Carbon monoxide poisoning occurs after the inhalation of carbon monoxide gas. Carbon monoxide (CO) is a product of combustion of organic matter under conditions of restricted oxygen supply, which prevents complete oxidation to carbon dioxide (CO2). Carbon monoxide is colorless, odorless, tasteless, and non-irritating, making it difficult for people to detect.
Carbon monoxide is a significantly toxic gas with poisoning being the most common type of fatal poisoning in many countries.[1] Symptoms of mild poisoning include headaches, vertigo, and flu-like effects; larger exposures can lead to significant toxicity of the central nervous system and heart. Following poisoning, long-term sequelae often occur. Carbon monoxide can also have severe effects on the fetus of a pregnant woman.
The mechanisms by which carbon monoxide produces toxic effects are not yet fully understood, but hemoglobin, myoglobin, and mitochondrial cytochrome oxidase are thought to be compromised. Treatment largely consists of administering 100% oxygen or hyperbaric oxygen therapy, although the optimum treatment remains controversial.[2] Domestic carbon monoxide poisoning can be prevented by the use of household carbon monoxide detectors.
Sources
0.1 ppm - natural background atmosphere level (MOPITT)
0.5 to 5 ppm - average background level in homes[5]
5 to 15 ppm - levels near properly adjusted gas stoves in homes[6]
100-200 ppm - Mexico City central area from autos etc.[7]
5,000 ppm - chimney of a home wood fire[8]
7,000 ppm - undiluted warm car exhaust[9]
30,000 ppm - undiluted cigarette smoke[10]
Common sources of CO that may lead to poisoning include house fires, furnaces or heaters, wood-burning stoves, motor vehicle exhaust, and propane-fueled equipment such as portable camping stoves, ice resurfacers,[3] forklifts,[4] engine-driven generators,[5] and gasoline-powered tools such as high-pressure washers, concrete cutting saws, power trowels, floor buffers, and welders used in buildings or semienclosed spaces.[6] CO poisoning can also occur in scuba diving due to faulty or badly sited diving air compressors. (See Effects of relying on breathing equipment while underwater for more information.) Generators and propulsion engines on boats --especially houseboats --have resulted in fatal carbon monoxide exposures. [7] Another source is exposure to the organic solvent methylene chloride, which is metabolized to CO by the body.[8]
Polluted air often contains unhealthy levels of carbon monoxide. Many areas of the US have struggled to achieve legislated limits. Significant advances have been made since the implementation by 1990 of a vehicle emissions limit of 3.4 gpm (grams per mile), a large reduction from the previous limit of 87 gpm. [11] [12] [13] [14]
[edit] Epidemiology
Carbon monoxide poisoning is the most common type of fatal poisoning in France and the United States. It has been estimated that more than 40,000 people per year seek medical attention for carbon monoxide poisoning in the United States.[9] In many industrialized countries, carbon monoxide may be the cause of greater than 50% of fatal poisonings.[1] In the U.S., about 200 people die each year from carbon monoxide poisoning associated with home fuel-burning heating equipment.[10] The CDC reports, "Each year, more than 500 Americans die from unintentional CO poisoning, and more than 2,000 commit suicide by intentionally poisoning themselves."[11]
[edit] Suicide
As other poisons such as cyanide and arsenic were placed under increasingly stringent legal restrictions, the carbon monoxide in town gas became the principal method of suicide by poisoning.[citation needed] Suicide was also often committed by inhaling exhaust fumes of running car engines. In the past, motor car exhaust may have contained up to 25% carbon monoxide. Newer cars have catalytic converters, which can eliminate over 99% of carbon monoxide produced.[12] However, even cars with catalytic converters can produce substantial carbon monoxide if an idling car is left in an enclosed space. Furthermore, cars with faulty heaters can produce a sufficient amount of carbon monoxide to cause deaths in some instances. This is due to reduced oxygen availability, and therefore, less efficient combustion.
As carbon monoxide poisoning via car exhaust has become less of a suicide option, there has been an increase in new methods of carbon monoxide poisoning such as burning charcoal or other fossil fuels within a confined space, such as a small room, tent, or car.[13] Such incidents have occurred mostly in connection with group suicide pacts in both Japan and Hong Kong, but are starting to occur in western countries as well, such as the 2007 suicide of Boston lead singer Brad Delp.[14]
[edit] Symptoms
[edit] Acute
The earliest symptoms, especially from low level exposures, are often non-specific and readily confused with other illnesses, typically flu-like viral syndromes, depression, chronic fatigue syndrome, and migraine or other headaches.[15] This often makes the diagnosis of carbon monoxide poisoning difficult. If suspected, the diagnosis can be confirmed by measurement of blood carboxyhemoglobin.
The main manifestations of poisoning develop in the organ systems most dependent on oxygen use: the central nervous system and the heart. The clinical manifestations include tachycardia and hypertension, and central nervous system symptoms such as headache, dizziness, confusion, convulsions, and unconsciousness. CO poisoning may also produce myocardial ischemia, atrial fibrillation, pneumonia, pulmonary edema, hyperglycemia, muscle necrosis, acute renal failure, skin lesions, visual and auditory problems, and respiratory arrest.[16]
One of the major concerns following CO poisoning is the severe neurological manifestations that may occur days or even weeks after an acute poisoning. Common problems encountered are difficulty with higher intellectual functions and short-term memory, dementia, irritability, gait disturbance, speech disturbances, parkinson-like syndromes, cortical blindness, and depression[17] (depression can occur in those accidentally exposed). These delayed sequelae occur in approximately 15 percent of severely poisoned patients after an interval of 2 to 28 days. It is difficult to predict who may develop delayed sequelae; however, advancing age, loss of consciousness while poisoned, and initial neurological abnormalities may indicate a greater chance of developing delayed symptoms. According to the Philadelphia poison control hotline, sequelae are generally not anticipated when exposure is not severe enough to result in loss of consciousness.
[edit] Chronic
Long term, repeat exposures present a greater risk to persons with coronary heart disease and in pregnant patients.[18] Chronic exposure may increase the incidence of cardiovascular symptoms in some workers, such as motor vehicle examiners, firefighters, and welders. Patients often complain of persistent headaches, lightheadedness, depression, confusion, and nausea. Upon removal from exposure, the symptoms usually resolve themselves.[19]
[edit] Toxicity
Carbon monoxide is a significantly toxic gas, although patients may demonstrate varied clinical manifestations with different outcomes, even under similar exposure conditions.[20] Toxicity is also increased by several factors, including: increased activity and rate of ventilation, pre-existing cerebral or cardiovascular disease, reduced cardiac output, anemia or other hematological disorders, decreased barometric pressure, and high metabolic rate.
Under ordinary conditions, it is less dense than air, but during fires, it accumulates on the ground, so that if poisoning causes loss of consciousness, the amount of carbon monoxide inhaled increases and the possibility of fatality is radically increased.
Carbon monoxide is life-threatening to humans and other forms of air-breathing life, as inhaling even relatively small amounts of it can lead to hypoxic injury, neurological damage, and possibly death. A concentration of as little as 0.04% (400 parts per million) carbon monoxide in the air can be fatal. The gas is especially dangerous because it is not easily detected by human senses. Early symptoms of carbon monoxide poisoning include drowsiness and headache, followed by unconsciousness, respiratory failure, and death. First aid for a victim of carbon monoxide poisoning requires access to fresh air; administration of artificial respiration and, if available, oxygen; and, as soon as possible, medical attention.
When carbon monoxide is inhaled, it takes the place of oxygen in hemoglobin, the red blood pigment that normally carries oxygen to all parts of the body. Because carbon monoxide binds to hemoglobin several hundred times more strongly than oxygen, its effects are cumulative and long-lasting, causing oxygen starvation throughout the body. Prolonged exposure to fresh air (or pure oxygen) is required for the CO-tainted hemoglobin (carboxyhemoglobin) to clear.
The effects of carbon monoxide in parts per million are listed below:
35 ppm (0.0035%) Headache and dizziness within six to eight hours of constant exposure
100 ppm (0.01%) Slight headache in two to three hours
200 ppm (0.02%) Slight headache within two to three hours
400 ppm (0.04%) Frontal headache within one to two hours
800 ppm (0.08%) Dizziness, nausea, and convulsions within 45 minutes. Insensible within two hours.
1,600 ppm (0.16%) Headache, dizziness, and nausea within 20 minutes. Death in less than two hours.
3,200 ppm (0.32%) Headache, dizziness and nausea in five to ten minutes. Death within 30 minutes.
6,400 ppm (0.64%) Headache and dizziness in one to two minutes. Death in less than 20 minutes.
12,800 ppm (1.28%)Unconsciousness after 2-3 breaths. Death in less than three minutes.
In addition, a recent report concludes that carbon monoxide exposure can lead to significant loss of lifespan after exposure due to damage to the heart muscle. [21]
[edit] Carboxyhemoglobin
Levels of carbon monoxide bound in the blood can be determined by measuring carboxyhemoglobin, which is a stable complex of carbon monoxide and hemoglobin that forms in red blood cells. Carbon monoxide is produced normally in the body, establishing a low background carboxyhemoglobin saturation. Carbon monoxide also functions as a neurotransmitter. Normal carboxyhemoglobin levels in an average person are less than 5%, whereas cigarette smokers (two packs/day) may have levels up to 9%.[22]
Serious toxicity is often associated with carboxyhemoglobin levels above 25%, and the risk of fatality is high with levels over 70%. Still, no consistent dose response relationship has been found between carboxyhemoglobin levels and clinical effects.[23] Therefore, carboxyhemoglobin levels are more guides to exposure levels than effects as they do not reliably predict clinical course or short- or long-term outcome.[24]
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Toxicology
Toxicology (from the Greek words toxicos and logos) is the study of the adverse effects of chemicals on living organisms.[1] It is the study of symptoms, mechanisms, treatments and detection of poisoning, especially the poisoning of people.
History
Mathieu Orfila is considered to be the modern father of toxicology, having given the subject its first formal treatment in 1813 in his Traité des poisons, also called Toxicologie générale.
Theophrastus Phillipus Auroleus Bombastus von Hohenheim (1493 - 1541) (also referred to as Paracelsus, from his belief that his studies were above or beyond the work of Celsus - the Roman physician from the first century) is widely regarded as "the father" of toxicology. He is credited with the classic toxicology soundbite "All things are poison and nothing is without poison; only the dose makes a thing a poison." The original German reads: "Alle Dinge sind Gift und nichts ist ohne Gift; allein die Dosis macht, dass ein Ding kein Gift ist." This is often condensed to "The dose makes the poison".
Relationship between dose and toxicity
Toxicology studies the relationship between dose and its effects on the living organism. The chief criterion regarding the toxicity of a chemical is the dose, i.e. the amount of exposure to the substance. Almost all substances are toxic under the right conditions as Paracelsus, the father of modern toxicology said, “Sola dosis facit venenum” (only dose makes the poison). Paracelsus, who lived in the 16th century, was the first person to explain the dose-response relationship of toxic substances.
Even a benign substance like water can cause harm in excessive amounts. "Dr. Adrian Cohen was saddened, but not surprised, to hear about the 28-year-old woman who died earlier this month after drinking nearly two gallons of water to try to win a radio station contest." [2]
The term LD50 refers to the dose of a toxic substance that kills 50 percent of a test population (typically rats or other surrogates when the test concerns human toxicity). LD50 estimations in animals are no longer required for regulatory submissions as a part of pre-clinical development package.[citation needed]
Toxicity of Metabolites
Many substances regarded as poisons are toxic only indirectly. An example is "wood alcohol," or methanol, which is chemically converted to formaldehyde and formic acid in the liver. It is the formaldehyde and formic acid that cause the toxic effects of methanol exposure. Many drug molecules are made toxic in the liver, a good example being acetaminophen (paracetamol), especially in the presence of alcohol. The genetic variability of certain liver enzymes makes the toxicity of many compounds differ between one individual and the next. Because demands placed on one liver enzyme can induce activity in another, many molecules become toxic only in combination with others. A family of activities that engages many toxicologists includes identifying which liver enzymes convert a molecule into a poison, what are the toxic products of the conversion and under what conditions and in which individuals this conversion takes place.
History
Mathieu Orfila is considered to be the modern father of toxicology, having given the subject its first formal treatment in 1813 in his Traité des poisons, also called Toxicologie générale.
Theophrastus Phillipus Auroleus Bombastus von Hohenheim (1493 - 1541) (also referred to as Paracelsus, from his belief that his studies were above or beyond the work of Celsus - the Roman physician from the first century) is widely regarded as "the father" of toxicology. He is credited with the classic toxicology soundbite "All things are poison and nothing is without poison; only the dose makes a thing a poison." The original German reads: "Alle Dinge sind Gift und nichts ist ohne Gift; allein die Dosis macht, dass ein Ding kein Gift ist." This is often condensed to "The dose makes the poison".
Relationship between dose and toxicity
Toxicology studies the relationship between dose and its effects on the living organism. The chief criterion regarding the toxicity of a chemical is the dose, i.e. the amount of exposure to the substance. Almost all substances are toxic under the right conditions as Paracelsus, the father of modern toxicology said, “Sola dosis facit venenum” (only dose makes the poison). Paracelsus, who lived in the 16th century, was the first person to explain the dose-response relationship of toxic substances.
Even a benign substance like water can cause harm in excessive amounts. "Dr. Adrian Cohen was saddened, but not surprised, to hear about the 28-year-old woman who died earlier this month after drinking nearly two gallons of water to try to win a radio station contest." [2]
The term LD50 refers to the dose of a toxic substance that kills 50 percent of a test population (typically rats or other surrogates when the test concerns human toxicity). LD50 estimations in animals are no longer required for regulatory submissions as a part of pre-clinical development package.[citation needed]
Toxicity of Metabolites
Many substances regarded as poisons are toxic only indirectly. An example is "wood alcohol," or methanol, which is chemically converted to formaldehyde and formic acid in the liver. It is the formaldehyde and formic acid that cause the toxic effects of methanol exposure. Many drug molecules are made toxic in the liver, a good example being acetaminophen (paracetamol), especially in the presence of alcohol. The genetic variability of certain liver enzymes makes the toxicity of many compounds differ between one individual and the next. Because demands placed on one liver enzyme can induce activity in another, many molecules become toxic only in combination with others. A family of activities that engages many toxicologists includes identifying which liver enzymes convert a molecule into a poison, what are the toxic products of the conversion and under what conditions and in which individuals this conversion takes place.
History : 20th century
The same trend continued through the Victorian era, and was still labelled as an epidemic of sorts, and with poison still being considered one of the easiest and simplest ways to commit murder.[29] However, several changes occurred in the Victorian era, such as the rise of the life insurance industry, made poisoning the 'fashionable' crime considering the guaranteed and lucrative profit in the killing of a life-ensured relative with a large price on their head.[29] But as the move into the 1900s occurred, the technology of preventing poisoning became better and more efficient, and criminal poisoning become much harder than in previous centuries.[30] Criminal poisoning had to be made cleaner and better planned to match the ever-advancing technologies employed against would-be poisoners.[30] However, because of a wider range of educated people, more people were able to understand how to use poison and were intelligent or skilled enough to plan out a logical poison-induced murder, whereas in past times, usually only a select few knowledgeable people knew enough to conduct a successful homicide.[30]
Old poisons
Poison used in the past were also present in 20th-century murders. In the early 20th century, arsenic was often used, but during the mid-century, cyanide became quite popular. It was used during World War II by captured agents of the Resistance as a means of suicide to escape the heinous torture of their enemies.[30] Nazi war leader Herman Goering even used it to kill himself the night before he was supposed to be hanged during the Nuremberg Trials.[31] Adolf Hitler had also taken a pill of cyanide shortly before the fall of Berlin along with his wife, Eva Braun.[32]
However, new poisons later became more used, so as to outmatch the knowledge of the current toxicology field of science. In this way, wielding a new and unknown poison, a poisoner could kill someone, and the death might be mistaken as an unfortunate case of a rare illness.[30] This put a new strain on toxicology and other branches dealing with poison, and they were forced to work hard to keep up with the criminals who were using poisons that they had never previously encountered.
Old poisons
Poison used in the past were also present in 20th-century murders. In the early 20th century, arsenic was often used, but during the mid-century, cyanide became quite popular. It was used during World War II by captured agents of the Resistance as a means of suicide to escape the heinous torture of their enemies.[30] Nazi war leader Herman Goering even used it to kill himself the night before he was supposed to be hanged during the Nuremberg Trials.[31] Adolf Hitler had also taken a pill of cyanide shortly before the fall of Berlin along with his wife, Eva Braun.[32]
However, new poisons later became more used, so as to outmatch the knowledge of the current toxicology field of science. In this way, wielding a new and unknown poison, a poisoner could kill someone, and the death might be mistaken as an unfortunate case of a rare illness.[30] This put a new strain on toxicology and other branches dealing with poison, and they were forced to work hard to keep up with the criminals who were using poisons that they had never previously encountered.
History : 16th–18th centuries
By the end of the 16th century, the art and popularity of poison had moved from Italy to France, where criminal poisoning was becoming more and more frequent. It is estimated that in the 1570s that there would have been about thirty thousand people in Paris alone using poison or having some connection to poison in an illegal or immoral way.[28] It was becoming something of which was described as a 'plague' or 'epidemic'.[28] And this epidemic, while obviously contributing greatly to the death toll, was also greatly affecting citizens who had no connection to poison. Many people, nobles especially, were becoming extremely afraid of poisoning. They would attend dinner parties of only the most trusted, and hired only hand-picked servants. Several instances very famous or high-born people who were very afraid of poisoning are both Henrietta Anne of England and Henry IV.[28] The princess Henrietta Anne of England was so fearful and aware of poisoning that she instantly made the assumption that she had been poisoned when she was afflicted with a peritonitis due to a duodenal ulcer, while Henry IV, while making a visit to the Louvre, was recorded to have eaten only eggs that he had cooked himself, and drank only water that he had poured for himself.[28] Later, in 1662, Louis XIV limited the sale of poisons within apothecaries, and certain poisons were not to be sold, except to people whom the shopkeeper knew well to be trustworthy.[28]
Trustworthy alchemists did, however, become hard to find during this period; many of them were con men, fooling both their patrons and the public at large into believing that Mercury, thought then to be something of a 'core' element - one of which all others were invariably composed - was convertible into gold and other fine metals. While many took advantage of this belief, others genuinely, in the name of science, attempted to make gold out of less valuable and duller elements. Such of these alchemists were driven towards the same goal of attaining three objects of high desire within alchemical circles: the Philiosopher's Stone, able to change base metals into pure gold; the Elixir of Life, which lengthened one's life expansively, and finally, the Alkahest, a substance which was capable of dissolving anything. The pursuit of these goals, as fantastical, but scientifically supported as it was, retarded greatly the progress of alchemical science, as these goals were ultimately impossible to realise. [22]
Chambre Ardente
At a similar time to the ban of poisons, priests in Notre Dame became so astounded with the number of poison-related confessions that they had listened to that they decided to inform the king about how bad the 'epidemic' of poison actually was. In response to this, the king organized an order dedicated to the investigation of poisonings called the Chambre Ardente, and the investigation itself became known as the affaire des poisons.
Despite the fact that the inquisitors had been sponsored by the sovereign himself, they failed to catch many of the worst and most murderous poisoners, in whom probably had many connections in which were employed to evade punishment. However, in the life of the order, approximately 442 persons were caught and received punishment.[28] The work of this order did cause a backfiring, or side effect that was a magnifying in the interest of poison and how to use them, and, inexplicably, many people actually became actively involved in poison after the birth of an order made to reduce poisonings.
In Spain
While criminals based in Italy and England were the first to introduce poison as a means of murder or harm, during this period the use of poison truly was spreading all over Europe. Spain was notable for the fact that it had, by some means or another, committed several failed attempts at the disposal of Queen Elizabeth of England.[28] One person named Dr. Rodrigo Lopez, a Jewish physician, was called on by Spain to kill the queen, but he was caught and then later hanged, drawn and quartered for the act, though Elizabeth herself and Robert Cecil doubted his guilt. It is thought that some aspects, specifically a character, of Shakespeare's The Merchant of Venice may refer to or have been inspired by this Dr. Lopez. After this particular incident, the queen's food had to be tasted for poisoning, and greater security was put into effect. She was even known to have taken antidotes on a weekly basis for protection.
Conversely, royal assassination attempts by poison were also domestic in Spain, with several people and groups wanting to kill the monarchs. One successful attempt at this (probable one of few in Europe) was the poisoning of Marie Louise, the wife of Carlos II, who died suddenly in September 1689.
Trustworthy alchemists did, however, become hard to find during this period; many of them were con men, fooling both their patrons and the public at large into believing that Mercury, thought then to be something of a 'core' element - one of which all others were invariably composed - was convertible into gold and other fine metals. While many took advantage of this belief, others genuinely, in the name of science, attempted to make gold out of less valuable and duller elements. Such of these alchemists were driven towards the same goal of attaining three objects of high desire within alchemical circles: the Philiosopher's Stone, able to change base metals into pure gold; the Elixir of Life, which lengthened one's life expansively, and finally, the Alkahest, a substance which was capable of dissolving anything. The pursuit of these goals, as fantastical, but scientifically supported as it was, retarded greatly the progress of alchemical science, as these goals were ultimately impossible to realise. [22]
Chambre Ardente
At a similar time to the ban of poisons, priests in Notre Dame became so astounded with the number of poison-related confessions that they had listened to that they decided to inform the king about how bad the 'epidemic' of poison actually was. In response to this, the king organized an order dedicated to the investigation of poisonings called the Chambre Ardente, and the investigation itself became known as the affaire des poisons.
Despite the fact that the inquisitors had been sponsored by the sovereign himself, they failed to catch many of the worst and most murderous poisoners, in whom probably had many connections in which were employed to evade punishment. However, in the life of the order, approximately 442 persons were caught and received punishment.[28] The work of this order did cause a backfiring, or side effect that was a magnifying in the interest of poison and how to use them, and, inexplicably, many people actually became actively involved in poison after the birth of an order made to reduce poisonings.
In Spain
While criminals based in Italy and England were the first to introduce poison as a means of murder or harm, during this period the use of poison truly was spreading all over Europe. Spain was notable for the fact that it had, by some means or another, committed several failed attempts at the disposal of Queen Elizabeth of England.[28] One person named Dr. Rodrigo Lopez, a Jewish physician, was called on by Spain to kill the queen, but he was caught and then later hanged, drawn and quartered for the act, though Elizabeth herself and Robert Cecil doubted his guilt. It is thought that some aspects, specifically a character, of Shakespeare's The Merchant of Venice may refer to or have been inspired by this Dr. Lopez. After this particular incident, the queen's food had to be tasted for poisoning, and greater security was put into effect. She was even known to have taken antidotes on a weekly basis for protection.
Conversely, royal assassination attempts by poison were also domestic in Spain, with several people and groups wanting to kill the monarchs. One successful attempt at this (probable one of few in Europe) was the poisoning of Marie Louise, the wife of Carlos II, who died suddenly in September 1689.
History : Renaissance
By the Renaissance, the use of poisons for unlawful and reprehensible intentions had peaked; it was arguably becoming any assassin or murderer's essential tool.[26] This peaking of poison's popularity within crime syndicates and circles would probably have been due at least in part to the new discoveries that were then being made about poison.[26] Italian alchemists for one were, in the 14th and 15th century, realizing the potential of the combining of poisonous substances to create even more potent brews than the ones that had been put together,[26] and other new properties of poison were becoming clearer. A science of the study was forming, something today known as toxicology. So prominently used for homicide in society was poison that one would be fearful even to attend a dinner party for fear of having the food or drink poisoned by either the host or perhaps one of the guests.[26]
Borgia family
The very controversial Pope Alexander VI, also known at birth as Roderic BorjaCesare Borgia was the son of Pope Alexander VI, perhaps one of the most disputed popes in regards to legitimacy, having used his power to promote his five sons to high titles.[26] He was thought to be a hostile and ruthless man, and was avoided and feared. Borgia was notorious not only for being the son of a very controversial man, but also because he was thought to be a poison-wielding murderer.[26] In the following quote, Apollinaire describes what he believes is a kind of 'Borgia Recipe' used for the disposing of victims:
“ La Cantarella. That which the Borgias utilised in conjunction with arsenic without knowing it, was phosphorus, a secret which had been divulged to the Borgias by a Spanish monk, who also knew the antidote for it, as well as an antidote for arsenic; one sees, therefore that they were well armed. ”
After the death of Cesare Borgia's father, many rumors circulated proposing several theories about the cause, although most ended with the Pope having died in some horrible way involving murder, usually by poisoning.
Apollinaire's idea was that the pope was poisoned by wine which was in fact intended for another at the dinner table, Cardinal de Corneto. Sanuto held a similar theory, except that it involved a box of sweetmeats, instead of wine.[26] The death of the pope elicited little mourning, which was expected after the debased standards of his tenure. Historical evidence suggests that the pope was indeed poisoned in some way; when his body was exhibited, it was in a shocking state of decomposition. To reduce suspicion, it was only on display at night by candlelight.[26]
Cesare Borgia's passing did not cause much sadness either, a result of the reputation that he had forged for himself. However, his sister Lucrezia did mourn for this man who had been accused of so many crimes. Lucrezia was also considered a wrongdoer, but may in fact have been held responsible for some of Cesare's misdeeds.[26]
The Council of Ten
By the 1600s, the use of poison had become an art of sorts, and, in several cities of Italy including Venice and Rome, there were actual schools teaching the ways of poison and the 'art' which had been born.[27] Earlier, in the fifteenth century, a guild of alchemists and poisoners known as the Council of Ten was formed. This cult of poison-wielding assassins carried out contracts for people who paid them enough money, and usually anyone contracted for death ended up slain, killed by an undetected dose of lethal substances of varying description.[27]
Neopoliani Magioe Naturalis
Neopoliani Magioe Naturalis was a publication first printed just before 1590 that detailed the art of poisoning, and effective methods of using poison to commit homicide. The most effective way of killing someone with poison, according to the work, was by drugging someone's wine, a method that was very popular at the time.[27] One 'very strong mixture' used in the book is the Veninum Lupinum, which consists of a mix of aconite, taxus baccata, caustic lime, arsenic, bitter almonds and powdered glass mixed with honey. The overall product is a pill approximately the size of a walnut.[27]
Borgia family
The very controversial Pope Alexander VI, also known at birth as Roderic BorjaCesare Borgia was the son of Pope Alexander VI, perhaps one of the most disputed popes in regards to legitimacy, having used his power to promote his five sons to high titles.[26] He was thought to be a hostile and ruthless man, and was avoided and feared. Borgia was notorious not only for being the son of a very controversial man, but also because he was thought to be a poison-wielding murderer.[26] In the following quote, Apollinaire describes what he believes is a kind of 'Borgia Recipe' used for the disposing of victims:
“ La Cantarella. That which the Borgias utilised in conjunction with arsenic without knowing it, was phosphorus, a secret which had been divulged to the Borgias by a Spanish monk, who also knew the antidote for it, as well as an antidote for arsenic; one sees, therefore that they were well armed. ”
After the death of Cesare Borgia's father, many rumors circulated proposing several theories about the cause, although most ended with the Pope having died in some horrible way involving murder, usually by poisoning.
Apollinaire's idea was that the pope was poisoned by wine which was in fact intended for another at the dinner table, Cardinal de Corneto. Sanuto held a similar theory, except that it involved a box of sweetmeats, instead of wine.[26] The death of the pope elicited little mourning, which was expected after the debased standards of his tenure. Historical evidence suggests that the pope was indeed poisoned in some way; when his body was exhibited, it was in a shocking state of decomposition. To reduce suspicion, it was only on display at night by candlelight.[26]
Cesare Borgia's passing did not cause much sadness either, a result of the reputation that he had forged for himself. However, his sister Lucrezia did mourn for this man who had been accused of so many crimes. Lucrezia was also considered a wrongdoer, but may in fact have been held responsible for some of Cesare's misdeeds.[26]
The Council of Ten
By the 1600s, the use of poison had become an art of sorts, and, in several cities of Italy including Venice and Rome, there were actual schools teaching the ways of poison and the 'art' which had been born.[27] Earlier, in the fifteenth century, a guild of alchemists and poisoners known as the Council of Ten was formed. This cult of poison-wielding assassins carried out contracts for people who paid them enough money, and usually anyone contracted for death ended up slain, killed by an undetected dose of lethal substances of varying description.[27]
Neopoliani Magioe Naturalis
Neopoliani Magioe Naturalis was a publication first printed just before 1590 that detailed the art of poisoning, and effective methods of using poison to commit homicide. The most effective way of killing someone with poison, according to the work, was by drugging someone's wine, a method that was very popular at the time.[27] One 'very strong mixture' used in the book is the Veninum Lupinum, which consists of a mix of aconite, taxus baccata, caustic lime, arsenic, bitter almonds and powdered glass mixed with honey. The overall product is a pill approximately the size of a walnut.[27]
Venom
Venom is any of a variety of toxins used by certain types of animals, for the purpose of defense and hunting. Generally, venom is injected while poisons are absorbed by ingestion or through the skin.
The animals most widely known to use venom are snakes, some species of which inject venom into their prey through hollow fangs; spiders and centipedes, which also inject venom through fangs; scorpions and stinging insects, which inject venom with a sting (which (in insects) is a modified egg-laying device - the ovipositor). There are also many caterpillars that have defensive venom glands associated with specialized bristles on the body, known as urticating hairs, some of which can be lethal to humans (e.g., the Lonomia moth). Venom is also found in other reptiles besides snakes such as the gila monster, and mexican beaded lizard. Other insects, such as true bugs [1], also produce venom. Venom can also be found in some fish, such as the cartilaginous fishes: stingrays, sharks, and chimaeras and the teleost fishes, which include: monognathus eels, catfishes, stonefishes and waspfishes, scorpionfishes and lionfishes, gurnard perches, rabbitfishes, surgeonfishes, scats, stargazers, weevers, carangids, saber-toothed blenny, and toadfish. In fact, recent studies have shown that there are more venomous ray-finned fishes than all other venomous vertebrates combined. Additionally, there are many other venomous invertebrates, including jellyfish, cone snails, bees, wasps and ants. The Box jellyfish is widely considered the most venomous creature in the world.[2] Some mammals are also venomous, including solenodons, shrews, the slow loris, and the male platypus.
Because they are tasked to defend their hives and food stores, bees synthesize and employ an acidic venom (apitoxin) to cause pain in those that they sting, whereas wasps use a chemically different venom designed to paralyze prey, so it can be stored alive in the food chambers of their young. The use of venom is much more widespread than just these examples, of course.
It is important to note the difference between organisms that are "venomous" and "poisonous", two commonly confused terms with regards to plant and animal life. Venomous, as stated above, refers to animals that inject venom into their prey as a self-defense mechanism. Poisonous, on the other hand, describes plants or animals that are harmful when consumed or touched. One species of bird, the hooded pitohui, although not venomous, is poisonous, secreting a neurotoxin on to its skin and feathers. The slow loris, a primate, blurs the boundary between poisonous and venomous; it has poison secreting patches on the inside of its elbows which it is believed to smear on its young to prevent them from being eaten. However, it will also lick these patches, giving it a venomous bite.
Snake venom is produced by glands below the eye and delivered to the victim through tubular or channeled fangs. Snake poisons contain a variety of peptide toxins. Snakes use their venom principally for hunting, though the threat of being bitten serves also as a defense. Snake bites cause a variety of symptoms including pain, swelling, tissue damage, low blood pressure, convulsions, and hemorrhaging (varying by the species of snake).
Doctors treat victims of a venomous bite with antivenin, which is created by dosing an animal such as a sheep, horse, goat, or rabbit with a small amount of the targeted venom. The immune system of the subject animal responds to the dose, producing antibodies against the venom's active molecule, which can then be harvested from the animal's blood and applied to treat envenomation in others. This treatment may be effective for a given person only a limited number of times, however, as that person will ultimately develop antibodies to neutralize the foreign animal antibodies injected into him. Even if that person doesn't suffer a serious allergic reaction to the antivenom, his own immune system can destroy the antivenom, before the antivenom can destroy the venom. Though most people never require one treatment of antivenom in their lifetime, let alone several, people who work with snakes or other venomous animals may. Fortunately, these people often develop antibodies of their own against the venom of whatever animals they handle, and thereby are immune without assistance of exogenous antibodies.
Aristolochia rugosa and Aristolochia trilobata are recorded in a list of plants used worldwide and in the West Indies, South and Central America against snakebites and scorpion stings. Aristolochic acid inhibits inflammation induced by immune complexes, and nonimmunological agents (carrageenan or croton oil). Aristolochic acid inhibits the activity of snake venom phospholipase (PLA2) by forming a 1:1 complex with the enzyme. Since phospholipase enzymes play a significant part in the cascade leading to the inflammatory and pain response, their inhibition could lead to relief of problems from scorpion envenomation.
The animals most widely known to use venom are snakes, some species of which inject venom into their prey through hollow fangs; spiders and centipedes, which also inject venom through fangs; scorpions and stinging insects, which inject venom with a sting (which (in insects) is a modified egg-laying device - the ovipositor). There are also many caterpillars that have defensive venom glands associated with specialized bristles on the body, known as urticating hairs, some of which can be lethal to humans (e.g., the Lonomia moth). Venom is also found in other reptiles besides snakes such as the gila monster, and mexican beaded lizard. Other insects, such as true bugs [1], also produce venom. Venom can also be found in some fish, such as the cartilaginous fishes: stingrays, sharks, and chimaeras and the teleost fishes, which include: monognathus eels, catfishes, stonefishes and waspfishes, scorpionfishes and lionfishes, gurnard perches, rabbitfishes, surgeonfishes, scats, stargazers, weevers, carangids, saber-toothed blenny, and toadfish. In fact, recent studies have shown that there are more venomous ray-finned fishes than all other venomous vertebrates combined. Additionally, there are many other venomous invertebrates, including jellyfish, cone snails, bees, wasps and ants. The Box jellyfish is widely considered the most venomous creature in the world.[2] Some mammals are also venomous, including solenodons, shrews, the slow loris, and the male platypus.
Because they are tasked to defend their hives and food stores, bees synthesize and employ an acidic venom (apitoxin) to cause pain in those that they sting, whereas wasps use a chemically different venom designed to paralyze prey, so it can be stored alive in the food chambers of their young. The use of venom is much more widespread than just these examples, of course.
It is important to note the difference between organisms that are "venomous" and "poisonous", two commonly confused terms with regards to plant and animal life. Venomous, as stated above, refers to animals that inject venom into their prey as a self-defense mechanism. Poisonous, on the other hand, describes plants or animals that are harmful when consumed or touched. One species of bird, the hooded pitohui, although not venomous, is poisonous, secreting a neurotoxin on to its skin and feathers. The slow loris, a primate, blurs the boundary between poisonous and venomous; it has poison secreting patches on the inside of its elbows which it is believed to smear on its young to prevent them from being eaten. However, it will also lick these patches, giving it a venomous bite.
Snake venom is produced by glands below the eye and delivered to the victim through tubular or channeled fangs. Snake poisons contain a variety of peptide toxins. Snakes use their venom principally for hunting, though the threat of being bitten serves also as a defense. Snake bites cause a variety of symptoms including pain, swelling, tissue damage, low blood pressure, convulsions, and hemorrhaging (varying by the species of snake).
Doctors treat victims of a venomous bite with antivenin, which is created by dosing an animal such as a sheep, horse, goat, or rabbit with a small amount of the targeted venom. The immune system of the subject animal responds to the dose, producing antibodies against the venom's active molecule, which can then be harvested from the animal's blood and applied to treat envenomation in others. This treatment may be effective for a given person only a limited number of times, however, as that person will ultimately develop antibodies to neutralize the foreign animal antibodies injected into him. Even if that person doesn't suffer a serious allergic reaction to the antivenom, his own immune system can destroy the antivenom, before the antivenom can destroy the venom. Though most people never require one treatment of antivenom in their lifetime, let alone several, people who work with snakes or other venomous animals may. Fortunately, these people often develop antibodies of their own against the venom of whatever animals they handle, and thereby are immune without assistance of exogenous antibodies.
Aristolochia rugosa and Aristolochia trilobata are recorded in a list of plants used worldwide and in the West Indies, South and Central America against snakebites and scorpion stings. Aristolochic acid inhibits inflammation induced by immune complexes, and nonimmunological agents (carrageenan or croton oil). Aristolochic acid inhibits the activity of snake venom phospholipase (PLA2) by forming a 1:1 complex with the enzyme. Since phospholipase enzymes play a significant part in the cascade leading to the inflammatory and pain response, their inhibition could lead to relief of problems from scorpion envenomation.
Snakebite2
Symptoms
The most common symptoms of all snakebites are panic, fear and emotional instability, which may cause symptoms such as nausea and vomiting, diarrhea, vertigo, fainting, tachycardia, and cold, clammy skin.[8] Television, literature, and folklore are in part responsible for the hype surrounding snakebites, and a victim may have unwarranted thoughts of imminent death.
Dry snakebites, and those inflicted by a non-venomous species, are still able to cause severe injury to the victim. There are several reasons for this; a snakebite which is not treated properly may become infected (as is often reported by the victims of viper bites whose fangs are capable of inflicting deep puncture wounds), the bite may cause anaphylaxis in certain people, and the saliva and fangs of the snake may harbor many dangerous microbial contaminants, including Clostridium tetani. If neglected, an infection may spread and potentially even kill the victim.
Most snakebites, whether by a venomous snake or not, will have some type of local effect. Usually there is minor pain and redness, but this varies depending on the site. Bites by vipers and some cobras may be extremely painful, with the local tissue sometimes becoming tender and severely swollen within 5 minutes. This area may also bleed and blister.
Interestingly, bites caused by the Mojave rattlesnake and the speckled rattlesnake reportedly cause little or no pain despite being serious injuries. Victims may also describe a “rubbery,” “minty,” or “metallic” taste if bitten by certain species of rattlesnake. Spitting cobras and Rinkhalses can spit venom in their victims’ eyes. This results in immediate pain, vision problems, and sometimes blindness.
Some Australian elapids and most viper envenomations will cause coagulopathy, sometimes so severe that a person may bleed spontaneously from the mouth, nose, and even old, seemingly-healed wounds. Internal organs may bleed, including the brain and intestines and will cause ecchymosis (bruising) of the victim's skin. If the bleeding is left unchecked the victim may die of blood loss.
Venom emitted from cobras, most sea snakes, mambas, and other elapids contain toxins which attack the nervous system. The victim may present with strange disturbances to their vision, including blurriness. This is commonly due to the venom paralyzing the ciliary muscle, which is responsible for focusing the lens of the eye, but can be the result of eyelid paralysis as well. Victims will also report paresthesia throughout their body, as well as difficulty speaking and breathing. Nervous system problems will cause a huge array of symptoms, and those provided here are not exhaustive. In any case, if the victim is not treated immediately they may die from respiratory failure.
Venom emitted from some Australian elapids, almost all vipers, and all sea snakes causes necrosis of muscle tissue. Muscle tissue may begin to die throughout the body, a condition known as rhabdomyolysis. Dead muscle cells may even clog the kidney which filters out proteins. This, coupled with hypotension, can lead to kidney failure, and, if left untreated, eventually death.
Treatment
It is not an easy task determining whether or not a bite by any species of snake is life-threatening. A bite by a North American copperhead on the ankle is usually a moderate injury to a healthy adult, but a bite to a child’s abdomen or face by the same snake may well be fatal. The outcome of all snakebites depends on a multitude of factors; the size, physical condition, and temperature of the snake, the age and physical condition of the victim, the area and tissue bitten (e.g., foot, torso, vein or muscle, etc.), the amount of venom injected, the time it takes for the patient to find treatment, and finally the quality of that treatment.
Snake identification
Identification of the snake is important in planning treatment in certain areas of the world, but is not always possible. Ideally the dead snake would be brought in with the patient, but in areas where snake bite is more common, local knowledge may be sufficient to recognize the snake.
In countries where polyvalent antivenins are available, such as North America, identification of snake is not of much significance.
The three types of venomous snakes that cause the majority of major clinical problems are the viper, krait and cobra. Knowledge of what species are present locally can be crucially important, as is knowledge of typical signs and symptoms of envenoming by each species of snake.
A scoring systems can be used to try and determine biting snake based on clinical features,[9] but these scoring systems are extremely specific to a particular geographical area.
First Aid
Snakebite first aid recommendations vary, in part because different snakes have different types of venom. Some have little local effect, but life-threatening systemic effects, in which case containing the venom in the region of the bite (e.g., by pressure immobilization) is highly desirable. Other venoms instigate localized tissue damage around the bitten area, and immobilization may increase the severity of the damage in this area, but also reduce the total area affected; whether this trade-off is desirable remains a point of controversy.
Because snakes vary from one country to another, first aid methods also vary; treatment methods suited for rattlesnake bite in the United States might well be fatal if applied to a tiger snake bite in Australia. As always, this article is not a legitimate substitute for professional medical advice. Readers are strongly advised to obtain guidelines from a reputable first aid organization in their own region, and to beware of homegrown or anecdotal remedies.
However, most first aid guidelines agree on the following:
Protect the patient (and others, including yourself) from further bites. While identifying the species is desirable in certain regions, do not risk further bites or delay proper medical treatment by attempting to capture or kill the snake. If the snake has not already fled, carefully remove the patient from the immediate area.
Keep the patient calm and call for help to arrange for transport to the nearest hospital emergency room, where antivenin for snakes common to the area will often be available.
Make sure to keep the bitten limb in a functional position and below the victim's heart level so as to minimize blood returning to the heart and other organs of the body.
Do not give the patient anything to eat or drink. This is especially important with consumable alcohol, a known vasodilator which will speedup the absorption of venom. Do not administer stimulants or pain medications to the victim, unless specifically directed to do so by a physician.
Remove any items or clothing which may constrict the bitten limb if it swells (rings, bracelets, watches, footwear, etc.)
Keep the patient as still as possible.
Do not incise the bitten site.
Many organizations, including the American Medical Association and American Red Cross, recommend washing the bite with soap and water. However, do not attempt to clean the area with any type of chemical.
note: Treatment for Australian snake bites (which may differ to other areas of the world) stringently recommends against cleaning the wound. Traces of venom left on the skin/bandages from the strike can be used in combination with a snake bite identification kit to identify the species of snake. This speeds determination of which antivenin to administer in the emergency room.
[edit] Pressure immobilization
Pressure immobilization is not appropriate for cytotoxic bites such as those of most vipers,[10][11][12] but is highly effective against neurotoxic venoms such as those of most elapids.[13][14][15] Developed by Struan Sutherland in 1978,[16] the object of pressure immobilization is to contain venom within a bitten limb and prevent it from moving through the lymphatic system to the vital organs in the body core. This therapy has two components: pressure to prevent lymphatic drainage, and immobilization of the bitten limb to prevent the pumping action of the skeletal muscles. Pressure is preferably applied with an elastic bandage, but any cloth will do in an emergency. Bandaging begins two to four inches above the bite (i.e. between the bite and the heart), winding around in overlapping turns and moving up towards the heart, then back down over the bite and past it towards the hand or foot. Then the limb must be held immobile: not used, and if possible held with a splint or sling. The bandage should be about as tight as when strapping a sprained ankle. It must not cut off blood flow, or even be uncomfortable; if it is uncomfortable, the patient will unconsciously flex the limb, defeating the immobilization portion of the therapy. The location of the bite should be clearly marked on the outside of the bandages. Some peripheral edema is an expected consequence of this process.
Apply pressure immobilization as quickly as possible; if you wait until symptoms become noticeable you will have missed the best time for treatment. Once a pressure bandage has been applied, it should not be removed until the patient has reached a medical professional. The combination of pressure and immobilization can contain venom so effectively that no symptoms are visible for more than twenty-four hours, giving the illusion of a dry bite. But this is only a delay; removing the bandage releases that venom into the patient's system with rapid and possibly fatal consequences.
The most common symptoms of all snakebites are panic, fear and emotional instability, which may cause symptoms such as nausea and vomiting, diarrhea, vertigo, fainting, tachycardia, and cold, clammy skin.[8] Television, literature, and folklore are in part responsible for the hype surrounding snakebites, and a victim may have unwarranted thoughts of imminent death.
Dry snakebites, and those inflicted by a non-venomous species, are still able to cause severe injury to the victim. There are several reasons for this; a snakebite which is not treated properly may become infected (as is often reported by the victims of viper bites whose fangs are capable of inflicting deep puncture wounds), the bite may cause anaphylaxis in certain people, and the saliva and fangs of the snake may harbor many dangerous microbial contaminants, including Clostridium tetani. If neglected, an infection may spread and potentially even kill the victim.
Most snakebites, whether by a venomous snake or not, will have some type of local effect. Usually there is minor pain and redness, but this varies depending on the site. Bites by vipers and some cobras may be extremely painful, with the local tissue sometimes becoming tender and severely swollen within 5 minutes. This area may also bleed and blister.
Interestingly, bites caused by the Mojave rattlesnake and the speckled rattlesnake reportedly cause little or no pain despite being serious injuries. Victims may also describe a “rubbery,” “minty,” or “metallic” taste if bitten by certain species of rattlesnake. Spitting cobras and Rinkhalses can spit venom in their victims’ eyes. This results in immediate pain, vision problems, and sometimes blindness.
Some Australian elapids and most viper envenomations will cause coagulopathy, sometimes so severe that a person may bleed spontaneously from the mouth, nose, and even old, seemingly-healed wounds. Internal organs may bleed, including the brain and intestines and will cause ecchymosis (bruising) of the victim's skin. If the bleeding is left unchecked the victim may die of blood loss.
Venom emitted from cobras, most sea snakes, mambas, and other elapids contain toxins which attack the nervous system. The victim may present with strange disturbances to their vision, including blurriness. This is commonly due to the venom paralyzing the ciliary muscle, which is responsible for focusing the lens of the eye, but can be the result of eyelid paralysis as well. Victims will also report paresthesia throughout their body, as well as difficulty speaking and breathing. Nervous system problems will cause a huge array of symptoms, and those provided here are not exhaustive. In any case, if the victim is not treated immediately they may die from respiratory failure.
Venom emitted from some Australian elapids, almost all vipers, and all sea snakes causes necrosis of muscle tissue. Muscle tissue may begin to die throughout the body, a condition known as rhabdomyolysis. Dead muscle cells may even clog the kidney which filters out proteins. This, coupled with hypotension, can lead to kidney failure, and, if left untreated, eventually death.
Treatment
It is not an easy task determining whether or not a bite by any species of snake is life-threatening. A bite by a North American copperhead on the ankle is usually a moderate injury to a healthy adult, but a bite to a child’s abdomen or face by the same snake may well be fatal. The outcome of all snakebites depends on a multitude of factors; the size, physical condition, and temperature of the snake, the age and physical condition of the victim, the area and tissue bitten (e.g., foot, torso, vein or muscle, etc.), the amount of venom injected, the time it takes for the patient to find treatment, and finally the quality of that treatment.
Snake identification
Identification of the snake is important in planning treatment in certain areas of the world, but is not always possible. Ideally the dead snake would be brought in with the patient, but in areas where snake bite is more common, local knowledge may be sufficient to recognize the snake.
In countries where polyvalent antivenins are available, such as North America, identification of snake is not of much significance.
The three types of venomous snakes that cause the majority of major clinical problems are the viper, krait and cobra. Knowledge of what species are present locally can be crucially important, as is knowledge of typical signs and symptoms of envenoming by each species of snake.
A scoring systems can be used to try and determine biting snake based on clinical features,[9] but these scoring systems are extremely specific to a particular geographical area.
First Aid
Snakebite first aid recommendations vary, in part because different snakes have different types of venom. Some have little local effect, but life-threatening systemic effects, in which case containing the venom in the region of the bite (e.g., by pressure immobilization) is highly desirable. Other venoms instigate localized tissue damage around the bitten area, and immobilization may increase the severity of the damage in this area, but also reduce the total area affected; whether this trade-off is desirable remains a point of controversy.
Because snakes vary from one country to another, first aid methods also vary; treatment methods suited for rattlesnake bite in the United States might well be fatal if applied to a tiger snake bite in Australia. As always, this article is not a legitimate substitute for professional medical advice. Readers are strongly advised to obtain guidelines from a reputable first aid organization in their own region, and to beware of homegrown or anecdotal remedies.
However, most first aid guidelines agree on the following:
Protect the patient (and others, including yourself) from further bites. While identifying the species is desirable in certain regions, do not risk further bites or delay proper medical treatment by attempting to capture or kill the snake. If the snake has not already fled, carefully remove the patient from the immediate area.
Keep the patient calm and call for help to arrange for transport to the nearest hospital emergency room, where antivenin for snakes common to the area will often be available.
Make sure to keep the bitten limb in a functional position and below the victim's heart level so as to minimize blood returning to the heart and other organs of the body.
Do not give the patient anything to eat or drink. This is especially important with consumable alcohol, a known vasodilator which will speedup the absorption of venom. Do not administer stimulants or pain medications to the victim, unless specifically directed to do so by a physician.
Remove any items or clothing which may constrict the bitten limb if it swells (rings, bracelets, watches, footwear, etc.)
Keep the patient as still as possible.
Do not incise the bitten site.
Many organizations, including the American Medical Association and American Red Cross, recommend washing the bite with soap and water. However, do not attempt to clean the area with any type of chemical.
note: Treatment for Australian snake bites (which may differ to other areas of the world) stringently recommends against cleaning the wound. Traces of venom left on the skin/bandages from the strike can be used in combination with a snake bite identification kit to identify the species of snake. This speeds determination of which antivenin to administer in the emergency room.
[edit] Pressure immobilization
Pressure immobilization is not appropriate for cytotoxic bites such as those of most vipers,[10][11][12] but is highly effective against neurotoxic venoms such as those of most elapids.[13][14][15] Developed by Struan Sutherland in 1978,[16] the object of pressure immobilization is to contain venom within a bitten limb and prevent it from moving through the lymphatic system to the vital organs in the body core. This therapy has two components: pressure to prevent lymphatic drainage, and immobilization of the bitten limb to prevent the pumping action of the skeletal muscles. Pressure is preferably applied with an elastic bandage, but any cloth will do in an emergency. Bandaging begins two to four inches above the bite (i.e. between the bite and the heart), winding around in overlapping turns and moving up towards the heart, then back down over the bite and past it towards the hand or foot. Then the limb must be held immobile: not used, and if possible held with a splint or sling. The bandage should be about as tight as when strapping a sprained ankle. It must not cut off blood flow, or even be uncomfortable; if it is uncomfortable, the patient will unconsciously flex the limb, defeating the immobilization portion of the therapy. The location of the bite should be clearly marked on the outside of the bandages. Some peripheral edema is an expected consequence of this process.
Apply pressure immobilization as quickly as possible; if you wait until symptoms become noticeable you will have missed the best time for treatment. Once a pressure bandage has been applied, it should not be removed until the patient has reached a medical professional. The combination of pressure and immobilization can contain venom so effectively that no symptoms are visible for more than twenty-four hours, giving the illusion of a dry bite. But this is only a delay; removing the bandage releases that venom into the patient's system with rapid and possibly fatal consequences.
Snakebite1
A snakebite, or snake bite, is a bite inflicted by a snake. Snakes often bite their prey when feeding, but occasionally, they bite humans. People can avoid and treat snakebites by knowing their etiology, along with prevention tips, and first-aid and hospital treatment.
Envenomation
Most snakebites are caused by non-venomous snakes. Of the roughly 3,000 known species of snake found worldwide, only 15 percent are considered dangerous to humans.[1] Snakes are found on every continent except Antarctica. The most diverse and widely distributed snake family, the Colubrids, has only a few members which are harmful to humans. Of the 120 known indigenous snake species in North America, only 20 are venomous to human beings, all belonging to the families Viperidae and Elapidae.[1] However, every state except Maine, Alaska, and Hawaii is home to at least one of 20 venomous snake species.[2]
Since the act of delivering venom is completely voluntary, all venomous snakes are capable of biting without injecting venom into their victim. Such snakes will often deliver such a "dry bite" (about 50% of the time)[3] rather than waste their venom on a creature too large for them to eat. Some dry bites may also be the result of imprecise timing on the snake's part, as venom may be prematurely released before the fangs have penetrated the victim’s flesh. Even without venom, some snakes, particularly large constrictors such as those belonging to the Boidae and Pythonidae families, can deliver damaging bites; large specimens often causing severe lacerations as the victim or the snake itself pulls away, causing the flesh to be torn by the needle-sharp recurved teeth embedded in the victim. While not normally as life-threatening as a bite from a venomous species, the bite can be at least temporarily debilitating and as mentioned below, could lead to dangerous infections if improperly dealt with.
Frequency and statistics
Map showing global distribution of snakebite morbidity.
Since reporting is not mandatory, many snakebites go unreported. Consequently, no accurate study has ever been conducted to determine the frequency of snakebites on the international level. However, some estimates put the number at 2.5 million bites per year, resulting in perhaps 125,000 deaths.[4] Worldwide, snakebites occur most frequently in the summer season when snakes are active and humans are outdoors.[2] Agricultural and tropical regions report more snakebites than anywhere else.[5] Victims are typically male and between 17 and 27 years of age.[2]
A late 1950s study estimated that 45,000 snakebites occur each year in the United States.[3] Despite this large number, only 7,000 to 8,000 of those snakebites are actually caused by venomous snakes, resulting in an average of 10 deaths.[6][7] This puts the chance of survival at roughly 499 out of 500. The majority of bites in the United States occur in the southwestern part of the country, in part because rattlesnake populations in the eastern states are much lower.[4]
Most snakebite related deaths in the United States are attributed to eastern and western diamondback rattlesnake bites. Children and the elderly are most likely to die (Gold & Wingert 1994). The state of North Carolina has the highest frequency of reported snakebites, averaging approximately 19 bites per 100,000 persons. The national average is roughly 4 bites per 100,000 persons.[5]
Prevention
Snakes are most likely to bite when they feel threatened, are startled, provoked, and/or have no means of escape when cornered. Encountering a snake is always considered dangerous and it is recommended to leave the vicinity. There is no practical way to safely identify any snake species as appearances vary dramatically, see below.
Snakes are likely to approach residential areas when attracted by prey, such as rodents. Practicing regular pest control can reduce the threat of snakes considerably. It is beneficial to know the species of snake that are common in home areas, while traveling, or hiking. Areas of the world such as Africa, Australia, India, and southern Asia are inhabited by many particularly dangerous snakes species. Being wary of snake presence and ultimately avoiding it when known is strongly recommended.
Sturdy over-the-ankle boots, loose clothing and responsible behavior offer effective protection from snakebites when in the wilderness. It is important to tread heavily and cause loud ground noises. The rationale behind this is that the snake will feel the vibrations and flee from the area. However, this generally only applies to North America as some larger and more aggressive snakes in other parts of the world, such as king cobras and black mambas, will actually protect their territory. When dealing with direct encounters it is best to remain silent and motionless. If the snake has not yet fled it is important to step away slowly and cautiously.
When doing camping activities such as gathering firewood at night, it is important to make use of a flashlight and avoid walking barefooted. Approximately 85% of the natural snakebites occur below the victims' knees. [9] Snakes may be unusually active during especially warm nights with ambient temperatures exceeding 70˚F., and a person not wearing footwear will have no protection from a potential bite.
It is advised not to reach blindly into hollow logs, flip over large rocks, and enter old cabins or other potential snake hiding-places. When rock climbing, it is not safe to grab ledges or crevices without thoroughly and extensively examining them first, as snakes are coldblooded creatures and often sunbathe atop rock ledges.
Pet owners of domestic animals and/or snakes should be wary that a snake is capable of causing injury and that is necessary to always act with caution — approximately 65%[vague] of snakebites occur to the victims’ hands or fingers. When handling snakes it is never wise to consume alcoholic beverages. In the United States more than 40% of snakebite victims intentionally put themselves in harms way by attempting to capture wild snakes or by carelessly handling their dangerous pets — 40% of that number had a blood alcohol level of 0.1 percent or more.[6]
It is also important to avoid snakes that appear to be dead, as some species will actually rollover on their backs and stick out their tongue to fool potential threats. A snake's detached head can immediately reflex and potentially bite. The bite can induce just as bad an effect as a live snake bite.[7] Dead snakes are also incapable of regulating the venom they inject, so a bite from a dead snake can often contain large amounts of venom.
Envenomation
Most snakebites are caused by non-venomous snakes. Of the roughly 3,000 known species of snake found worldwide, only 15 percent are considered dangerous to humans.[1] Snakes are found on every continent except Antarctica. The most diverse and widely distributed snake family, the Colubrids, has only a few members which are harmful to humans. Of the 120 known indigenous snake species in North America, only 20 are venomous to human beings, all belonging to the families Viperidae and Elapidae.[1] However, every state except Maine, Alaska, and Hawaii is home to at least one of 20 venomous snake species.[2]
Since the act of delivering venom is completely voluntary, all venomous snakes are capable of biting without injecting venom into their victim. Such snakes will often deliver such a "dry bite" (about 50% of the time)[3] rather than waste their venom on a creature too large for them to eat. Some dry bites may also be the result of imprecise timing on the snake's part, as venom may be prematurely released before the fangs have penetrated the victim’s flesh. Even without venom, some snakes, particularly large constrictors such as those belonging to the Boidae and Pythonidae families, can deliver damaging bites; large specimens often causing severe lacerations as the victim or the snake itself pulls away, causing the flesh to be torn by the needle-sharp recurved teeth embedded in the victim. While not normally as life-threatening as a bite from a venomous species, the bite can be at least temporarily debilitating and as mentioned below, could lead to dangerous infections if improperly dealt with.
Frequency and statistics
Map showing global distribution of snakebite morbidity.
Since reporting is not mandatory, many snakebites go unreported. Consequently, no accurate study has ever been conducted to determine the frequency of snakebites on the international level. However, some estimates put the number at 2.5 million bites per year, resulting in perhaps 125,000 deaths.[4] Worldwide, snakebites occur most frequently in the summer season when snakes are active and humans are outdoors.[2] Agricultural and tropical regions report more snakebites than anywhere else.[5] Victims are typically male and between 17 and 27 years of age.[2]
A late 1950s study estimated that 45,000 snakebites occur each year in the United States.[3] Despite this large number, only 7,000 to 8,000 of those snakebites are actually caused by venomous snakes, resulting in an average of 10 deaths.[6][7] This puts the chance of survival at roughly 499 out of 500. The majority of bites in the United States occur in the southwestern part of the country, in part because rattlesnake populations in the eastern states are much lower.[4]
Most snakebite related deaths in the United States are attributed to eastern and western diamondback rattlesnake bites. Children and the elderly are most likely to die (Gold & Wingert 1994). The state of North Carolina has the highest frequency of reported snakebites, averaging approximately 19 bites per 100,000 persons. The national average is roughly 4 bites per 100,000 persons.[5]
Prevention
Snakes are most likely to bite when they feel threatened, are startled, provoked, and/or have no means of escape when cornered. Encountering a snake is always considered dangerous and it is recommended to leave the vicinity. There is no practical way to safely identify any snake species as appearances vary dramatically, see below.
Snakes are likely to approach residential areas when attracted by prey, such as rodents. Practicing regular pest control can reduce the threat of snakes considerably. It is beneficial to know the species of snake that are common in home areas, while traveling, or hiking. Areas of the world such as Africa, Australia, India, and southern Asia are inhabited by many particularly dangerous snakes species. Being wary of snake presence and ultimately avoiding it when known is strongly recommended.
Sturdy over-the-ankle boots, loose clothing and responsible behavior offer effective protection from snakebites when in the wilderness. It is important to tread heavily and cause loud ground noises. The rationale behind this is that the snake will feel the vibrations and flee from the area. However, this generally only applies to North America as some larger and more aggressive snakes in other parts of the world, such as king cobras and black mambas, will actually protect their territory. When dealing with direct encounters it is best to remain silent and motionless. If the snake has not yet fled it is important to step away slowly and cautiously.
When doing camping activities such as gathering firewood at night, it is important to make use of a flashlight and avoid walking barefooted. Approximately 85% of the natural snakebites occur below the victims' knees. [9] Snakes may be unusually active during especially warm nights with ambient temperatures exceeding 70˚F., and a person not wearing footwear will have no protection from a potential bite.
It is advised not to reach blindly into hollow logs, flip over large rocks, and enter old cabins or other potential snake hiding-places. When rock climbing, it is not safe to grab ledges or crevices without thoroughly and extensively examining them first, as snakes are coldblooded creatures and often sunbathe atop rock ledges.
Pet owners of domestic animals and/or snakes should be wary that a snake is capable of causing injury and that is necessary to always act with caution — approximately 65%[vague] of snakebites occur to the victims’ hands or fingers. When handling snakes it is never wise to consume alcoholic beverages. In the United States more than 40% of snakebite victims intentionally put themselves in harms way by attempting to capture wild snakes or by carelessly handling their dangerous pets — 40% of that number had a blood alcohol level of 0.1 percent or more.[6]
It is also important to avoid snakes that appear to be dead, as some species will actually rollover on their backs and stick out their tongue to fool potential threats. A snake's detached head can immediately reflex and potentially bite. The bite can induce just as bad an effect as a live snake bite.[7] Dead snakes are also incapable of regulating the venom they inject, so a bite from a dead snake can often contain large amounts of venom.
Poison and toxic signs
Anticholinergic poisoning is given physostigmine sulfate as the antidote.
Anticholinesterase poisoning is given atropine sulfate and pralidoxime chloride 2-PAM as the antidote.
Benzodiazepine poisoning is given flumazenil as the antidote.
Beta blocker poisoning is given glucagon as the antidote.
Carbon monoxide poisoning is given oxygen as the antidote.
Cyanide poisoning is given amyl nitrite, sodium nitrite, and thiosulfate as the antidote.
Digoxin poisoning is given Fragment antigen binding(Fab) fragments that bind to digoxin (trade names Digibind and Digifab) as the antidote.
Ethylene glycol poisoning is given ethanol or fomepizole as the antidote.
Extrapyramidal reactions associated with antipsychotic poisoning is given diphenhydramine hydrochloride and benztropine mesylate as the antidote.
Heavy metal poisoning is given chelators, calcium disodium edetate (EDTA), dimercaprol (BAL), penicillamine, and 2,3-dimercaptosuccinic acid (DMSA, succimer) as the antidote.
Heparin poisoning is given protamine sulfate as the antidote.
Iron poisoning is given deferoxamine mesylate as the antidote.
Isoniazid poisoning is given pyridoxine as the antidote.
Methanol poisoning is given ethanol or fomepizole as the antidote.
Methemoglobinemia poisoning is given methylene blue as the antidote.
Opioid poisoning is given naloxone hydrochloride as the antidote.
Paracetamol (acetaminophen) poisoning is given N-acetylcysteine as the antidote.
Thallium poisoning is given Prussian blue as the antidote.
Warfarin poisoning is given vitamin K phytonadione and fresh frozen plasma as the antidote.
Antidote
An antidote is a substance which can counteract a form of poisoning.
Sometimes, the antidote for a particular toxin is manufactured by injecting the toxin into an animal in small doses and the resulting antibodies are extracted from the animals' blood. The venom produced by some snakes, spiders, and other venomous animals is often treatable by the use of these antivenoms, although a number do lack one, and a bite or sting from such an animal often results in death. Some animal venoms, especially those produced by arthropods (e.g. certain spiders, scorpions, bees, etc.) are only potentially lethal when they provoke allergic reactions and induce anaphylactic shock; as such, there is no "antidote" for these venoms because it is not a form of poisoning, though anaphylactic shock can be treated (e.g., by the use of epinephrine).
Some other toxins have no known antidote. For example, the poison ricin, which is produced from the waste byproduct of castor oil manufacture, has no antidote, and as a result is often fatal if it enters the human body in sufficient quantities.
Ingested poisons are frequently treated by the oral administration of activated charcoal, which absorbs the poison, and then it is flushed from the digestive tract, removing a large part of the toxin.
Poisons which are injected into the body (such as those from bites or stings from venomous animals) are usually treated by the use of a constriction band which limits the flow of lymph and/or blood to the area, thus slowing circulation of the poison around the body.
Sometimes, the antidote for a particular toxin is manufactured by injecting the toxin into an animal in small doses and the resulting antibodies are extracted from the animals' blood. The venom produced by some snakes, spiders, and other venomous animals is often treatable by the use of these antivenoms, although a number do lack one, and a bite or sting from such an animal often results in death. Some animal venoms, especially those produced by arthropods (e.g. certain spiders, scorpions, bees, etc.) are only potentially lethal when they provoke allergic reactions and induce anaphylactic shock; as such, there is no "antidote" for these venoms because it is not a form of poisoning, though anaphylactic shock can be treated (e.g., by the use of epinephrine).
Some other toxins have no known antidote. For example, the poison ricin, which is produced from the waste byproduct of castor oil manufacture, has no antidote, and as a result is often fatal if it enters the human body in sufficient quantities.
Ingested poisons are frequently treated by the oral administration of activated charcoal, which absorbs the poison, and then it is flushed from the digestive tract, removing a large part of the toxin.
Poisons which are injected into the body (such as those from bites or stings from venomous animals) are usually treated by the use of a constriction band which limits the flow of lymph and/or blood to the area, thus slowing circulation of the poison around the body.
History : Middle ages
Europe
Later, in Europe during the Middle Ages, when the nature of poisons were known better than simply magic and witchcraft, there were sellers and suppliers of potions and poisons, known as apothecaries.[21] Despite the fact that the medicinal uses of poisons were now known, it was no secret that people bought poisons for less useful and lawful reasons. The alchemists who worked in these apothecaries suffered a considerable risk to their health, working so invariably close to poisonous substances. [22]
At the same time, in other areas of the world, the technological advancement of poisons was expanding, and, in the Arab nations, some had succeeded in making arsenic transparent, odourless and tasteless when applied to a drink, a method which would allow poison murderers to remain undetected for at least one millennia.[23]
An excerpt from Chaucer's The Canterbury Tales, a text that existed sometime in the 14th century to the 15th century describes a killer buying poison from an apothecary to rid a rat infestation:
And forth he goes – no longer he would tarry –Into the town unto a ‘pothecaryAnd prayed him that he woulde sellSome poison, that he might his rattes quell…The ‘pothecary answered: "And thou shalt haveA thing that, all so God my soule save,In all this world there is no creatureThat ate or drunk has of this confitureNot but the montance of a corn of wheatThat he ne shall his life anon forlete.Yea, starve (die) he shall, and that in lesse whileThan thou wilt go a pace but not a mileThe poison is so strong and violent—Canterbury Tales - The Pardoner's Tale. Lines 565-581.
This is one example of a large literature related to poison, and poisons and potions were a very popular subject in fiction. There were also academic texts discussing the subject, and both non-fiction and fiction were written for the most part by monks, whose knowledge and wisdom were respected, and as such authored a large portion of published works.[21]
One example of a non-fiction work is The Book of Venoms, a book describing the known poisons of the time, their effects and uses, written by Magister Santes de Ardoynis in 1424. It also recommended the best known treatments for a given poison. Despite this, it is considered probable that these factual works were not released to the public, but kept within appropriate learned circles for study and research.[21]
The troubled 14th and 15th centuries in Rajasthan, India saw invasions in the Rajput heartlands. Rajput women practiced a custom of jauhar ( literally the taking of life) when their sons, brothers, or husbands faced certain death in battle. Jauhar was practiced within the Kshatriya warrior class to avoid the fate of subservience, slavery, rape, or slaughter at the hands of the invading forces.[24]
[edit] Public reaction
If the truth was indeed kept from the public, it did not prevent the spawning of folklore and rumors about poisons, and use of them for purposes that were distasteful to the public. This caused a level of paranoia within some areas of the societies of England and Europe.[21] This wave of concern was furthered by the availability of 'medicine' potent enough to be lethal when secretly administered in sufficient quantity - it provided an easy way to kill, and one which was subtle, quiet, and generally allowed the criminal to remain undetected.[21] Perhaps it was this wave of paranoia that swept the streets, or the public need for answers about these toxins, but books about ways of counteracting poisons became sought for, and fed off the mounting anxiety, even though generally being wholly inaccurate.[21]
Naturally, crafty book salesmen would have sought to inflame the issue as a marketing ploy, and exaggerate the risk so that people would buy their books in search of a non-existent security. Other salesmen such as jewelry traders offering a supposedly poison-weakening amulet, or a doctor selling a magical cure would have profited greatly in such times of doubt. The information the public craved was kept from them, a treasure only for scholars and scientists, and so the public was left to make their own assumptions.[21]
[edit] Persia
Despite the negative effects of poison, which were so evident in these times, cures were being found in poison, even at such a time where it was hated by the most of the general public. An example can be found in the works of Iranian born Persian physician, philosopher, and scholar Rhazes, writer of Secret of Secrets, which was a long list of chemical compounds, minerals and appratus, the first man to distil alcohol and use it as an anti-septic, and the person who suggested mercury be used as a laxative. He made discoveries relating to a mercury chloride called corrosive sublimate. An ointment derived from this sublimate was used to cure what Rhazes described as 'the itch', which is now referred to as scabies. This proved an effective treatment because of mercury's poisonous nature and ability to penetrate the skin, allowing it to eliminate the disease and the itch. [25]
Later, in Europe during the Middle Ages, when the nature of poisons were known better than simply magic and witchcraft, there were sellers and suppliers of potions and poisons, known as apothecaries.[21] Despite the fact that the medicinal uses of poisons were now known, it was no secret that people bought poisons for less useful and lawful reasons. The alchemists who worked in these apothecaries suffered a considerable risk to their health, working so invariably close to poisonous substances. [22]
At the same time, in other areas of the world, the technological advancement of poisons was expanding, and, in the Arab nations, some had succeeded in making arsenic transparent, odourless and tasteless when applied to a drink, a method which would allow poison murderers to remain undetected for at least one millennia.[23]
An excerpt from Chaucer's The Canterbury Tales, a text that existed sometime in the 14th century to the 15th century describes a killer buying poison from an apothecary to rid a rat infestation:
And forth he goes – no longer he would tarry –Into the town unto a ‘pothecaryAnd prayed him that he woulde sellSome poison, that he might his rattes quell…The ‘pothecary answered: "And thou shalt haveA thing that, all so God my soule save,In all this world there is no creatureThat ate or drunk has of this confitureNot but the montance of a corn of wheatThat he ne shall his life anon forlete.Yea, starve (die) he shall, and that in lesse whileThan thou wilt go a pace but not a mileThe poison is so strong and violent—Canterbury Tales - The Pardoner's Tale. Lines 565-581.
This is one example of a large literature related to poison, and poisons and potions were a very popular subject in fiction. There were also academic texts discussing the subject, and both non-fiction and fiction were written for the most part by monks, whose knowledge and wisdom were respected, and as such authored a large portion of published works.[21]
One example of a non-fiction work is The Book of Venoms, a book describing the known poisons of the time, their effects and uses, written by Magister Santes de Ardoynis in 1424. It also recommended the best known treatments for a given poison. Despite this, it is considered probable that these factual works were not released to the public, but kept within appropriate learned circles for study and research.[21]
The troubled 14th and 15th centuries in Rajasthan, India saw invasions in the Rajput heartlands. Rajput women practiced a custom of jauhar ( literally the taking of life) when their sons, brothers, or husbands faced certain death in battle. Jauhar was practiced within the Kshatriya warrior class to avoid the fate of subservience, slavery, rape, or slaughter at the hands of the invading forces.[24]
[edit] Public reaction
If the truth was indeed kept from the public, it did not prevent the spawning of folklore and rumors about poisons, and use of them for purposes that were distasteful to the public. This caused a level of paranoia within some areas of the societies of England and Europe.[21] This wave of concern was furthered by the availability of 'medicine' potent enough to be lethal when secretly administered in sufficient quantity - it provided an easy way to kill, and one which was subtle, quiet, and generally allowed the criminal to remain undetected.[21] Perhaps it was this wave of paranoia that swept the streets, or the public need for answers about these toxins, but books about ways of counteracting poisons became sought for, and fed off the mounting anxiety, even though generally being wholly inaccurate.[21]
Naturally, crafty book salesmen would have sought to inflame the issue as a marketing ploy, and exaggerate the risk so that people would buy their books in search of a non-existent security. Other salesmen such as jewelry traders offering a supposedly poison-weakening amulet, or a doctor selling a magical cure would have profited greatly in such times of doubt. The information the public craved was kept from them, a treasure only for scholars and scientists, and so the public was left to make their own assumptions.[21]
[edit] Persia
Despite the negative effects of poison, which were so evident in these times, cures were being found in poison, even at such a time where it was hated by the most of the general public. An example can be found in the works of Iranian born Persian physician, philosopher, and scholar Rhazes, writer of Secret of Secrets, which was a long list of chemical compounds, minerals and appratus, the first man to distil alcohol and use it as an anti-septic, and the person who suggested mercury be used as a laxative. He made discoveries relating to a mercury chloride called corrosive sublimate. An ointment derived from this sublimate was used to cure what Rhazes described as 'the itch', which is now referred to as scabies. This proved an effective treatment because of mercury's poisonous nature and ability to penetrate the skin, allowing it to eliminate the disease and the itch. [25]
History : Ancient times and Dark Ages
Archaeological findings provide proof that, while primitive mankind used conventional weapons such as axes and clubs, and later swords, they probably sought more subtle, destructive means of causing death—something that could be achieved through poison.[2] Grooves for storing or holding poisons such as tubocurarine have been found in their hunting weapons and tools, showing that early humans had discovered poisons of varying potency and been applying them to their weapons.[2] Some speculate that this use and existence of these strange and noxious substances would have been kept within the more important and higher-ranked members of a tribe or clan, and were seen as emblems of a greater power. This may have also given birth to the stereotypical 'medicine man' or 'witch doctor'.[2]
The discovery of poisons had both advantages and disadvantages in probably every civilisation in which it was discovered. The use of poisons for homicide and assassination also caused the need for antidotes for these poisons, and soon after the potential of the poison was realised, the search for ways to detract from or reverse its power began.
Once the use and danger of poison was realized, it became apparent that something had to be done. Mithridates, King of Pontos (ancient Greece, now modern Turkey) from around 114-63 BC, lived in constant fear of being assassinated by the use of poison, and so became a hard-working pioneer in the search for a cure for poisons.[2] In his position of power, he was able to test poisons on criminals facing execution, and then to test if there was a possible antidote. So paranoid was he that he administered daily amounts of poisons in an attempt to make himself immune to as many poisons as he could.[2]
Eventually, he discovered a formula that combined small portions of dozens of the best-known herbal remedies of the time, which he named 'Mithridatium'.[2] This was kept totally secret until the invasion of Pompey, who was able to take it back to Rome. Pliny the Younger describes over 7000 different poisons. One he describes as:
“
The blood of a duck found in a certain district of Pontus, which was supposed to live on poisonous food, and the blood of this duck was afterwards used in the preparation of the Mithridatum, because it fed on poisonous plants and suffered no harm.[2]
”
After being defeated by Pompey, Mithridates' antidote prescriptions and notes of medicinal plants were taken by the Romans and translated into Latin.[3]
Indian surgeon Sushruta defined the stages of slow poisoning and the remedies of slow poisoning. He also mentions antidotes and the use of traditional substances to counter the effects of poisoning.[4]
[edit] In ancient mythology
References to poison or poison-like substances are present in the mythological canon of many ancient civilizations and up to the almost-universal 'death' of mythological beliefs.
Some of the first mythological depictions of the use of poisons come from translations of ancient, Mesopotamian Sumerian texts, in which a being named 'Gula' is mentioned as 'the mistress of spells and witchcraft'. These texts have been dated to c. 4500 BC;[2] a translated piece of text follows:
“
Gula, the woman, the mighty one, the prince of all womenHis seed with a poison not curableWithout issue; in his body may she placeAll the days of his life,Blood and pus like water may he pour forth.[5]
”
The Rigveda mentions visha, which is Sanskrit for poison.[6] References are also made in hymns to poison liquids that produce ecstasy.[7]
In the Puranic legend mention of poison is made during the mythological process of churning the cosmic ocean, before the drink of immortality is won, and thus it symbolizes the unavoidable phenomenon of death within the samsara realm of Maya.[8]
In Hindu mythology, only Shiva is capable of drinking poison without harm and he is the popular Hindu symbol of spiritual progress through Yoga.[8]
In Greek mythology, Medea attempted to poison Theseus with a cup of wine poisoned with wolfsbane. However, his father Aegeus interceded when he discerned his identity, knocking the cup out of his hand and sending Medea away.[9]
[edit] India
Some economic concepts and ideas find mention in the Buddhist literature during the 6th and 5th centuries BC. Among these the economic enterprise and price and taxation are the main issues discussed in this literature. Some specific economic activities such as the sale of meat, living creatures, poison, arms and armaments were forbidden.[10]
Poisoned weapons were used in ancient India.[11] Tactics related to war in ancient India have references to poison. A verse in Sanskrit is given below:
Jalam visravayet sarmavamavisravyam ca dusayet.
Waters of wells were to be mixed with poison and thus polluted.[11]
Chānakya (c. 350-283 BC), also known as Kautilya, was adviser and prime minister[12] to the first Maurya Emperor Chandragupta (c. 340-293 BC). Kautilya suggests employing means such as seduction, secret use of weapons, poison, etc.[13] Kautilya urged detailed precautions against assassination - tasters for food, elaborate ways to detect poison.[14] Death penalty for violations of royal decrees was frequently administered through the use of poison.[15]
An example of a flint sword and spear, weapons used for hunting in ancient times.
[edit] Egypt
Unlike many civilizations, records of Egyptian knowledge and use of poisons can only be dated back to approx. 300 BCE. However, it is believed that the earliest known Egyptian pharaoh, Menes, studied the properties of poisonous plants and venoms, according to early records.[2]
Before this, however, evidence of poison-related knowledge in Egypt can be traced to the writings of an ancient Egyptian alchemist, Agathodiamon (100BC approx.), who spoke of an (unidentified) mineral that when mixed with natron produced a 'fiery poison'. He described this poison as 'disappearing in water', giving a clear solution. This 'fiery poison' may exist as the roots for some of the later poisons that were invisible when mixed with water, and indicates that such an elusive poison may have been available to some civilisations such as Egypt as early as 100 BC.[16] As to the 'fiery poison' which this alchemist had concocted, it appears that he must surely have created arsenic trioxide, the unidentified mineral having to have been either realgar or orpiment, due to the relation between the unidentified mineral and his other writings. [16]
The Egyptians are also thought to have come into knowledge about elements such as antimony, copper, crude arsenic, lead, opium, and mandrake (among others). Other such secrets were revealed in papyri. Egyptians are now thought to be the first to properly master distillation, and to manipulate the poison that can be retrieved from peach kernels.[2]
Finally, Cleopatra is said to have poisoned herself with an asp after hearing of Marc Antony's demise. Prior to her death, she was said to have sent many of her maidservants to act as guinea pigs to test different poisons, including belladonna, henbane, and the strychnine tree's seed.[17]
[edit] Rome
A bust of the Roman Emperor Nero, who used cyanide to dispose of unwanted family members
In Roman times, poisoning carried out at the dinner table or common eating or drinking area was not unheard of, or probably even uncommon, and was happening as early as 331 BC.[2] These poisonings would have been used for self-advantageous reasons in every class of the social order. The writer Livy describes the poisoning of members of the upper class and nobles of Rome, and Roman emperor Nero is known to have favored the use of poisons on his relatives, even hiring a personal poisoner. His preferred poison was, according to Livy, cyanide.[2]
His predecessor Claudius was allegedly poisoned with mushrooms or alternatively poison herbs.[18] However, accounts of the way Claudius died vary greatly. Halotus, his taster, Xenophon, his doctor, and the infamous poisoner Locusta have all been accused of possibly being the administrator of the fatal substance, but Agrippina, his final wife, is considered to be the most likely to have arranged his murder and may have even administered the poison herself. Some report that he died after prolonged suffering following a single dose at his evening meal, while some say that he recovered somewhat, only to be poisoned once more by a feather dipped in poison which was pushed down his throat under the pretence of helping him to vomit,[19] or by poisoned gruel or an enema.[18] Agrippina is considered to be the most likely have had Claudius murdered, because she was ambitious for her son, Nero, and Claudius had become suspicious of her intrigues.[20]
The discovery of poisons had both advantages and disadvantages in probably every civilisation in which it was discovered. The use of poisons for homicide and assassination also caused the need for antidotes for these poisons, and soon after the potential of the poison was realised, the search for ways to detract from or reverse its power began.
Once the use and danger of poison was realized, it became apparent that something had to be done. Mithridates, King of Pontos (ancient Greece, now modern Turkey) from around 114-63 BC, lived in constant fear of being assassinated by the use of poison, and so became a hard-working pioneer in the search for a cure for poisons.[2] In his position of power, he was able to test poisons on criminals facing execution, and then to test if there was a possible antidote. So paranoid was he that he administered daily amounts of poisons in an attempt to make himself immune to as many poisons as he could.[2]
Eventually, he discovered a formula that combined small portions of dozens of the best-known herbal remedies of the time, which he named 'Mithridatium'.[2] This was kept totally secret until the invasion of Pompey, who was able to take it back to Rome. Pliny the Younger describes over 7000 different poisons. One he describes as:
“
The blood of a duck found in a certain district of Pontus, which was supposed to live on poisonous food, and the blood of this duck was afterwards used in the preparation of the Mithridatum, because it fed on poisonous plants and suffered no harm.[2]
”
After being defeated by Pompey, Mithridates' antidote prescriptions and notes of medicinal plants were taken by the Romans and translated into Latin.[3]
Indian surgeon Sushruta defined the stages of slow poisoning and the remedies of slow poisoning. He also mentions antidotes and the use of traditional substances to counter the effects of poisoning.[4]
[edit] In ancient mythology
References to poison or poison-like substances are present in the mythological canon of many ancient civilizations and up to the almost-universal 'death' of mythological beliefs.
Some of the first mythological depictions of the use of poisons come from translations of ancient, Mesopotamian Sumerian texts, in which a being named 'Gula' is mentioned as 'the mistress of spells and witchcraft'. These texts have been dated to c. 4500 BC;[2] a translated piece of text follows:
“
Gula, the woman, the mighty one, the prince of all womenHis seed with a poison not curableWithout issue; in his body may she placeAll the days of his life,Blood and pus like water may he pour forth.[5]
”
The Rigveda mentions visha, which is Sanskrit for poison.[6] References are also made in hymns to poison liquids that produce ecstasy.[7]
In the Puranic legend mention of poison is made during the mythological process of churning the cosmic ocean, before the drink of immortality is won, and thus it symbolizes the unavoidable phenomenon of death within the samsara realm of Maya.[8]
In Hindu mythology, only Shiva is capable of drinking poison without harm and he is the popular Hindu symbol of spiritual progress through Yoga.[8]
In Greek mythology, Medea attempted to poison Theseus with a cup of wine poisoned with wolfsbane. However, his father Aegeus interceded when he discerned his identity, knocking the cup out of his hand and sending Medea away.[9]
[edit] India
Some economic concepts and ideas find mention in the Buddhist literature during the 6th and 5th centuries BC. Among these the economic enterprise and price and taxation are the main issues discussed in this literature. Some specific economic activities such as the sale of meat, living creatures, poison, arms and armaments were forbidden.[10]
Poisoned weapons were used in ancient India.[11] Tactics related to war in ancient India have references to poison. A verse in Sanskrit is given below:
Jalam visravayet sarmavamavisravyam ca dusayet.
Waters of wells were to be mixed with poison and thus polluted.[11]
Chānakya (c. 350-283 BC), also known as Kautilya, was adviser and prime minister[12] to the first Maurya Emperor Chandragupta (c. 340-293 BC). Kautilya suggests employing means such as seduction, secret use of weapons, poison, etc.[13] Kautilya urged detailed precautions against assassination - tasters for food, elaborate ways to detect poison.[14] Death penalty for violations of royal decrees was frequently administered through the use of poison.[15]
An example of a flint sword and spear, weapons used for hunting in ancient times.
[edit] Egypt
Unlike many civilizations, records of Egyptian knowledge and use of poisons can only be dated back to approx. 300 BCE. However, it is believed that the earliest known Egyptian pharaoh, Menes, studied the properties of poisonous plants and venoms, according to early records.[2]
Before this, however, evidence of poison-related knowledge in Egypt can be traced to the writings of an ancient Egyptian alchemist, Agathodiamon (100BC approx.), who spoke of an (unidentified) mineral that when mixed with natron produced a 'fiery poison'. He described this poison as 'disappearing in water', giving a clear solution. This 'fiery poison' may exist as the roots for some of the later poisons that were invisible when mixed with water, and indicates that such an elusive poison may have been available to some civilisations such as Egypt as early as 100 BC.[16] As to the 'fiery poison' which this alchemist had concocted, it appears that he must surely have created arsenic trioxide, the unidentified mineral having to have been either realgar or orpiment, due to the relation between the unidentified mineral and his other writings. [16]
The Egyptians are also thought to have come into knowledge about elements such as antimony, copper, crude arsenic, lead, opium, and mandrake (among others). Other such secrets were revealed in papyri. Egyptians are now thought to be the first to properly master distillation, and to manipulate the poison that can be retrieved from peach kernels.[2]
Finally, Cleopatra is said to have poisoned herself with an asp after hearing of Marc Antony's demise. Prior to her death, she was said to have sent many of her maidservants to act as guinea pigs to test different poisons, including belladonna, henbane, and the strychnine tree's seed.[17]
[edit] Rome
A bust of the Roman Emperor Nero, who used cyanide to dispose of unwanted family members
In Roman times, poisoning carried out at the dinner table or common eating or drinking area was not unheard of, or probably even uncommon, and was happening as early as 331 BC.[2] These poisonings would have been used for self-advantageous reasons in every class of the social order. The writer Livy describes the poisoning of members of the upper class and nobles of Rome, and Roman emperor Nero is known to have favored the use of poisons on his relatives, even hiring a personal poisoner. His preferred poison was, according to Livy, cyanide.[2]
His predecessor Claudius was allegedly poisoned with mushrooms or alternatively poison herbs.[18] However, accounts of the way Claudius died vary greatly. Halotus, his taster, Xenophon, his doctor, and the infamous poisoner Locusta have all been accused of possibly being the administrator of the fatal substance, but Agrippina, his final wife, is considered to be the most likely to have arranged his murder and may have even administered the poison herself. Some report that he died after prolonged suffering following a single dose at his evening meal, while some say that he recovered somewhat, only to be poisoned once more by a feather dipped in poison which was pushed down his throat under the pretence of helping him to vomit,[19] or by poisoned gruel or an enema.[18] Agrippina is considered to be the most likely have had Claudius murdered, because she was ambitious for her son, Nero, and Claudius had become suspicious of her intrigues.[20]
History of poison
The history of poisons stretches over a period from before 4500 BC to the present day. Poisons have been used for many purposes across the span of human existence as weapons, anti-venoms and medicines. Indeed, poison has allowed much progress in the branches of medicine, toxicology, and technology, among others.
The use of poison varies greatly. Historically, its employment in assassination and homicide incited fear in the public. Other times, it has been used for political implosion and elements of espionage.
In the present day, poison is still used for a variety of mostly mundane purposes involving agriculture and food preservation, but is also still used for the starker purposes of murder. Due to more modern-day technology, however, poisons can be more easily detected.
The use of poison varies greatly. Historically, its employment in assassination and homicide incited fear in the public. Other times, it has been used for political implosion and elements of espionage.
In the present day, poison is still used for a variety of mostly mundane purposes involving agriculture and food preservation, but is also still used for the starker purposes of murder. Due to more modern-day technology, however, poisons can be more easily detected.
Types of poisons
The majority of this section is sorted by ICD-10 code, which classifies poisons based upon the nature of the poison itself. However, it is also possible to classify poisons based upon the effect the poison has (for example, "Metabolic poisons" such as Antimycin, Malonate, and 2,4-Dinitrophenol act by adversely disrupting the normal metabolism of an organism.)
(T36-T50) Poisoning by drugs, medicaments and biological substances
(T36.) Poisoning by systemic antibiotics
(T37.) Poisoning by other systemic anti-infectives and antiparasitics
(T38.) Poisoning by hormones and their synthetic substitutes and antagonists, not elsewhere classified
(T39.) Poisoning by nonopiod analgesics, antipyretics and antirheumatics
(T40.) Poisoning by narcotics and psychodysleptics (hallucinogens)
(T41.) Poisoning by anaesthetics and therapeutic gases
(T42.) Poisoning by antiepileptic, sedative-hypnotic and antiparkinsonism drugs
(T43.) Poisoning by psychotropic drugs, not elsewhere classified
(T44.) Poisoning by drugs primarily affecting the autonomic nervous system Neurotoxins interfere with nervous system functions and often lead to near-instant paralysis followed by rapid death. They include most spider and snake venoms, as well as many modern chemical weapons. One class of toxins of interest to neurochemical researchers are the various cone snail toxins known as conotoxins.
Atropine
Poison hemlock
Anticholinesterases (T44.0)
Fasciculin
Nerve agents
Acetylcholine antagonists
Curare
Pancuronium
Cell membrane disrupters Others
Nicotine - not strictly a neurotoxin, but capable in large doses of causing heart attack
(T45.) Poisoning by primarily systemic and haematological agents, not elsewhere classified
Phytohaemagglutinin (Red kidney bean poisoning)
(T46.) Poisoning by agents primarily affecting the cardiovascular system
Digitoxin
Digoxin
Ouabain
(T47.) Poisoning by agents primarily affecting the gastrointestinal system
Solanine
Hyoscyamine
(T48.) Poisoning by agents primarily acting on smooth and skeletal muscles and the respiratory system
Strychnine
Aconite
(T49.) Poisoning by topical agents primarily affecting skin and mucous membrane and by ophthalmological, otorhinolaryngological and dental drugs
(T50.) Poisoning by diuretics and other unspecified drugs, medicaments and biological substances
(T51-T65) Toxic effects of substances chiefly nonmedicinal as to source
(T51.) Toxic effect of alcohol
(T51.0) Ethanol
(T51.1) Methanol
(T52.) Toxic effect of organic solvents
(T53.) Toxic effect of halogen derivatives of aliphatic and aromatic hydrocarbons
(T54.) Toxic effect of corrosive substances Corrosives mechanically damage biological systems on contact. Both the sensation and injury caused by contact with a corrosive resembles a burn injury.
Acids and bases, corrosives
Various light metal oxides, hydroxides, superoxides
Bleach, some pool chemicals, other hypochlorates (acidic and oxydizing effect)
Hydrofluoric acid
Acids (T54.2) Strong inorganic acids, such as concentrated sulfuric acid, nitric acid or hydrochloric acid, destroy any biological tissue with which they come in contact within seconds.
Bases (T54.3) Strong inorganic bases, such as lye, gradually dissolve skin on contact but can cause serious damage to eyes or mucous membranes much more rapidly. Ammonia is a far weaker base than lye, but has the distinction of being a gas and thus may more easily come into contact with the sensitive mucous membranes of the respiratory system. Quicklime, which has household uses, is a particularly common cause of poisoning. Some of the light metals, if handled carelessly, can not only cause thermal burns, but also produce very strongly basic solutions in sweat.
(T55.) Toxic effect of soaps and detergents
(T56.) Toxic effect of metals A common trait shared by toxic metals is the chronic nature of their toxicity (a notable exception would be bismuth, which is considered entirely non-toxic). Low levels of toxic metal salts ingested over time accumulate in the body until toxic levels are reached. Toxic metals are often inaccurately referred to as "heavy metals", although not all heavy metals are necessarily harmful and not all toxic metals are heavy metals.
Toxic metals are generally far more toxic when ingested in the form of soluble salts than in elemental form. For example, metallic mercury passes through the human digestive tract without interaction and is commonly used in dental fillings—even though mercury salts and inhaled mercury vapor are highly toxic.
Examples:
(T56.0) Lead poisoning
(T56.1) Mercury
(T56.2) Chromium
(T56.3) Cadmium
(T56.7) Beryllium (a highly but subtly toxic light metal)
Antimony
Barium
Thallium
Uranium
(T57.) Toxic effect of other inorganic substances
(T57.0) Arsenic (see arsenic poisoning)
Arsenic compounds
Arsenic trioxide
Fowler's solution
Reducing agents
(T57.1) The most notable substance in this class is phosphorus.
(T58.) Toxic effect of carbon monoxide
(T58) By far the most notable metabolic poison is carbon monoxide, which blocks the ability of red blood cells to transport oxygen.
(T59.) Toxic effect of other gases, fumes and vapours
Formaldehyde (T59.2)
Phosgene
Phosphine
Hydrogen sulfide
Oxidizers Poisons of this class are generally not very harmful to higher life forms such as humans (for whom the outer layer of cells are more or less disposable), but lethal to microorganisms such as bacteria. Typical examples are ozone and chlorine (T59.4), either of which is added to nearly every municipal water supply in order to kill any harmful microorganisms present.
All halogens are strong oxidizing agents, fluorine (T59.5) being the strongest of all.
See also: Free radical
(T60.) Toxic effect of pesticides
Pesticide poisoning
Fluoroacetate is a metabolic poison that blocks a vital step in the citric acid cycle.
Rotenone is a metabolic poison that disrupts electron transport in cellular respiration.
(T61.) Toxic effect of noxious substances eaten as seafood
Ciguatera poisoning
Scombroid poisoning
Shellfish toxins (PSP, DSP, NSP, ASP )
Domoic acid (or Amnesic shellfish poisoning, ASP)
Tetrodotoxin
(T62.) Toxic effect of other noxious substances eaten as food
Food poisoning
Botulin toxin
Hemlock water dropwort
Grayanotoxin (Honey intoxication)
Tetanospasmin (Tetanos Toxin)
(T63.) Toxic effect of venomous animals
Snake and spider venoms
(T64.) Toxic effect of aflatoxin and other mycotoxin food contaminants
Fungal toxins
Amanita toxin, see Amanita phalloides
Muscarine
Aflatoxins
(T65.) Toxic effect of other and unspecified substances
(T65.0) Cyanide is a metabolic poison that bonds with an enzyme involved in ATP production.
Antidotes
Some poisons have specific antidotes:
Poison/DrugAntidote
paracetamol (acetaminophen) / N-acetylcysteine
vitamin K anticoagulants, e.g. warfarin / vitamin K
opioids / naloxone
iron (and other heavy metals) / desferrioxamine, Deferasirox or Deferiprone
benzodiazepines / flumazenil
ethylene glycol / ethanol, fomepizole or Thiamine
methanol / ethanol or fomepizole
cyanide / amyl nitrite, sodium nitrite & sodium thiosulfate
Organophosphates / Atropine & Pralidoxime
Magnesium / Calcium Gluconate
Calcium Channel Blockers (Verapamil, Diltiazem) / Calcium Gluconate
Beta-Blockers (Propranolol, Sotalol) / Calcium Gluconate and/or Glucagon
Isoniazid / Pyridoxine
Enhanced excretion
In some situations elimination of the poison can be enhanced using diuresis, hemodialysis, hemoperfusion, peritoneal dialysis, or exchange transfusion.
Further treatment
In the majority of poisonings the mainstay of management is providing supportive care for the patient, i.e. treating the symptoms rather than the poison.
Poison/DrugAntidote
paracetamol (acetaminophen) / N-acetylcysteine
vitamin K anticoagulants, e.g. warfarin / vitamin K
opioids / naloxone
iron (and other heavy metals) / desferrioxamine, Deferasirox or Deferiprone
benzodiazepines / flumazenil
ethylene glycol / ethanol, fomepizole or Thiamine
methanol / ethanol or fomepizole
cyanide / amyl nitrite, sodium nitrite & sodium thiosulfate
Organophosphates / Atropine & Pralidoxime
Magnesium / Calcium Gluconate
Calcium Channel Blockers (Verapamil, Diltiazem) / Calcium Gluconate
Beta-Blockers (Propranolol, Sotalol) / Calcium Gluconate and/or Glucagon
Isoniazid / Pyridoxine
Enhanced excretion
In some situations elimination of the poison can be enhanced using diuresis, hemodialysis, hemoperfusion, peritoneal dialysis, or exchange transfusion.
Further treatment
In the majority of poisonings the mainstay of management is providing supportive care for the patient, i.e. treating the symptoms rather than the poison.
Poisoning management
Poison Control Centers (In the US reachable at 1-800-222-1222 at all hours) provide immediate, free, and expert treatment advice and assistance over the telephone in case of suspected exposure to poisons or toxic substances.
Initial medical management
Initial management for all poisonings includes ensuring adequate cardiopulmonary function and providing treatment for any symptoms such as seizures, shock, and pain.
Decontamination
Emesis (i.e. induced by ipecac) is no longer recommended in poisoning situations.
Biological poisoning
Acute poisoning is exposure to a poison on one occasion or during a short period of time. Symptoms develop in close relation to the exposure. Absorption of a poison is necessary for systemic poisoning. In contrast, substances that destroy tissue but do not absorb, such as lye, are classified as corrosives rather than poisons.
Chronic poisoning is long-term repeated or continuous exposure to a poison where symptoms do not occur immediately or after each exposure. The patient gradually becomes ill, or becomes ill after a long latent period. Chronic poisoning most commonly occurs following exposure to poisons that bioaccumulate such as mercury and lead.
Contact or absorption of poisons can cause rapid death or impairment. Agents that act on the nervous system can paralyze in seconds or less, and include both biologically derived neurotoxins and so-called nerve gases, which may be synthesized for warfare or industry.
Inhaled or ingested cyanide as used as method of execution on US gas chambers almost instantly starves the body of energy by inhibiting the enzymes in mitochondria that make ATP. Intravenous injection of an unnaturally high concentration of potassium chloride, such as in the execution of prisoners in parts of the United States, quickly stops the heart by eliminating the cell potential necessary for muscle contraction.
Most (but not all) biocides, including pesticides, are created to act as poisons to target organisms, although acute or less observable chronic poisoning can also occur in non-target organism, including the humans who apply the biocides and other beneficial organisms. For example, the herbicide 2,4-D imitates the action of a plant hormone, to the effect that the lethal toxicity is specific to plants. Indeed, 2,4-D is not a poison, but classified as "harmful" (EU).
Many substances regarded as poisons are toxic only indirectly, by toxication. An example is "wood alcohol" or methanol, which is not poisonous itself, but is chemically converted to toxic formaldehyde and formic acid in the liver. Many drug molecules are made toxic in the liver, and the genetic variability of certain liver enzymes makes the toxicity of many compounds differ between individuals.
The study of the symptoms, mechanisms, treatment and diagnosis of biological poisoning is known as toxicology.
Exposure to radioactive substances can produce radiation poisoning, an unrelated phenomenon
Chronic poisoning is long-term repeated or continuous exposure to a poison where symptoms do not occur immediately or after each exposure. The patient gradually becomes ill, or becomes ill after a long latent period. Chronic poisoning most commonly occurs following exposure to poisons that bioaccumulate such as mercury and lead.
Contact or absorption of poisons can cause rapid death or impairment. Agents that act on the nervous system can paralyze in seconds or less, and include both biologically derived neurotoxins and so-called nerve gases, which may be synthesized for warfare or industry.
Inhaled or ingested cyanide as used as method of execution on US gas chambers almost instantly starves the body of energy by inhibiting the enzymes in mitochondria that make ATP. Intravenous injection of an unnaturally high concentration of potassium chloride, such as in the execution of prisoners in parts of the United States, quickly stops the heart by eliminating the cell potential necessary for muscle contraction.
Most (but not all) biocides, including pesticides, are created to act as poisons to target organisms, although acute or less observable chronic poisoning can also occur in non-target organism, including the humans who apply the biocides and other beneficial organisms. For example, the herbicide 2,4-D imitates the action of a plant hormone, to the effect that the lethal toxicity is specific to plants. Indeed, 2,4-D is not a poison, but classified as "harmful" (EU).
Many substances regarded as poisons are toxic only indirectly, by toxication. An example is "wood alcohol" or methanol, which is not poisonous itself, but is chemically converted to toxic formaldehyde and formic acid in the liver. Many drug molecules are made toxic in the liver, and the genetic variability of certain liver enzymes makes the toxicity of many compounds differ between individuals.
The study of the symptoms, mechanisms, treatment and diagnosis of biological poisoning is known as toxicology.
Exposure to radioactive substances can produce radiation poisoning, an unrelated phenomenon
Uses of poison
Poisons are usually not used for their toxicity, but may be used for their other properties. The property of toxicity itself has limited applications: mainly for controlling pests and weeds, and for preserving building materials and food stuffs. Where possible, specific agents which are less poisonous to humans have come to be preferred, but exceptions such as phosphine continue in use.
Throughout human history, intentional application of poison has been used as a method of assassination, murder, suicide and execution. As a method of execution, poison has been ingested, as the ancient Athenians did (see Socrates), inhaled, as with carbon monoxide or hydrogen cyanide (see gas chamber), or injected (see lethal injection). Many languages describe lethal injection with their corresponding words for "poison shot". Poison was also employed in gunpowder warfare. For example, the 14th century Chinese text of the Huo Long Jing written by Jiao Yu outlined the use of a poisonous gunpowder mixture to fill cast iron grenade bombs.
Poisonous materials are often used for their chemical or physical properties other than being poisonous. The most effective, easiest, safest, or cheapest option for use in a chemical synthesis may be a poisonous material. Particularly in experimental laboratory syntheses a specific reactivity is used, despite the toxicity of the reagent. Chromic acid is an example of such a "simple to use" reagent. Many technical applications call for some specific physical properties; a toxic substance may possess these properties and therefore be superior. Reactivity, in particular, is important. Hydrogen fluoride, for example, is poisonous and extremely corrosive. However, it has a high affinity for silicon, which is exploited by using HF to etch glass or to manufacture silicon semiconductor chips.
Throughout human history, intentional application of poison has been used as a method of assassination, murder, suicide and execution. As a method of execution, poison has been ingested, as the ancient Athenians did (see Socrates), inhaled, as with carbon monoxide or hydrogen cyanide (see gas chamber), or injected (see lethal injection). Many languages describe lethal injection with their corresponding words for "poison shot". Poison was also employed in gunpowder warfare. For example, the 14th century Chinese text of the Huo Long Jing written by Jiao Yu outlined the use of a poisonous gunpowder mixture to fill cast iron grenade bombs.
Poisonous materials are often used for their chemical or physical properties other than being poisonous. The most effective, easiest, safest, or cheapest option for use in a chemical synthesis may be a poisonous material. Particularly in experimental laboratory syntheses a specific reactivity is used, despite the toxicity of the reagent. Chromic acid is an example of such a "simple to use" reagent. Many technical applications call for some specific physical properties; a toxic substance may possess these properties and therefore be superior. Reactivity, in particular, is important. Hydrogen fluoride, for example, is poisonous and extremely corrosive. However, it has a high affinity for silicon, which is exploited by using HF to etch glass or to manufacture silicon semiconductor chips.
Terminology
Some poisons are also toxins, usually referring to naturally produced substances, such as the bacterial proteins that cause tetanus and botulism. A distinction between the two terms is not always observed, even among scientists.
Animal toxins that are delivered subcutaneously (e.g. by sting or bite) are also called venom. In normal usage, a poisonous organism is one that is harmful to consume, but a venomous organism uses poison to defend itself while still alive. A single organism can be both venomous and poisonous.
The derivative forms "toxic" and "poisonous" are synonymous.
Within chemistry and physics, a poison is a substance that obstructs or inhibits a reaction, for example by binding to a catalyst. For example, see nuclear poison.
The phrase "poison" is often used colloquially to describe any harmful substance, particularly corrosive substances, carcinogens, mutagens, teratogens and harmful pollutants, and to exaggerate the dangers of chemicals. The legal definition of "poison" is stricter.
Animal toxins that are delivered subcutaneously (e.g. by sting or bite) are also called venom. In normal usage, a poisonous organism is one that is harmful to consume, but a venomous organism uses poison to defend itself while still alive. A single organism can be both venomous and poisonous.
The derivative forms "toxic" and "poisonous" are synonymous.
Within chemistry and physics, a poison is a substance that obstructs or inhibits a reaction, for example by binding to a catalyst. For example, see nuclear poison.
The phrase "poison" is often used colloquially to describe any harmful substance, particularly corrosive substances, carcinogens, mutagens, teratogens and harmful pollutants, and to exaggerate the dangers of chemicals. The legal definition of "poison" is stricter.
Begin poison
In the context of biology, poisons are substances that can cause damage, illness, or death to organisms, usually by chemical reaction or other activity on the molecular scale, when a sufficient quantity is absorbed by an organism. Paracelsus, the father of toxicology, once wrote: "Everything is poison, there is poison in everything. Only the dose makes a thing not a poison."
In medicine (particularly veterinary) and in zoology, a poison is often distinguished from a toxin and a venom. Toxins are poisons produced via some biological function in nature, and venoms are usually defined as biologic toxins that are injected by a bite or sting to cause their effect, while other poisons are generally defined as substances which are absorbed through epithelial linings such as the skin or gut.
In medicine (particularly veterinary) and in zoology, a poison is often distinguished from a toxin and a venom. Toxins are poisons produced via some biological function in nature, and venoms are usually defined as biologic toxins that are injected by a bite or sting to cause their effect, while other poisons are generally defined as substances which are absorbed through epithelial linings such as the skin or gut.
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