Instruct: Given a question, retrieve passages that answer the question.
Query: What is an organophosphate?
Organophosphates (also known as phosphate esters) are a class of organophosphorus compounds with the general structure O=P(OR)3. They can be considered as esters of phosphoric acid. Like most functional groups organophosphates occur in a diverse range of forms, with important examples including key biomolecules such as DNA, RNA and ATP, as well as many insecticides, herbicides, and nerve agents.
Furthermore, certain organophosphates can cause OPIDN, organophosphate-induced delayed polyneuropathy. This is a disease, which is characterized by degeneration of axons in the peripheral and central nervous system. This disease will show a few weeks after contamination with the organophosphate. It is believed that the neuropathy target esterase (NTE) is affected by the organophosphate which induces the disease. However, there are no references found, which indicate that TEPP is one of the organophosphates that can cause OPIDN.
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.
Anatoxin-a(S) is a naturally occurring organophosphate produced by cyanobacteria.
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]
The symptoms of organophosphate poisoning include muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis. Other symptoms include hypertension, and hypoglycemia.
Effective organophosphates have the following structural features:
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.
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]
An organic diet is an effective way to reduce exposure to the organophosphorus pesticides commonly used in agricultural production.[19] Organophosphate metabolite levels rapidly drop, and for some metabolites, become undetectable in children's urine when an organic diet is consumed.[19] This is speculative based on a short study of 23 children, in which only a few organophosphate compounds were potentially reduced, no effect was shown for the majority of them that were found in the samples.
Clothianidin is an alternative to organophosphate, carbamate, and pyrethroid pesticides. It poses lower risks to mammals, including humans, when compared to organophosphates and carbamates. It has helped prevent insect pests build up resistance to organophosphate and pyrethroid pesticides.
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.
Various routes exist for the synthesis of organophosphates
In 1999, the EPA banned most uses of methyl parathion and azinphos methyl, citing the risks they pose to children. Both methyl parathion and azinphos methyl are organophosphates. Organophosphates are pesticides that kill insects by disrupting nerve impulses. Unfortunately, these pesticides have the same effect on humans. In 2000, the EPA banned another organophosphate, (chlorpyrifos), that was common in the agriculture industry, household cleaners and commercial pest control products, due to a study showing that chlorpyrifos caused weakness, vomiting and diarrhea in baby rats.
Organophosphate is the general name for esters of phosphoric acid and is one of the organophosphorus compounds. They can be found as part of insecticides, herbicides, and nerve gases, amongst others. Some less-toxic organophosphates can be used as solvents, plasticizers, and EP additives. The use of organophosphates accounts for approximately 38% of all pesticide use globally.
Organophosphate pesticides (OPPs), like some nerve agents, inhibit this neuromuscular enzyme, which is broadly essential for normal function in insects, but also in humans and many other animals.[2] OPPs affect this enzyme in varied ways, a principle one being through irreversible covalent inhibition,[3] and so create potentials for poisoning that vary in degree. The brain sends out neurotransmitters to the nerve endings in the body; organophosphates disrupt this process from occurring.This chemical, organophosphate works by disrupting the enzyme acetylcholinesterase. Acetylcholinesterase break down the acetylcholine neurotransmitter, which sends out signals to other nerve endings in the body.[1]
Bacterial species that had the ability to degrade organophosphate pesticides have been isolated from soil samples from different parts of the world. The first bacterial strain identified to be able to hydrolyze organophosphates was "Flavobacterium" sp. ATCC 27551, found by Sethunathan and Yoshida in 1973 from a soil sample originally from the Philippines. Since then, other species were found to also have organophosphate-degrading enzymes similar to that found in "Flavobacterium""."
Organophosphites can be readily oxidised to give organophosphates
According to the EPA, organophosphate use in 2004 accounts for 40% of all insecticide products used in the United States.[22]Out of concerns for potential hazards of organophosphate exposure to child development, the EPA began phasing out forms of organophosphates used indoors in 2001.[22] While it is used in forestry, urban, and public health spraying (mosquito abatement programs, etc.) as well, the general population has been observed to have low exposure.[23] Thus, the primary affected population that faces exposure to organophosphates are farmworkers, especially those in countries that have fewer restrictions on its usage, such as in India.[24]
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.
Organophosphates are another large class of contact insecticides. These also target the insect's nervous system. Organophosphates interfere with the enzymes acetylcholinesterase and other cholinesterases, disrupting nerve impulses and killing or disabling the insect. Organophosphate insecticides and chemical warfare nerve agents (such as sarin, tabun, soman, and VX) work in the same way. Organophosphates have a cumulative toxic effect to wildlife, so multiple exposures to the chemicals amplifies the toxicity. In the US, organophosphate use declined with the rise of substitutes.
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.
Activity-based protein profiling using organophosphate-containing activity-based probes Pesticide toxicity to bees Toxic oil syndrome
Tris(1,3-dichloroisopropyl)phosphate (TDCPP) is a chlorinated organophosphate. Organophosphate chemicals have a wide variety of applications and are used as flame retardants, pesticides, plasticizers, and nerve gases. TDCPP is structurally similar to several other organophosphate flame retardants, such as tris(2-chloroethyl) phosphate (TCEP) and tris(chloropropyl)phosphate (TCPP). TDCPP and these other chlorinated organophosphate flame retardants are all sometimes referred to as "chlorinated tris".
As of 2013, thirty-six types of organophosphates were registered for use in the United States.[33] Organophosphates are currently used in a variety of environments (e.g. agriculture, gardens and veterinary practices), however, several notable OPs have been discontinued for use.[33] This includes parathion, which is no longer registered for any use, and chlorpyrifos (as mentioned previously), which is no longer registered for home use.[33] And again, other than for agricultural use, the OP diazinon has been banned in the U.S.