Seven accused “spies” are fitted with explosive cables dubbed “decapitation necklaces
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Mustard agents are usually classified as "blistering agents" owing to the similarity of the wounds caused by these substances resembling burns and blisters. However, since mustard agents also cause severe damage to the eyes, respiratory system and internal organs, they should preferably be described as "blistering and tissue-injuring agents". Normal mustard agent, bis-(2-chloroethyl)sulphide, reacts with a large number of biological molecules. The effect of mustard agent is delayed and the first symptoms do not occur until 2-24 hours after exposure.
Mustard agent was produced for the first time in 1822 but its harmful effects were not discovered until 1860. Mustard agent was first used as a CW agent during the latter part of the First World War and caused lung and eye injuries to a very large number of soldiers. Many of them still suffered pain 30-40 years after they had been exposed, mainly as a result of injuries to the eyes and chronic respiratory disorders.
During the war between Iran and Iraq in 1979-88, Iraq used large quantities of chemical agents. About 5 000 Iranian soldiers have been reported killed, 10-20 per cent by mustard agent. In addition, there were 40 000 to 50 000 injured. A typical result of warfare with mustard agent is that the medical system is overloaded with numerous victims who require long and demanding care.
Incidents are still occurring annually in the neighbourhood of Sweden where people risk injury from mustard agent. This largely involves fishermen who are exposed to mustard agent brought to the surface by fishing nets. The background is found in the dumping of chemical weapons after the Second World War in waters off the Danish and Swedish coasts. Many fishing ports in south Sweden and Denmark have resources to care for injured people and to decontaminate equipment contaminated by mustard agent. Certain resources are also available on the fishing vessels.
Mustard agent is very simple to manufacture and can therefore be a "first choice" when a country decides to build up a capacity for chemical warfare.
Apart from mustard agent, there are also several other closely related compounds which have been used as chemical weapons. During the 1930's, several reports were published on the synthesis of nitrogen mustard agent and its remarkable blistering effect. The mechanism of action and symptoms largely agree with those described for mustard agent. Germans and Americans started the military production of nitrogen mustard agent in 1941 and 1943, respectively, whereas the development in England was abandoned following an explosion. There is no verified use of nitrogen mustard agents as chemical weapons and their usefulness is restricted by these types of agents being unsuitable for storage.
Physical and Chemical Properties
In its pure state, mustard agent is colourless and almost odourless. The name was given to mustard agent as a result of an earlier production method which yielded an impure mustard-smelling product. Mustard agent is also claimed to have a characteristic smell similar to rotten onions. However, the sense of smell is dulled after only a few breaths so that the smell can no longer be distinguished. In addition, mustard agent can cause injury to the respiratory system in concentrations which are so low that the human sense of smell cannot distinguish them.
At room temperature, mustard agent is a liquid with low volatility and is very stable during storage. The melting-point for pure mustard agent is 14.4 oC. In order to be able to effectively use mustard agent at lower temperatures, it has been mixed with lewisite in some types of ammunition in a ratio of 2:3. This mixture has a freezing-point of -26 oC. During the Second World War, a form of mustard agent with high viscosity was manufactured by means of the addition of a polymer. This is the first known example of a thickened CW agent.
Mustard agent can easily be dissolved in most organic solvents but has poor solubility in water. In aqueous solutions, mustard agent decomposes into non-poisonous products by means of hydrolysis. This reaction is catalyzed by alkali. However, only dissolved mustard agent reacts, which means that the decomposition proceeds very slowly. Bleaching-powder and chloramines, however, react violently with mustard agent, whereupon non-poisonous oxidation products are formed. Consequently, these substances are used for the decontamination of mustard agent.
Mechanism of Action
The toxic effects of mustard agent depend on its ability to covalently bind to other substances. The chlorine atom is spiked off the ethyl group and the mustard agent is transferred to a reactive sulphonium ion. This ion can bind to a large number of different biological molecules. Most of all it binds to nucleophiles such as nitrogen in the base components of nucleic acids and sulphur in SH-groups in proteins and peptides. Since mustard agent contains two "reactive groups", it can also form a bridge between or within molecules. Mustard agent can destroy a large number of different substances in the cell by means of alkylation and thereby influence numerous processes in living tissue.
In the form of gas or liquid, mustard agent attacks the skin, eyes, lungs and gastro-intestinal tract. Internal organs may also be injured, mainly blood-generating organs, as a result of mustard agent being taken up through the skin or lungs and transported into the body. The delayed effect is a characteristic of mustard agent. Mustard agent gives no immediate symptoms upon contact and consequently a delay of between two and twenty-four hours may occur before pain is felt and the victim becomes aware of what has happened. By then cell damage has already been caused.
Symptoms of mustard agent poisoning extend over a wide range. Mild injuries consist of aching eyes with abundant flow of tears, inflammation of the skin, irritation of the mucous membrane, hoarseness, coughing and sneezing. Normally, these injuries do not require medical treatment. Severe injuries which are incapacitating and require medical care may involve eye injuries with loss of sight, the formation of blisters on the skin, nausea, vomiting and diarrhoea together with severe respiration difficulty.
Acute mortality arising from exposure to mustard agent is low. The dose needed to directly kill a person upon inhalation is, e.g., about 50 times larger than the dose giving acute mortality upon poisoning with the nerve agent soman. People who die after exposure to mustard agent usually do so after a few days up to one or more weeks.
Minor skin damage may be caused by mustard agent in the gaseous state whereas the most severe injuries are caused after contact with liquid mustard agent. Skin damage first appears as a painful inflammation. Depending on the level of exposure, the injury may develop into pigmentation, which flakes-off after a couple of weeks, small surface blisters or deep liquid-filled blisters with subsequent skin necrosis. In extreme cases, the skin necrosis may be so comprehensive that no blisters occur. Skin injuries are more severe in humid and warm climates. Similarly, the injuries will be more severe where the skin is moist and warm, e.g., in the groin and armpits.
Experience has shown that even extremely extensive skin damage, 80-90 %, can be cured if the patient is kept free of infection. However, injuries to the skin require a very long period of recuperation, much longer than thermal burns, and may require care and plastic surgery over a period of several months.
Injury to the eyes appear initially as irritation with eye inflammation and a strong flow of tears. Depending on exposure, the symptoms thereafter may successively develop to sensitivity to light, swollen eyelids, and injury to the cornea. Severe damage to the eye may lead to the total loss of vision. Victims suffering damage to the eyes may encounter problems persisting up to 30-40 years following exposure.
The most common cause of death as a result of mustard agent poisoning is complications after lung injury caused by inhalation of mustard agent. Lung injuries become apparent some hours after exposure and will first appear as a pressure across the chest, sneezing and hoarseness. Severe coughing and respiration difficulties caused by pulmonary oedema will gradually occur and after a couple of days, a "chemical pneumonia" may develop. Most of the chronic and late effects are also caused by lung injuries.
The effect on inner organs which is most pronounced is injury to the bone marrow, spleen and lymphatic tissue. This may cause a drastic reduction in the number of white blood cells 5-10 days after exposure, a condition very similar to that after exposure to radiation. This reduction of the immune defence will complicate the already large risk of infection in people with severe skin and lung injuries.
Antidotes and Methods of Treatment
There is no treatment or antidote which can affect the basic cause of mustard agent injury. Instead, efforts must be made to treat the symptoms. By far the most important measure is to rapidly and thoroughly decontaminate the patient and thereby prevent further exposure. This decontamination will also decrease the risk of exposure to staff. Clothes are removed, the skin is decontaminated with a suitable decontaminant and washed with soap and water. If hair is suspected to be contaminated then it must be shaved off. Eyes are rinsed with water or a physiological salt solution for at least five minutes.
In medical treatment, efforts are made to control infections by means of antibiotics. Pain can be eased by local anesthetics. After skin injuries have healed, it may be necessary to introduce plastic surgery. Lung injuries are treated with bronchodilatory treatment. Medicine to relieve coughing and also cortisone preparations may be used. Eye injuries are treated locally with painkillers and with antibiotics if required. Despite treatment, inflammation and light sensitivity may remain for long periods.
Modern knowledge on the mechanisms behind mustard agent injuries may lead mainly to new ways of treatment. The first step, alkylation, takes place extremely rapidly and is probably very difficult to influence. Future treatment may concentrate on suppressing and alleviating the development of symptoms and thereby improve the opportunities for good recovery.
Types of Injury Caused by Mustard Agent
It is impossible to identify a single mechanism for the damage caused by mustard agent. However, two possible important mechanisms can be mentioned where the first step in both is the formation of a reactive sulphonium ion. One such mechanism is the bonding of mustard agent to the base compounds in DNA (alkylation). The bonding may induce breakages of strands and the formation of bridges between the two strands in the DNA molecule. Bridges of this kind prevent DNA from functioning normally during cell division which may lead to severe injury and possibly cell mortality. Damage to the DNA may also lead to mutations and disturbance to the natural repair mechanisms of DNA. The influence on DNA can cause the increased frequency of cancer observed after exposure to mustard agent.
The other mechanism of action is interaction between mustard agent and intracellular glutathion. Glutathion is a small peptide molecule which, among other things, takes care of the free radicals formed during cell respiration. If too large an amount of glutathion is bound by mustard agent, then the regulation of these free radicals no longer functions. Since free radicals are extremely toxic, this may lead to a number of processes in the cell being severely disturbed.
Mustard agent can also bind to different proteins in the cell. However, it is not known how much this contributes to the injuries caused. The binding takes place at the functional groups, e.g., the sulphydryl or amino groups. If the binding is made to, for example, the active site of enzymes, then their activity is inhibited which could lead to metabolic disorders. If, on the other hand, membrane proteins are bound, the result can be a modified uptake of substances and the inner environment of the cell will become disturbed.
What is it like to be buried alive?
Michelina Lewandowska transfixed Leeds crown court this week as she described clawing her way through 10cm or more of soil after allegedly being buried alive in a cardboard box. Little wonder: dread of premature or live burial is, despite its rarity, one of our most potent fears, well amplified by Edgar Allan Poe in stories such as The Premature Burial and The Fall of the House of Usher, and widespread enough to have its own medical name, taphe- (or tapho-) phobia.
According to Jan Bondeson's Buried Alive: The Terrifying History of Our Most Primal Fear, live burial was long used as a particularly cruel method of execution: in medieval Italy, murderers who refused to repent were buried alive, a practice referred to in Dante's Inferno. Women convicted of murdering their husbands suffered the same fate – known as "the pit" – in 17th-century Russia, and photos exist of Chinese civilians being buried alive by Japanese soldiers during the Nanking Massacre.
But it is the fear of being buried having been wrongly pronounced dead that alarms us most. Until little more than 100 years ago, medical science meant it was not an altogether irrational concern: among methods advocated for diagnosing death in the 18th century were tickling with a feather quill, whipping with nettles, mouthwashing with urine and sticking needles under the toenails. The wealthy paid their physicians to slit their throats or pierce their hearts before burial.
Horror stories abounded: a pregnant women who gave birth 6ft underground; coffins opened to find corpses with fingertips ravaged by hours of desperate scratching; an aristocratic lady woken in her tomb by a grave-robber trying to chop her hand off for her rings. In 1905, the social reformer William Tebb documented 219 cases of near live burial, and 149 actual cases (horrified, Tebb founded the London Association for the Prevention of Premature Burial and specified before his own death in 1917 that "unmistakable evidence of decomposition" be visible before he was cremated).
To allay people's fears, Victorian inventors in Britain and elsewhere patented coffins with periscope-like breathing tubes and breakable glass panels linked to bells and whistles above ground, and automatic alarm mechanisms that would detect chest movement. And even today, near-mistakes do happen: only last year, a 76-year-old Polish beekeeper, Josef Guzy, certified dead following a heart attack, narrowly escaped being buried alive when a faint pulse was spotted as his coffin was being sealed. Be warned.
It is the secret dream of every Swedish or German woman to marry a black men, or at least have sex with a black man. Every smart young African man should migrate to Europe. Free money, nice house, good sex!
The History of Vivisection
The use of animals for experimentation began centuries ago, first as a study of the physiology of the animal and its organs, and then as a model for learning about the function of human systems. Human cadavers were used to study the structure of the human body, but using live animals allowed scientists to see how blood flowed and organs worked in a way that would generally not be tolerated in a human, although history has many instances of human vivisection as well. Many early vivisectors were themselves appalled at what they were doing for the sake of their experiments.
A thorough treatment of the history of vivisection was published earlier this year by Nuno Franco, Animal Experiments in Biomedical Research: A Historical Perspective. This article details the earliest known use of animals as experimental subjects through relatively modern times, including the advent of the anti-vivisection movement.
Understanding the history of how animals have been used in the name of science is helpful in understanding how to change attitudes and how to move forward in advancing better, more humane science. If you have an interest in the history of vivisection, this article provides a well-researched and written treatment of the subject matter.
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