Chlorpyrifos

Chlorpyrifos
Names
IUPAC name
O,O-Diethyl O-3,5,6-trichloropyridin-2-yl phosphorothioate
Other names
Brodan, Chlorpyrifos-ethyl, Detmol UA, Dowco 179, Dursban, Empire, Eradex, Lorsban, Paqeant, Piridane, Scout, Stipend and Tricel.
Identifiers
2921-88-2 YesY
ChEBI CHEBI:34631 YesY
ChEMBL ChEMBL463210 YesY
ChemSpider 2629 YesY
Jmol interactive 3D Image
KEGG D07688 YesY
PubChem 2730
UNII JCS58I644W YesY
Properties
C9H11Cl3NO3PS
Molar mass 350.59 g/mol
Appearance colourless crystals[1]
Odor mercaptan-like[2]
Density 1.398 g/cm3 (43.5 °C)
Melting point 43 °C (109 °F; 316 K)[3]
Boiling point 160 °C; 320 °F; 433 K (decomposes)[2]
2 mg/L (25 °C)
log P 4.96 (octanol/water)[4]
Hazards
Main hazards combustible, reacts strongly with amines, strong acids, caustics[2]
US health exposure limits (NIOSH):
none[2]
TWA 0.2 mg/m3 ST 0.6 mg/m3 [skin][2]
N.D.[2]
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
YesY verify (what is YesYN ?)
Infobox references

Chlorpyrifos (IUPAC name: O,O-diethyl O-3,5,6-trichloropyridin-2-yl phosphorothioate) is a crystalline organophosphate insecticide, acaracide and miticide. It was introduced in 1965 by Dow Chemical Company and is known by many trade names (see table), including Dursban and Lorsban. It acts on the nervous system of insects by inhibiting acetylcholinesterase.

Chlorpyrifos is moderately toxic to humans, and exposure has been linked to neurological effects, persistent developmental disorders and autoimmune disorders. Exposure during pregnancy retards the mental development of children, and most home use was banned in 2001 in the U.S.[5] In agriculture, it is "one of the most widely used organophosphate insecticides" in the United States, according to the United States Environmental Protection Agency (EPA), and before being phased out for residential use was one of the most used residential insecticides.[6]

Manufacture

Chlorpyrifos is produced via a multistep synthesis from 3-methylpyridine, eventually reacting 3,5,6-trichloro-2-pyridinol with diethylthiophosphoryl chloride.[1]

Uses

Chlorpyrifos is used around the world to control pest insects in agricultural, residential and commercial settings. Its use in residential applications is restricted in multiple countries. According to Dow, chlorpyrifos is registered for use in nearly 100 countries and is annually applied to approximately 8.5 million crop acres.[7] The crops with the most use are cotton, corn, almonds and fruit trees including oranges, bananas and apples.[8]

Chlorpyrifos was first registered for use in the United States in 1965 for control of foliage and soil-born insects.[6] The chemical became widely used in residential settings, on golf course turf, as a structural termite control agent, and in agricultural use. Most residential use has been phased out in the United States; however it remains a common agricultural insecticide.[6]

EPA estimated that between 1987 and 1998 about 21 million pounds of chlorpyrifos were annually used in the US.[6] In 2007, chlorpyrifos was the most commonly used organophosphate pesticide in the United States, with an estimated 8 to 11 million pounds applied, and the 14th most common agricultural pesticide ingredient overall in 2007 in the United States.[9]

Application

Chlorpyrifos is normally supplied as a 23.5% or 50% liquid concentrate. The recommended concentration for direct-spray pin point application is 0.5% and for wide area application a 0.03 – 0.12% mix is recommended (US).[10][11]

Toxicity and safety

Chlorpyrifos exposure may lead to acute toxicity at higher doses. Persistent health effects follow acute poisoning or from long-term exposure to low doses. developmental effects appear in fetuses and children even at very small doses.

Persistent health effects

Gestation, infancy and childhood

Epidemiological and experimental animal studies suggest that infants and children are more susceptible than adults to effects from low dose exposure.[12][13] The young have a decreased capacity to detoxify chlorpyrifos and its metabolites. This results in disruption in nervous system developmental processes, as observed in animal experiments.[12]

Human studies: In multiple epidemiological studies, chlorpyrifos exposure during gestation or childhood has been linked with lower birth weight and neurological changes such as slower motor development and attention problems.[13] Exposure to organophosphate pesticides in general has been increasingly associated with changes in children's cognitive, behavioral and motor performance.[14]

Animal experiments: In experiments with rats, early, short-term low-dose exposure to chlorpyrifos resulted in lasting neurological changes, with larger effects on emotional processing and cognition than on motor skills.[13] Such rats exhibited behaviors consistent with depression and reduced anxiety.[13] In rats, low-level exposure during development has its greatest neurotoxic effects during the period in which sex differences in the brain develop. Exposure leads to reductions or reversals of normal gender differences.[15] Exposure to low levels of chlorpyrifos early in rat life or as adults also affects metabolism and body weight.[16] These rats show increased body weight as well as changes in liver function and chemical indicators similar to prediabetes, likely associated with changes to the cyclic AMP system.[16]

Adulthood

Adults may develop lingering health effects following acute exposure or repeated low-dose exposure. Among agricultural workers, chlorpyrifos has been associated with slightly increased risk of wheeze, a whistling sound while breathing due to airway obstruction in the airways.[17]

Among 50 farm pesticides studied, chlorpyrifos was associated with higher risks of lung cancer among frequent pesticide applicators than among infrequent or non-users. Pesticide applicators as a whole were found to have a 50% lower cancer risk than the general public, likely due to their nearly 50% lower smoking rate. However, chlorpyrifos applicators had a 15% lower cancer risk than the general public, which the study suggests indicates a link between chlorpyrifos application and lung cancer.[18][19]

Acute health effects

For acute effects, the World Health Organization classifies chlorpyrifos as Class II: moderately toxic.[20] The oral LD50 in experimental animals is 32 to 1000 mg/kg. The dermal LD50 in rats is greater than 2000 mg/kg and 1000 to 2000 mg/kg in rabbits. The 4-hour inhalation LC50 for chlorpyrifos in rats is greater than 200 mg/m3.[21]

Symptoms of acute exposure

Acute poisoning results mainly from interference with the acetylcholine neurotransmission pathway, leading to a range of neuromuscular symptoms. Relatively mild poisoning can result in eye watering, increased saliva and sweating, nausea and headache. Intermediate exposure may lead to muscle spasms or weakness, vomiting or diarrhea and impaired vision. Symptoms of severe poisoning include seizures, unconsciousness, paralysis, and suffocation from lung failure.[22]

Children are more likely to experience muscle weakness rather than twitching; excessive saliva rather than sweat or tears; seizures; and sleepiness or coma.[22]

Frequency of acute exposure

Acute poisoning is probably most common in agricultural areas in Asia, where many small farmers are affected.[23] Poisoning may be due to occupational or accidental exposure or intentional self-harm. Precise numbers of chlorpyrifos poisonings globally are not available.[24] Pesticides are used in an estimated 200,000+ suicides annually. Organophosphates are thought to constitute two-thirds of ingested pesticides in rural Asia. Chlorpyrifos is among the commonly used pesticides used for self-harm.[23][24][25]

In the US, the number of incidents of chlorpyrifos exposure reported to the US National Pesticide Information Center shrank sharply from over 200 in the year 2000 to less than 50 in 2003, following the residential ban.[26]

Treatment

Poisoning is treated with atropine and simultaneously with oximes such as pralidoxime.[27] Atropine blocks acetylcholine from binding with muscarinic receptors, which reduces the pesticide's impact. However, atropine does not affect acetylcholine at nicotinic receptors and thus is a partial treatment. Pralidoxime is intended to reactivate acetylcholinesterase, but the benefit of oxime treatment is questioned.[27] A randomized controlled trial (RCT) supported the use of higher doses of pralidoxime rather than lower doses.[28] A subsequent double-blind RCT, that treated patients who self-poisoned, found no benefit of pralidoxime, including specifically in chlorpyrifos patients.[29]

Tourist deaths

Chlorpyrifos poisoning was described by New Zealand scientists as the likely cause of death of several tourists in Chiang Mai, Thailand who developed myocarditis in 2011.[30][31][32] Thai investigators came to no conclusion on the subject,[33] but maintain that chlorpyrifos was not responsible and that the deaths were not linked.[34]

Mechanisms of toxicity

Acetylcholine neurotransmission

Primarily, chlorpyrifos and other organophosphate pesticides interfere with signaling from the neurotransmitter acetylcholine.[22] One chlorpyrifos metabolite, chlorpyrifos-oxon, binds permanently to the enzyme acetylcholinesterase, preventing this enzyme from deactivating acetylcholine in the synapse.[12][22] By irreversibly inhibiting acetylcholinesterase, chlorpyrifos leads to a build-up of acetylcholine between neurons and a stronger, longer-lasting signal to the next neuron. Only when new molecules of acetylcholinesterase have been synthesized can normal function return. Acute symptoms of chlorpyrifos poisoning only occur when more than 70% of acetylcholinesterase molecules are inhibited.[15] This mechanism is well established for acute chlorpyrifos poisoning and also some lower-dose health impacts. It is also the primary insecticidal mechanism.

Non-cholinesterase mechanisms

Chlorpyrifos may affect other neurotransmitters, enzymes and cell signaling pathways, potentially at doses below those that substantially inhibit acetylcholinesterase. The extent of and mechanisms for these effects remain to be fully characterized.[35][36] Laboratory experiments in rats and cell cultures suggest that exposure to low doses of chlorpyrifos may alter serotonin signaling and increase rat symptoms of depression; change the expression or activity of several serine hydrolase enzymes, including neuropathy target esterase and several endocannabinoid enzymes; affect components of the cyclic AMP system; and influence other chemical pathways.[15][36][37][38]

Paraoxonase activity

The enzyme paraoxonase 1 (PON1) detoxifies chlorpyrifos oxon, the more toxic metabolite of chlorpyrifos, via hydrolysis. In laboratory animals, additional PON1 protects against chlorpyrifos toxicity while individuals that do not produce PON1 are particularly susceptible.[39] In humans, studies about the effect of PON1 activity on the toxicity of chlorpyrifos and other organophosphates are mixed, with modest yet inconclusive evidence that higher levels of PON1 activity may protect against chlorpyrifos exposure in adults; PON1 activity may be most likely to offer protection from low-level chronic doses.[39] Human populations have genetic variation in the sequence of PON1 and its promoter region that may influence the effectiveness of PON1 at detoxifying chlorpyrifos oxon and the amount of PON1 available to do so.[39] Some evidence indicates that children born to women with low PON1 may be particularly susceptible to chlorpyrifos exposure. Further, infants produce low levels of PON1 until six months to several years after birth, likely increasing the risk from chlorpyrifos exposure early in life.[39]

Combined exposures

Several studies have examined the effects of combined exposure to chlorpyrifos and other chemical agents, and these combined exposures can result in different effects during development. Female rats exposed first to dexamethasone, a treatment for premature labor, for three days in utero and then to low levels of chlorpyrifos for four days after birth experienced additional damage to the acetylcholine system upstream of the synapse that was not observed with either exposure alone.[40] In both male and female rats, combined exposures to dexamethasone and chlorpyrifos decreased serotonin turnover in the synapse, for female rats with a greater-than-additive result.[41] Rats that were co-exposed to dexamethasone and chlorpyrifos also exhibited complex behavioral differences from exposure to either chemical alone, including lessening or reversing normal sex differences in behavior.[42] In the lab, in rats and neural cells co-exposed to both nicotine and chlorpyrifos, nicotine appears to protect against chlorpyrifos acetylcholinesterase inhibition and reduce its effects on neurodevelopment.[43][44][45] In at least one study, nicotine appeared to enhance chlorpyrifos detoxification.[43]

Human exposure

In 2011, EPA estimated that, in the general US population, people consume 0.009 micrograms of chlorpyrifos per kilogram of their body weight per day directly from food residue.[46] Children are estimated to consume a greater quantity of chlorpyrifos per unit of body weight from food residue, with toddlers the highest at 0.025 micrograms of chlorpyrifos per kilogram of their body weight per day. People may also ingest chlorprifos from drinking water or from residue in food handling establishments. The EPA’s acceptable daily dose is 0.3 micrograms/kg/day.[46]

Before residential use was restricted in the US, data from 1999-2000 in the national NHANES study detected the metabolite TCPy in 91% of human urine samples tested.[47] In samples collected between 2007 and 2009 from families living in Northern California, TCPy was found in 98.7% of floor wipes tested and in 65% of urine samples tested. For both children and adults, the average concentrations of TCPy in urine were lower in the later study.[47] A 2008 study found dramatic drops in the urinary levels of chlorpyrifos metabolites when children in the general population switched from conventional to organic diets.[48]

Certain populations with higher likely exposure to chlorpyrifos, such as people who apply pesticides, work on farms, or live in agricultural communities, have been measured in the US to excrete TCPy in their urine that are 5 to 10 times greater than levels in the general population.[49][50][51]

Air monitoring studies conducted by the California Air Resources Board (CARB) documented chlorpyrifos in the air of California communities.[52] Analyses indicate that children living in areas of high chlorpyrifos use are often exposed to levels that exceed EPA dosages.[53][54] Advocacy groups monitored air samples in Washington and Lindsay, CA, in 2006 with comparable results.[55][56] Grower and pesticide industry groups argued that the air levels documented in these studies are not high enough to cause significant exposure or adverse effects,[57] but a follow-up biomonitoring study in Lindsay showed that people there display above-normal chlorpyrifos levels.[58][59]

Effects on wildlife

Aquatic life

Among freshwater aquatic organisms, crustaceans and insects appear to be more sensitive to acute exposure than are fish.[60] Aquatic insects and animals appear to absorb chlorpyrifos directly from water rather than ingesting it with their diet or through sediment exposure.[60]

Concentrated chlorpyrifos released into rivers killed insects, shrimp and fish. In Britain, the rivers Roding (1985), Ouse (2001), Wey (2002 & 2003), and Kennet (2013) all experienced insect, shrimp, and/or fish kills as a result of small releases of concentrated chlorpyrifos.[61] The July 2013 release along the River Kennet poisoned insect life and shrimp along 15 km of the river, potentially from several teaspoonsful of concentrated chlorpyrifos washed down a drain.[62]

Bees

Acute exposure to chlorpyrifos can be toxic to bees, with an oral LD50 of 360 ng/bee and a contact LD50 of 70 ng/bee.[22] Guidelines for Washington state recommend that chlorpyrifos products should not be applied to flowering plants such as fruit trees within 4–6 days of blossoming to prevent bees from directly contacting the residue.[63]

Risk assessments have primarily considered acute exposure, but more recently researchers have begun to investigate the effects of chronic, low-level exposure through residue in pollen and components of bee hives.[64] A review of US studies, several European countries, Brazil and India found chlorpyrifos in nearly 15% of hive pollen samples and just over 20% of honey samples. Because of its high toxicity and prevalence in pollen and honey, bees are considered to have higher risk from chlorpyrifos exposure via their diet than from many other pesticides.[64]

When exposed in the laboratory to chlorpyrifos at levels roughly estimated from measurements in hives, bee larvae experienced 60% mortality over 6 days, compared with 15% mortality in controls.[65] Adult bees exposed to sub-lethal effects of chlorpyrifos (0.46 ng/bee) exhibited altered behaviors: less walking; more grooming, particularly of the head; more difficulty righting themselves; and unusual abdominal spasms.[66] Chlorpyrifos oxon appears to particularly inhibit acetylcholinesterase in bee gut tissue as opposed to head tissue.[66] Other organophosphate pesticides impaired bee learning and memory of smells in the laboratory.[67]

Regulation

International law

Chlorpyrifos is not regulated under international law or treaty. Organizations such as PANNA and the NRDC state that chlorpyrifos meets the four criteria (persistence, bioaccumulation, long-range transport, and toxicity) in Annex D of the Stockholm Convention on Persistent Organic Pollutants and should be restricted.[68]

National regulations

Chlorpyrifos is restricted from termite control in Singapore as of 2009.[69]

It was banned from residential use in South Africa as of 2010.[70]

In 2010, India barred Dow from commercial activity for 5 years[71] after India’s Central Bureau of Investigation found Dow guilty of bribing Indian officials in 2007 to allow the sale of chlorpyrifos.[72]

United States

In the United States, several laws directly or indirectly regulate the use of pesticides. These laws, which are implemented by the EPA, NIOSH, USDA and FDA, include: the Clean Water Act (CWA); the Endangered Species Act (ESA); the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA); the Federal Food, Drug, and Cosmetic Act (FFDCA); the Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA); and the Emergency Planning and Community Right-to-Know Act (EPCRA). As a pesticide, chlorpyrifos is not regulated under the Toxic Substances Control Act (TSCA).[73]

Chlorpyrifos is sold in restricted-use products for certified pesticide applicators to use in agriculture and other settings, such as golf courses or for mosquito control.[74] It may also be sold in ant and roach baits with childproof packaging.[75] In 2000, manufacturers reached an agreement with the EPA to voluntarily restrict the use of chlorpyrifos in places where children may be exposed, including homes, schools and day care centers.[76][77]

On August 10, 2015, the Ninth Circuit Court of Appeals ordered the EPA to respond no later than October 2015 to a petition from pesticide activists requesting a chlorpyrifos ban. The court called the EPA's failure to respond for more than eight years (neither granting nor denying the petition) an "egregious" delay.[78] In late October, 2015, the EPA released a proposal to end the use of chlorpyrifos due to a possible risk to certain water supplies. Dow AgroSciences disagreed with the EPA’s proposal and said the product had been thoroughly tested for health, safety and environmental effects and said, “no other pesticide has been more thoroughly tested.”

Residue

The use of chlorpyrifos in agriculture can leave chemical residue on food commodities. The FFDCA requires EPA to set limits, known as tolerances, for pesticide residue in human food and animal feed products based on risk quotients for acute and chronic exposure from food in humans.[79][80] These tolerances limit the amount of chlorpyrifos that can be applied to crops. FDA enforces EPA's pesticide tolerances and determines “action levels” for the unintended drift of pesticide residues onto crops without tolerances.[81]

Chlorpyrifos has a tolerance of 0.1 part per million (ppm) residue on all food items unless a different tolerance has been set for that item or chlorpyrifos is not registered for use on that crop.[82] EPA set approximately 112 tolerances pertaining to food products and supplies.[80][83] In 2006, to reduce childhood exposure, the EPA amended its chlorpyrifos tolerance on apples, grapes and tomatoes, reducing the grape and apple tolerances to 0.01 ppm and eliminating the tolerance on tomatoes.[80] Chlorpyrifos is not allowed on crops such as spinach, squash, carrots, and tomatoes; any chlorpyrifos residue on these crops normally represents chlorpyrifos misuse or spray drift.[80]

Food handling establishments (places where food products are held, processed, prepared or served) are included in the food tolerance of 0.1 ppm for chlorpyrifos. Food handling establishments may use a 0.5% solution of chlorpyrifos solely for spot and/or crack and crevice treatments.[83] Food items are to be removed or protected during treatment. Food handling establishment tolerances may be modified or exempted under FFDCA sec. 408.[84]

Water

Chlorpyrifos in waterways is regulated as a hazardous substance under section 311(b)(2)(A) of the Federal Water Pollution Control Act and falls under the CWA amendments of 1977 and 1978.[85] The regulation is inclusive of all chlorpyrifos isomers and hydrates in any solution or mixture. EPA has not set a drinking water regulatory standard for chlorpyrifos, but has established a drinking water guideline of 2 ug/L.[86]

In 2009, in order to protect threatened salmon and steelhead under CWA and ESA, EPA and National Marine Fisheries Service (NMFS) recommended limits on the use of chlorpyrifos in California, Idaho, Oregon and Washington and requested that manufacturers voluntarily add buffer zones, application limits and fish toxicity to the standard labeling requirements for all chlorpyrifos-based products.[87] Manufacturers rejected the request.[88] In February 2013 in Dow AgroSciences vs NMFS, the Fourth Circuit Court of Appeals vacated EPA’s order for these labeling requirements.[89] In August 2014, in the settlement of a suit brought by environmental and fisheries advocacy groups against EPA in the U.S. District Court for the Western District of Washington, EPA agreed to re-instate no-spray stream buffer zones in California, Oregon and Washington, restricting aerial spraying (300 ft.) and ground-based applications (60 ft.) near salmon populations.[90] These buffers will remain until EPA makes a permanent decision in consultation with NMFS.[91]

Reporting

EPCRA designates the chemicals that facilities must report to the Toxics Release Inventory (TRI), based on EPA assessments. Chlorpyrifos is not on the reporting list. It is on the list of hazardous substances under CERCLA (aka the Superfund Act). In the event of an environmental release above its reportable quantity of 1 lb or 0.454 kg, facilities are required to immediately notify the National Response Center (NRC) .[92]

In 1995, Dow paid a $732,000 EPA penalty for not forwarding reports it had received on 249 chlorpyrifos poisoning incidents.[93]

Occupational exposure

In 1989, OSHA established a workplace permissible exposure limit (PEL) of 0.2 mg/m3 for chlorpyrifos, based on an 8-hour time weighted average (TWA) exposure. However, the rule was remanded by the U.S. Circuit Court of Appeals and no PELs are in place presently.[94]

EPA’s Worker Protection Standard requires owners and operators of agricultural businesses to comply with safety protocols for agricultural workers and pesticide handlers (those who mix, load and apply pesticides). For example, in 2005, the EPA filed an administrative complaint against JSH Farms, Inc. (Wapato, Washington) with proposed penalties of $1,680 for using chlorpyrifos in 2004 without proper equipment. An adjacent property was contaminated with chlorpyrifos due to pesticide drift and the property owner suffered from eye and skin irritation.[95]

State Laws

Additional laws and guidelines may apply for individual states. For example, Florida has a drinking water guideline for chlorpyrifos of 21 ug/L.[86] Other states are reviewing chlorpyrifos following the federal government’s recommendations for pesticide surveillance.

In 2003, Dow agreed to pay $2 million to New York state, in response to a lawsuit to end Dow's advertising of Dursban as "safe".[96]

Oregon’s Department of Environmental Quality added chlorpyrifos to the list of targeted reductions in the Clackamas Subbasin as part of the Columbia River National Strategic Plan, which is based on EPA’S 2006-11 National Strategic Plan.1[97]

In 2008, chlorpyrifos was evaluated for inclusion in California’s Proposition 65,[98] a state law that prohibits businesses from discharging substances known to cause birth defects and reproductive harm into the drinking water, but the California’s Office of Environmental Health Hazard Assessment decided against the move.[99]

California included regulation limits for chlorpyrifos in waterways and established maximum and continuous concentration limits of 0.025 ppb and 0.015 pbb, respectively.[100]

See also

References

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