents 98% of the global population.
As of June 2016, 66,368 of 72,525 metric tonnes, have been verified as destroyed. The OPCW has conducted 6,327 inspections at 235 chemical weapon-related sites and 2,255 industrial sites; these inspections have affected the sovereign territory of 86 States Parties since April 1997. Worldwide, 4,732 industrial facilities are subject to inspection under provisions of the CWC. Chemical warfare involves using the toxic properties of chemical substances as weapons; this type of warfare is distinct from nuclear warfare and biological warfare, which together make up NBC, the military initialism for Nuclear and Chemical. None of these fall under the term conventional weapons, which are effective because of their destructive potential. Chemical warfare does not depend upon explosive force to achieve an objective, it depends upon the unique properties of the chemical agent weaponized. A lethal agent is designed to injure, incapacitate, or kill an opposing force, or deny unhindered use of a particular area of terrain.
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A hallucinogen is a psychoactive agent which can cause hallucinations, perceptual anomalies, other substantial subjective changes in thoughts and consciousness. The common types of hallucinogens are psychedelics and deliriants. Although hallucinations are a common symptom of amphetamine psychosis, amphetamines are not considered hallucinogens, as they are not a primary effect of the drugs themselves. While hallucinations can occur when abusing stimulants, the nature of stimulant psychosis is not unlike delirium. A debate persists on criteria which would differentiate a substance which is'psychedelic' from one'hallucinogenic'. Sir Thomas Browne in 1646 coined the term'hallucination' from the Latin word "alucinari" meaning "to wander in the mind"; the term'psychedelic' is derived from the Ancient Greek words psychē and dēloun, or "mind-revealing".'A hallucinogen' and'a psychedelic' may refer to the same substance.'Hallucinations' and'psychedelia' may both refer to the same aspects of subjective experience in a given instance.
The term psychedelia carries an added reference to psychedelic substance culture, and'psychedelics' are considered by many to be the'traditional' or'classical hallucinogens' including DMT, Psilocybin, LSD.'A hallucinogen' in this sense broadly refers to any substance which causes changes in perception or hallucinations, while psychedelics carry a positive connotation of general perceptual enhancement. In contrast to Hollister's original criteria, adverse effects may predominate with some hallucinogens with this application of the term; the word psychedelic was coined to express the idea of a drug that makes manifest a hidden but real aspect of the mind. It is applied to any drug with perception-altering effects such as LSD and other ergotamine derivatives, DMT and other tryptamines including the alkaloids of Psilocybe spp. mescaline and other phenethylamines. The term "psychedelic" is applied somewhat interchangeably with "psychotomimetic" and "hallucinogen", The classical hallucinogens are considered to be the representative psychedelics and LSD is considered the prototypical psychedelic.
In order to refer to the LSD-like psychedelics, scientific authors have used the term "classical hallucinogen" in the sense defined by Glennon: "The classical hallucinogens are agents that meet Hollister's original definition, but are agents that: bind at 5-HT2 serotonin receptors, are recognized by animals trained to discriminate 1--2-aminopropane from vehicle. Otherwise, when the term "psychedelic" is used to refer only to the LSD-like psychedelics, authors explicitly point that they intend "psychedelic" to be understood according to this more restrictive interpretation. One explanatory model for the experiences provoked by psychedelics is the "reducing valve" concept, first articulated in Aldous Huxley's book The Doors of Perception. In this view, the drugs disable the brain's "filtering" ability to selectively prevent certain perceptions, emotions and thoughts from reaching the conscious mind; this effect has been described as mind expanding, or consciousness expanding, for the drug "expands" the realm of experience available to conscious awareness.
While possessing a unique mechanism of action, cannabis or marijuana has been regarded alongside the classic psychedelics. A designer drug is a structural or functional analog of a controlled substance, designed to mimic the pharmacological effects of the original drug while at the same time avoid being classified as illegal and/or avoid detection in standard drug tests. Many designer drugs and research chemicals are hallucinogenic in nature, such as those in the 2C and 25-NB families. Dissociatives produce analgesia and catalepsy at anesthetic doses, they produce a sense of detachment from the surrounding environment, hence "the state has been designated as dissociative anesthesia since the patient seems disassociated from his environment." Dissociative symptoms include the disruption or compartmentalization of "...the integrated functions of consciousness, identity or perception."p. 523 Dissociation of sensory input can cause derealization, the perception of the outside world as being dream-like or unreal.
Other dissociative experiences include depersonalization, which includes feeling detached from one's body. Simeon offered "...common descriptions of depersonalisation experiences: watching oneself from a distance. However, dissociation is remarkably administered by salvinorin A's potent κ-opioid receptor agonism, though sometimes described as an atypical psychedelic; some dissociatives can have CNS depressant effects, thereby carrying similar risks as opioids, which can slow breathing or heart rate to levels resulting in death (w
Sarin (NATO designation GB, is an toxic synthetic organophosphorus compound. A colorless, odorless liquid, it is used as a chemical weapon due to its extreme potency as a nerve agent. Exposure is lethal at low concentrations, where death can occur within one to ten minutes after direct inhalation of a lethal dose, due to suffocation from lung muscle paralysis, unless antidotes are administered. People who absorb a non-lethal dose, but do not receive immediate medical treatment, may suffer permanent neurological damage. Sarin is considered a weapon of mass destruction. Production and stockpiling of Sarin was outlawed as of April 1997 by the Chemical Weapons Convention of 1993, it is classified as a Schedule 1 substance. In June 1994, the UN Special Commission on Iraqi Disarmament reported that it had destroyed Iraq's stockpiles of Sarin. Like some other nerve agents that affect the neurotransmitter acetylcholine, Sarin attacks the nervous system by interfering with the degradation of the neurotransmitter acetylcholine at neuromuscular junctions.
Death will occur as a result of asphyxia due to the inability to control the muscles involved in breathing. Initial symptoms following exposure to Sarin are a runny nose, tightness in the chest and constriction of the pupils. Soon after, the person will have difficulty breathing and they will experience nausea and drooling; as they continue to lose control of bodily functions, they may vomit and urinate. This phase is followed by jerking; the person becomes comatose and suffocates in a series of convulsive spasms. Moreover, common mnemonics for the symptomatology of organophosphate poisoning, including Sarin gas, are the "killer B's" of bronchorrhea and bronchospasm because they are the leading cause of death, SLUDGE – salivation, urination, gastrointestinal distress, emesis. Death may follow in 1 to 10 minutes after direct inhalation. Sarin has a high volatility relative to similar nerve agents, therefore inhalation can be dangerous and vapor concentrations may penetrate the skin. A person’s clothing can release sarin for about 30 minutes after it has come in contact with sarin gas, which can lead to exposure of other people.
Treatment measures have been described. Treatment is with the antidotes and pralidoxime. Atropine, an antagonist to muscarinic acetylcholine receptors, is given to treat the physiological symptoms of poisoning. Since muscular response to acetylcholine is mediated through nicotinic acetylcholine receptors, atropine does not counteract the muscular symptoms. Pralidoxime can regenerate cholinesterases if administered within five hours. Biperiden, a synthetic acetylcholine antagonist, has been suggested as an alternative to atropine due to its better blood–brain barrier penetration and higher efficacy. Sarin is a potent inhibitor of acetylcholinesterase, an enzyme that degrades the neurotransmitter acetylcholine after it is released into the synaptic cleft. In vertebrates, acetylcholine is the neurotransmitter used at the neuromuscular junction, where signals are transmitted between neurons from the central nervous systems to muscle fibres. Acetylcholine is released from the neuron to stimulate the muscle, after which it is degraded by acetylcholinesterase, allowing the muscle to relax.
A build-up of acetylcholine in the synaptic cleft, due to the inhibition of cholinesterase, means the neurotransmitter continues to act on the muscle fibre, so that any nerve impulses are continually transmitted. Sarin acts on cholinesterase by forming a covalent bond with the particular serine residue at the active site. Fluoride is the leaving group, the resulting phosphoester is robust and biologically inactive, its mechanism of action resembles that of some used insecticides, such as malathion. In terms of biological activity, it resembles carbamate insecticides, such as Sevin, the medicines pyridostigmine and physostigmine. Controlled studies in healthy men have shown that a nontoxic 0.43 mg oral dose administered in several portions over a 3-day interval caused average maximum depressions of 22 and 30% in plasma and erythrocyte cholinesterase levels. A single acute 0.5 mg dose caused mild symptoms of intoxication and an average reduction of 38% in both measures of cholinesterase activity.
Sarin in blood is degraded either in vivo or in vitro. Its primary inactive metabolites have in vivo serum half-lives of 24 hours; the serum level of unbound isopropylmethylphosphonic acid, a Sarin hydrolysis product, ranged from 2-135 µg/L in survivors of a terrorist attack during the first 4 hours post-exposure. Sarin or its metabolites may be determined in blood or urine by gas or liquid chromatography, while cholinesterase activity is measured by enzymatic methods. A newer method called "fluoride regeneration" or "fluoride reactivation" detects the presence of nerve agents for a longer period after exposure than the methods described above. Fluoride reactivation is a technique, explored since at least the early 2000s; this technique obviates some of the deficiencies of older procedures. Sarin not only reacts with the water in the blood plasma through hydrolysis, but reacts with various proteins to form ‘protein adducts’; these protein adducts are not so removed from the body, remain for a longer period of time than the free metabolites.
One clear advantage of this process is that the period, post-exposure, for determination of Sarin exposure is much longer 5 to 8 weeks according to at least one study. As a nerve
A blister agent, or vesicant, is a chemical compound that causes severe skin and mucosal pain and irritation. They are named for their ability to cause severe chemical burns, resulting in painful water blisters on the bodies of those affected. Although the term is used in connection with large-scale burns caused by chemical spills or chemical warfare agents, some occurring substances such as cantharidin are blister-producing agents. Furanocoumarin, another occurring substance, causes vesicant-like effects indirectly, for example, by increasing skin photosensitivity greatly. Vesicants have medical uses including wart removal but can be fatal if small amounts are ingested. Most blister agents fall into one of three groups: Sulfur mustards – A family of sulfur-based agents, including mustard gas. Nitrogen mustards – A family of agents similar to the sulfur mustards, but based on nitrogen instead of sulfur. Lewisite – An early blister agent, developed, but not used, during World War I, it was rendered obsolete with the development of British anti-Lewisite in the 1940s.
Phosgene oxime is included among the blister agents, although it is more properly termed a nettle agent. Exposure to a weaponized blister agent can cause a number of life-threatening symptoms, including: Severe skin and mucosal pain and irritation Skin erythema with large fluid blisters that heal and may become infected Tearing, corneal damage Mild respiratory distress to marked airway damageAll blister agents known are denser than air, are absorbed through the eyes and skin. Effects of the two mustard agents are delayed: exposure to vapors becomes evident in 4 to 6 hours, skin exposure in 2 to 48 hours; the effects of Lewisite are immediate. Medterms.com Medical Aspects of Biological and Chemical Warfare, Chapter 7: Vesicants
The Jmol applet, among other abilities, offers an alternative to the Chime plug-in, no longer under active development. While Jmol has many features that Chime lacks, it does not claim to reproduce all Chime functions, most notably, the Sculpt mode. Chime requires plug-in installation and Internet Explorer 6.0 or Firefox 2.0 on Microsoft Windows, or Netscape Communicator 4.8 on Mac OS 9. Jmol operates on a wide variety of platforms. For example, Jmol is functional in Mozilla Firefox, Internet Explorer, Google Chrome, Safari. Chemistry Development Kit Comparison of software for molecular mechanics modeling Jmol extension for MediaWiki List of molecular graphics systems Molecular graphics Molecule editor Proteopedia PyMOL SAMSON Official website Wiki with listings of websites and moodles Willighagen, Egon. "Fast and Scriptable Molecular Graphics in Web Browsers without Java3D". Doi:10.1038/npre.2007.50.1
European Chemicals Agency
The European Chemicals Agency is an agency of the European Union which manages the technical and administrative aspects of the implementation of the European Union regulation called Registration, Evaluation and Restriction of Chemicals. ECHA is the driving force among regulatory authorities in implementing the EU's chemicals legislation. ECHA helps companies to comply with the legislation, advances the safe use of chemicals, provides information on chemicals and addresses chemicals of concern, it is located in Finland. The agency headed by Executive Director Bjorn Hansen, started working on 1 June 2007; the REACH Regulation requires companies to provide information on the hazards and safe use of chemical substances that they manufacture or import. Companies register this information with ECHA and it is freely available on their website. So far, thousands of the most hazardous and the most used substances have been registered; the information is technical but gives detail on the impact of each chemical on people and the environment.
This gives European consumers the right to ask retailers whether the goods they buy contain dangerous substances. The Classification and Packaging Regulation introduces a globally harmonised system for classifying and labelling chemicals into the EU; this worldwide system makes it easier for workers and consumers to know the effects of chemicals and how to use products safely because the labels on products are now the same throughout the world. Companies need to notify ECHA of the labelling of their chemicals. So far, ECHA has received over 5 million notifications for more than 100 000 substances; the information is available on their website. Consumers can check chemicals in the products. Biocidal products include, for example, insect disinfectants used in hospitals; the Biocidal Products Regulation ensures that there is enough information about these products so that consumers can use them safely. ECHA is responsible for implementing the regulation; the law on Prior Informed Consent sets guidelines for the import of hazardous chemicals.
Through this mechanism, countries due to receive hazardous chemicals are informed in advance and have the possibility of rejecting their import. Substances that may have serious effects on human health and the environment are identified as Substances of Very High Concern 1; these are substances which cause cancer, mutation or are toxic to reproduction as well as substances which persist in the body or the environment and do not break down. Other substances considered. Companies manufacturing or importing articles containing these substances in a concentration above 0,1% weight of the article, have legal obligations, they are required to inform users about the presence of the substance and therefore how to use it safely. Consumers have the right to ask the retailer whether these substances are present in the products they buy. Once a substance has been identified in the EU as being of high concern, it will be added to a list; this list is available on ECHA's website and shows consumers and industry which chemicals are identified as SVHCs.
Substances placed on the Candidate List can move to another list. This means that, after a given date, companies will not be allowed to place the substance on the market or to use it, unless they have been given prior authorisation to do so by ECHA. One of the main aims of this listing process is to phase out SVHCs where possible. In its 2018 substance evaluation progress report, ECHA said chemical companies failed to provide “important safety information” in nearly three quarters of cases checked that year. "The numbers show a similar picture to previous years" the report said. The agency noted that member states need to develop risk management measures to control unsafe commercial use of chemicals in 71% of the substances checked. Executive Director Bjorn Hansen called non-compliance with REACH a "worry". Industry group CEFIC acknowledged the problem; the European Environmental Bureau called for faster enforcement to minimise chemical exposure. European Chemicals Bureau Official website
Nerve agents, sometimes called nerve gases, are a class of organic chemicals that disrupt the mechanisms by which nerves transfer messages to organs. The disruption is caused by the blocking of acetylcholinesterase, an enzyme that catalyzes the breakdown of acetylcholine, a neurotransmitter. Poisoning by a nerve agent leads to constriction of pupils, profuse salivation and involuntary urination and defecation, with the first symptoms appearing in seconds after exposure. Death by asphyxiation or cardiac arrest may follow in minutes due to the loss of the body's control over respiratory and other muscles; some nerve agents are vaporized or aerosolized, the primary portal of entry into the body is the respiratory system. Nerve agents can be absorbed through the skin, requiring that those to be subjected to such agents wear a full body suit in addition to a respirator. Nerve agents are colorless to amber-colored, tasteless liquids that may evaporate to a gas. Agents sarin and VX are odorless. Nerve agents attack the nervous system.
All such agents function the same way resulting in cholinergic crisis: they inhibit the enzyme acetylcholinesterase, responsible for the breakdown of acetylcholine in the synapses between nerves that control muscle contraction. If the agent cannot be broken down, muscles are prevented from relaxing and they are paralyzed; this includes the muscles used for breathing. Because of this, the first symptoms appear within seconds of exposure and death can occur via asphyxiation or cardiac arrest in a few minutes. Initial symptoms following exposure to nerve agents are a runny nose, tightness in the chest, constriction of the pupils. Soon after, the victim will experience nausea and salivation; as the victim continues to lose control of bodily functions, involuntary salivation, urination, gastrointestinal pain and vomiting will be experienced. Blisters and burning of the eyes and/or lungs may occur; this phase is followed by myoclonic jerks followed by status epilepticus -type epileptic seizure. Death comes via complete respiratory depression, most via the excessive peripheral activity at the neuromuscular junction of the diaphragm.
The effects of nerve agents increase with continued exposure. Survivors of nerve agent poisoning invariably suffer chronic neurological damage and related psychiatric effects. Possible effects that can last at least up to 2–3 years after exposure include blurred vision, declined memory, hoarse voice, sleeplessness, shoulder stiffness and eye strain. In people exposed to nerve agents and erythrocyte acetylcholinesterase in the long-term are noticeably lower than normal and tend to be lower the worse the persisting symptoms are; when a functioning motor nerve is stimulated, it releases the neurotransmitter acetylcholine, which transmits the impulse to a muscle or organ. Once the impulse is sent, the enzyme acetylcholinesterase breaks down the acetylcholine in order to allow the muscle or organ to relax. Nerve agents disrupt the nervous system by inhibiting the function of the enzyme acetylcholinesterase by forming a covalent bond with its active site, where acetylcholine would be broken down. Acetylcholine thus builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop.
This same action occurs at the gland and organ levels, resulting in uncontrolled drooling, tearing of the eyes and excess production of mucus from the nose. The reaction product of the most important nerve agents, including soman, tabun and VX, with acetylcholinesterase were solved by the U. S. Army using X-ray crystallography in the 1990s; the reaction products have been confirmed subsequently using different sources of acetylcholinesterase and the related target enzyme, butyrylcholinesterase. The X-ray structures clarify important aspects of the reaction mechanism at atomic resolution and provide a key tool for antidote development. Atropine and related anticholinergic drugs act as antidotes to nerve agent poisoning because they block acetylcholine receptors, but they are poisonous in their own right; some synthetic anticholinergics, such as biperiden, may counteract the central symptoms of nerve agent poisoning better than atropine, since they pass the blood–brain barrier better than atropine.
While these drugs will save the life of a person affected by nerve agents, that person may be incapacitated or for an extended period, depending on the extent of exposure. The endpoint of atropine administration is the clearing of bronchial secretions. Atropine for field use by military personnel is loaded in an autoinjector, for ease of use in stressful conditions. Pralidoxime chloride known as 2-PAM chloride, is used as an antidote. Rather than counteracting the initial effects of the nerve agent on the nervous system as does atropine, pralidoxime chloride reactivates the poisoned enzyme by scavenging the phosphoryl group attached on the functional hydroxyl group of the enzyme. Though safer to use than atropine, it takes longer to act. Revival of acetylcholinesterase with pralidoxime chloride works more on nicotinic receptors while blocking acetylcholine receptors with atropine is more effective on muscarinic receptors. Severe cases of poisoning are treated with both drugs. Butyrylcholinesterase is under development by the U.
S. Department of Defense as a prophylactic counter