Instruct: Given a question, retrieve relevant documents that answer the question.
Query: How many people get organophosphate poisoning each year in the US?
OPs are one of the most common causes of poisoning worldwide.[2] There are nearly 3 million poisonings per year resulting in two hundred thousand deaths.[2][3] Around 15% of people who are poisoned die as a result.[2] Organophosphate poisoning has been reported at least since 1962.[7]
To treat the ethion-exposure itself is done in the same way as exposure with other organophosphates. The main danger lies in respiratory problems, if symptoms are present then artificial respiration with an endotracheal tube is used as a treatment. The effect of ethion on muscles or nerves is counteracted with Atropine. Pralidoxime can be used to act against organophosphate poisoning, this must be given as fast as possible after the ethion poisoning for its efficacy is inhibited by the chemical change of ethion-enzyme in the body that occurs over time.
Acute poisoning is probably most common in agricultural areas in Asia, where many small farmers are affected. Poisoning may be due to occupational or accidental exposure or intentional self-harm. Precise numbers of chlorpyrifos poisonings globally are not available. Pesticides are used in an estimated 200,000+ suicides annually with tens of thousands due to chlorpyrifos. Organophosphates are thought to constitute two thirds of ingested pesticides in rural Asia. Chlorpyrifos is among the commonly used pesticides used for self-harm.
Neuromuscular junction diseases in this category include snake venom poisoning, botulism, arthropod poisoning, organophosphates and hypermagnesemia.(reference 13) Organophosphates are present in many insecticides and herbicides. They are also the basis of many nerve gases.(reference 27) Hypermagnesmia is a condition where the balance of magnesium in the body is unstable and concentrations are higher than normal baseline values.(reference 28)
Many "organophosphates" are potent nerve agents, functioning by inhibiting the action of acetylcholinesterase (AChE) in nerve cells. They are one of the most common causes of poisoning worldwide, and are frequently intentionally used in suicides in agricultural areas. Organophosphosphate pesticides can be absorbed by all routes, including inhalation, ingestion, and dermal absorption. Their inhibitory effects on the acetylcholinesterase enzyme lead to a pathological excess of acetylcholine in the body. Their toxicity is not limited to the acute phase, however, and chronic effects have long been noted. Neurotransmitters such as acetylcholine (which is affected by organophosphate pesticides) are profoundly important in the brain's development, and many organophosphates have neurotoxic effects on developing organisms, even from low levels of exposure. Other organophosphates are not toxic, yet their main metabolites, such as their oxons, are. Treatment includes both a pralidoxime binder and an anticholinergic such as atropine.
The effects of organophosphate poisoning on muscarinic receptors are recalled using the mnemonic SLUDGEM (salivation, lacrimation, urination, defecation, gastrointestinal motility, emesis, miosis)[10] An additional mnemonic is MUDDLES: miosis, urination, diarrhea, diaphoresis, lacrimation, excitation, and salivation.[11]
Sulfotep causes an organophosphate poisoning. This means that it had an effect on the activity of cholinesterase. There are differences for the indications of a sulfotep poisoning between inhalation, ingestion, intake by the skin and intake by the eyes. However, examples of poisoned greenhouse workers teach us an overall route of symptoms for a sulfotepp poisoning. Within the first hour after a poisonous intake of sulfotep people often suffer from nausea or headaches. After some hours diarrhea and vomiting may occur. People who inhaled sulfotep are often disorientated and have difficulties to breath. A poisonous dose may lead to a coma or death after 24 hours. The point at 24 hours after the poisoning is very important. If the dose is not lethal, the symptoms will slowly disappear after the point of 24 hours.
In any part of the world that uses organophosphates, "C. megacephala" could prove to be beneficial. Organophosphate compounds are used in agriculture and are highly toxic. Organophosphate poisoning often causes death, and in many cases, by evaluating the body tissue and fluids, the toxin can be identified as the source of the poisoning. However, it is somewhat difficult to evaluate the body tissue in a body that is exceedingly decomposed. Nevertheless, a medical examiner in Hawaii worked on a case in which poisoning by malathion, an organophosphate insecticide, was thought to be the cause of death. The victim’s stomach contents and body fat were examined and found to have contained malathion. The fly larvae of "Chrysomya megacephala" and "Chrysomya rufifacies" were also present at the scene on the body and were tested for malathion. Both of these species did contain malathion, but there had been no previous record of organophosphates in their larvae. Studying larvae from decomposed remains may provide an effective method of determining the presence of these toxins in a body that is extremely decayed.
Carbophenothion is a highly toxic organophosphate insecticide and acaricide. Organophosphates are acetylcholinesterase inhibitors and disrupt the signal transduction at the cholinergic synapse. It is classified as Restricted Use Pesticide (RUP) by the Environmental Protection Agency (EPA). Carbophenothion is used in different brands like Trithion. This pesticide contains 80% carbophenothion as its only active ingredient. Because of the widespread use of those organophosphates in the nineties in the US, it was the most common cause of agricultural poisonings.
Prevention includes banning very toxic types of organophosphates.[2] Among those who work with pesticides the use of protective clothing and showering before going home is also useful.[6] In those who have organophosphate poisoning the primary treatments are atropine, oximes such as pralidoxime, and diazepam.[2][4] General measures such as oxygen and intravenous fluids are also recommended.[2] Attempts to decontaminate the stomach, with activated charcoal or other means, has not been shown to be useful.[2] While there is a theoretical risk of health care workers taking care of a poisoned person becoming poisoned themselves, the degree of risk appears to be very small.[2]
Under a 1988 amendment to the Federal Insecticide, Fungicide and Rodenticide Act (FIFRA), the U.S. Environmental Protection Agency (EPA) regulates organophosphate pesticides[43] Its focus was initially on registering pesticides for use on food crops. No pesticide can be sold in the United States before the EPA has reviewed the manufacture's application for registration and determined that the use of the product will not present an unreasonable risk to the public or the environment.[44] In 1996, with the passage of the Food Quality Protection Act, Congress required the EPA to reassess all existing pesticide tolerances with specific consideration for children.[45] This resulted in a 10-year review process of the health and environmental effects of all pesticides, beginning with the organophosphates. As part of that process, in 1999 the EPA announced a ban the use of organophosphate pesticide methyl parathion and significant restrictions on the use of another OP, azinphos methyl, in what they called "kid's food".[46] The review process was concluded in 2006 and eliminated or modified thousands of other uses of pesticides.[47] Other legislative action has been taken to protect children from the risks of organophosphates.
Research has linked the neurological abnormalities found in Persian Gulf War veterans who suffer from chronic multisymptom ilnesses to exposure to wartime combinations of organophosphate chemical nerve agents. Before, it was believed that veterans were suffering from a psychologically based disorder or depression, most likely post-traumatic stress disorder (PTSD). Many veterans were given pyridostigmine bromide (PB) pills to protect against nerve gas agents such as sarin and soman. During the war veterans were exposed to combinations of organophosphate pesticides and nerve agents, which produced symptoms associated with chronic organophosphate-induced delayed polyneuropathy (OPIDP) syndrome. Similar symptoms found in the veterans were the same symptoms reported for individuals in occupational settings who were acutely poisoned by organophosphates, such as chlorpyrifos. Studies found veterans experienced deficits in intellectual and academic abilities, simple motor skills, memory impairment, and impaired emotional function. These symptoms indicate brain damage, not a psychologically based disorder.[40][41][42]
Atropine is not an actual antidote for organophosphate poisoning. However, by blocking the action of acetylcholine at muscarinic receptors, atropine also serves as a treatment for poisoning by organophosphate insecticides and nerve gases, such as tabun (GA), sarin (GB), soman (GD) and VX. Troops who are likely to be attacked with chemical weapons often carry autoinjectors with atropine and obidoxime, for rapid injection into the muscles of the thigh. In a developed case of nerve-gas poisoning, maximum atropinization is desirable. Atropine is often used in conjunction with pralidoxime chloride.
Organophosphate and carbamate insecticides have a similar mode of action. They affect the nervous system of target pests (and non-target organisms) by disrupting acetylcholinesterase activity, the enzyme that regulates acetylcholine, at nerve synapses. This inhibition causes an increase in synaptic acetylcholine and over-stimulation of the parasympathetic nervous system. Many of these insecticides, first developed in the mid 20th century, are very poisonous. Although commonly used in the past, many older chemicals have been removed from the market due to their health and environmental effects ("e.g." DDT, chlordane, and toxaphene). However, many organophosphates are not persistent in the environment.
It has been estimated that more than 40,000 people per year seek medical attention for carbon monoxide poisoning in the United States. 95% of carbon monoxide poisoning deaths in the United States are due to gas space heaters. In many industrialized countries carbon monoxide is the cause of more than 50% of fatal poisonings. In the United States, approximately 200 people die each year from carbon monoxide poisoning associated with home fuel-burning heating equipment. Carbon monoxide poisoning contributes to the approximately 5613 smoke inhalation deaths each year in the United States. The CDC reports, "Each year, more than 500 Americans die from unintentional carbon monoxide poisoning, and more than 2,000 commit suicide by intentionally poisoning themselves." For the 10-year period from 1979 to 1988, 56,133 deaths from carbon monoxide poisoning occurred in the United States, with 25,889 of those being suicides, leaving 30,244 unintentional deaths. A report from New Zealand showed that 206 people died from carbon monoxide poisoning in the years of 2001 and 2002. In total carbon monoxide poisoning was responsible for 43.9% of deaths by poisoning in that country. In South Korea, 1,950 people had been poisoned by carbon monoxide with 254 deaths from 2001 through 2003. A report from Jerusalem showed 3.53 per 100,000 people were poisoned annually from 2001 through 2006. In Hubei, China, 218 deaths from poisoning were reported over a 10-year period with 16.5% being from carbon monoxide exposure.
Neurotoxic effects have also been linked to poisoning with OP pesticides causing four neurotoxic effects in humans: cholinergic syndrome, intermediate syndrome, organophosphate-induced delayed polyneuropathy (OPIDP), and chronic organophosphate-induced neuropsychiatric disorder (COPIND). These syndromes result after acute and chronic exposure to OP pesticides.
Chemical and pesticide use causes many health ailments as in chemical or pesticide poisoning and reproductive issues in women. Some common chemicals used in agriculture are bipyridyls, organophosphates, and carbamates. Exposure to pesticides can occur through not just the process of making pesticides, but also in other agricultural tasks like harvesting crop or irrigating fields. Part of the problem arises in the lack of more strict safety measures as well as utilization of personal protective equipment, but the use of pesticides requires care in itself of set safety measures. The United States' use of pesticides resides heavily in agriculture, with 75% being used in this industry. In a study by the California Department of Pesticide Regulation and the SENSOR- Pesticides program, regarding pesticide poisoning incidence rates out of 3,271 cases, 402 individuals had medium severity illnesses from pesticide exposure with high severity cases being rare and lower severity being more common. From this study, the pesticides that were deemed to cause most cases of diseases were cholinesterase, pyrethroids, inorganic compounds, and dithiocarbamates. Insecticides, specifically cholinesterase inhibitors (N-methyl carbamates and organophosphates) cause a majority of the illnesses in 54% of the individuals in the case. Some of the more common symptoms seen in pesticide poisoning were nervous system impairments, headaches, gastrointestinal issues, respiratory impairments, skin impairments, inflammations, and many more.
The use of the organophosphates in aviation lubricating oils and hydraulic fluids and its impact on health and flight safety is currently being researched. Aerotoxic syndrome is a medical condition allegedly caused by exposure to contaminated bleed air.
A number of measurements exist to assess exposure and early biological effects for organophosphate poisoning. Measurements of OP metabolites in both the blood and urine can be used to determine if a person has been exposed to organophosphates. Specifically in the blood, metabolites of cholinesterases, such as butyrylcholinesterase (BuChE) activity in plasma, neuropathy target esterase (NTE) in lymphocytes, and of acetylcholinesterase (AChE) activity in red blood cells.[23] Due to both AChE and BuChE being the main targets of organophosphates, their measurement is widely used as an indication of an exposure to an OP. The main restriction on this type of diagnosis is that depending on the OP the degree to which either AChE or BuChE are inhibited differs; therefore, measure of metabolites in blood and urine do not specify for a certain OP.[23][25] However, for fast initial screening, determining AChE and BuChE activity in the blood are the most widely used procedures for confirming a diagnosis of OP poisoning.[25] The most widely used portable testing device is the Test-mate ChE field test,[26][27]:13 which can be used to determine levels of Red Blood Cells (RBC), AChE and plasma (pseudo) cholinesterase (PChE) in the blood in about four minutes. This test has been shown to be just as effective as a regular laboratory test and because of this, the portable ChE field test is frequently used by people who work with pesticides on a daily basis.[28]
In combination with analysis of reductions in cholinesterase activity in the blood, symptoms of organophosphate poisoning can be used to identify victims of organophosphate poisoning. These symptoms are not specific for chlorfenvinphos, but for anticholinesterase compounds in general.
Pesticide use is widespread in Latin America, as around US $3 billion are spend each year in the region. It has been recorded that pesticide poisonings have been increasing each year for the past two decades. It was estimated that 50–80% of the cases are unreported. It is indicated by studies that organophosphate and carbamate insecticides are the most frequent source of pesticide poisoning.
Organophosphate-induced delayed neuropathy (OPIDN), also called organophosphate-induced delayed polyneuropathy (OPIDP), is a neuropathy caused by killing of neurons in the central nervous system, especially in the spinal cord, as a result of acute or chronic organophosphate poisoning.
It is sometimes reported that people poisoned by organophosphate insecticides experience the same symptoms as nicotine poisoning. Organophosphates inhibit an enzyme called acetylcholinesterase, causing a buildup of acetylcholine, excessive stimulation of all types of cholinergic neurons, and a wide range of symptoms. Nicotine is specific for nicotinic cholinergic receptors only and has some, but not all of the symptoms of organophosphate poisoning.
Pralidoxime (2-pyridine aldoxime methyl chloride) or 2-PAM, usually as the chloride or iodide salts, belongs to a family of compounds called oximes that bind to organophosphate-inactivated acetylcholinesterase. It is used to treat organophosphate poisoning in conjunction with atropine and diazepam. It is a white solid.
Organophosphate poisoning is poisoning due to organophosphates (OPs).[4] Organophosphates are used as insecticides, medications, and nerve agents.[4] Symptoms include increased saliva and tear production, diarrhea, vomiting, small pupils, sweating, muscle tremors, and confusion.[2] While onset of symptoms is often within minutes to hours, some symptoms can take weeks to appear.[5][1] Symptoms can last for days to weeks.[2]