Template:Chembox UNII
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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.
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2921-88-2 7pxY
ChEBI CHEBI:34631 7pxY
ChEMBL ChEMBL463210 7pxY
ChemSpider 2629 7pxY
Jmol-3D images Image
KEGG D07688 7pxY
PubChem Template:Chembox PubChem/format
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Molar mass 350.59 g/mol
Appearance colourless crystals[1]
Odor mercaptan-like[2]
Density 1.398 g/cm3 (43.5 °C)
Melting point Script error: No such module "convert".[4]
Boiling point Script error: No such module "convert". (decomposes)[2]
2 mg/L (25 °C)
log P 4.96 (octanol/water)[3]
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Main hazards combustible, reacts strongly with amines, strong acids, caustics[2]
US health exposure limits (NIOSH):

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This page is a soft redirect. TWA 0.2 mg/m3 ST 0.6 mg/m3 [skin][2] #REDIRECTmw:Help:Magic words#Other
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Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
 14pxY verify (what is10pxY/10pxN?)
Infobox references

Chlorpyrifos (IUPAC name: O,O-diethyl O-3,5,6-trichloropyridin-2-yl phosphorothioate) is a crystalline organophosphate insecticide. 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 use in homes has been banned since 2001 in the U.S.[5] In agriculture, it remains "one of the most widely used organophosphate insecticides", according to the United States Environmental Protection Agency (EPA).[6]

Manufacture and its uses

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

Chlorpyrifos is used around the world to control pest insects in agricultural, residential, and commercial settings, although its use in certain residential applications has been restricted in several countries. According to the Dow Chemical Company, chlorpyrifos is registered for use in nearly 100 countries and is applied to approximately 8.5 million crop acres each year.[7] The crops with the most intense chlorpyrifos use are cotton, corn, almonds, and fruit trees including oranges, bananas and apples.[8]

The U.S. EPA estimated that between 1987 and 1998 about 21 million pounds of chlorpyrifos were used in the United States each year.[9] In 2007, chlorpyrifos was the most commonly used organophosphate pesticide in the United States, with an estimated 8 to 11 million pounds applied.[10]

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).[11][12]

Toxicity and Safety

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

Persistent health effects

Effects from exposure during pregnancy, infancy, and childhood

Epidemiological and experimental animal studies suggest that infants and children are more susceptible than adults to effects from low exposure to chlorpyrifos.[13][14] This susceptibility derives in part because the very young have a decreased capacity to detoxify chlorpyrifos and its metabolites and in part from disruption, observed in animal experiments, in normal developmental processes in the nervous system.[13]

Human studies: In the growing number of epidemiological studies, exposure to chlorpyrifos during pregnancy or childhood has been potentially linked with lower birth weight and neurological changes such as slower motor development and attention problems.[14] Exposure to organophosphate pesticides in general has been increasingly associated with changes in children's cognitive, behavioral, and motor performance.[15]

Animal experiments: In experiments with rats, short-term low-dose exposure to chlorpyrifos early in life has resulted in lasting neurological changes, with larger effects on emotional processing and cognition than on motor skills.[14] Such rats can also exhibit behaviors consistent with depression and reduced anxiety.[14] In rats, low-level exposure during development to chlorpyrifos has its greatest neurotoxic effects during a window in which sex differences in the brain develops, and exposure leads to reductions or reversals of normal rat male-female differences.[16]

In laboratory rats, exposure to low levels of chlorpyrifos early in life or as adults also appears to affect metabolism and body weight.[17] 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.[17]

Effects from exposure during adulthood

Adults may develop lingering health effects following acute exposure or repeated low-level exposure to chlorpyrifos. Among agricultural growers, use of chlorpyrifos has been associated with slightly increased risk of wheeze, a whistling sound while breathing due to obstruction in the airways.[18]

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 likely link between chlorpyrifos application and lung cancer.[19][20]

Acute health effects

For acute effects, the World Health Organization classifies chlorpyrifos as Class II: moderately toxic.[21] The oral LD50 for chlorpyrifos 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.[22]

Symptoms of acute exposure

Acute poisoning with chlorpyrifos results mainly from interference with the acetylcholine neurotransmission pathway (see Mechanisms of Toxicity), leading to a range of neuromuscular symptoms. Relatively mild poisoning can result in watering of the eyes, increased saliva and sweating, nausea, and headache. More 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 inability of the lungs to operate.[23]

Children may exhibit different symptoms than adults. Children are more likely to experience muscle weakness rather than twitching; excessive saliva rather than sweat or tears; seizures; and sleepiness or coma.[23]

Frequency of acute exposure

Acute poisoning with chlorpyrifos is probably most common in agricultural areas in Asia, where many small farmers have access to pesticides.[24] Poisoning may be due to occupational or accidental exposure or intentional self-harm. Precise numbers of chlorpyrifos poisonings globally are not available.[25] Pesticides are estimated to be used in over 200,000 deaths by suicide annually, organophosphate pesticides are thought to contribute two-thirds of ingested pesticides in rural Asia, and chlorpyrifos is among the pesticides commonly used for self-harm in some areas.[24][25][26]

In the United States, the number of incidents of chlorpyrifos exposure reported to the U.S. National Pesticide Information Center reduced sharply from over 200 in the year 2000 to less than 50 in 2003 following the U.S. ban on chlorpyrifos for residential use.[27]


Poisoning by chlorpyrifos and other organophosphate pesticides has been treated with atropine and simultaneously with oximes such as pralidoxime.[28] Atropine blocks acetylcholine from binding with muscarinic receptors, which clearly reduces the impact of organophosphate poisoning. 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.[28] A small randomized controlled trial supported the use of higher doses of pralidoxime rather than lower doses.[29] A subsequent small randomized, controlled, double-blind trial treating patients who self-poisoned with organophosphates found no benefit of treatment with pralidoxime, including specifically in patients poisoned by chlorpyrifos.[30]

In news coverage

Chlorpyrifos poisoning has been described by New Zealand scientists as the likely cause of death of several tourists in Chiang Mai, Thailand who developed myocarditis in 2011.[31][32][33] Thai investigators have come to no conclusion as to what caused the deaths,[34] but maintain that chlorpyrifos was not responsible and that the deaths were not linked.[35]

Mechanisms of toxicity

Acetylcholine neurotransmission

Primarily, chlorpyrifos and other organophosphate pesticides interfere with signaling from the neurotransmitter acetylcholine.[23] One metabolite of chlorpyrifos, chlorpyrifos-oxon, binds permanently to the enzyme acetylcholinesterase, preventing this enzyme from deactivating acetylcholine in the synapse.[13][23] 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.[16] 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 also 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.[36][37] 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.[16][37][38][39]

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.[40] 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.[40] 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.[40] 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.[40]

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.[41] 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.[42] 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.[43] In the lab, in rats and neural cells co-exposed to both nicotine and chlorpyrifos, nicotine appears to protect against acetylcholinesterase inhibition by chlorpyrifos and reduce its effects on neurodevelopment.[44][45][46] In at least one study, nicotine appeared to enhance chlorpyrifos detoxification.[44]

Human exposure

In 2011, EPA estimated that, in the general U.S. population, people consume 0.009 micrograms of chlorpyrifos per kilogram of their body weight per day directly from food residue.[47] 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 maximum acceptable daily dose is 0.3 micrograms/kg/day.[47]

Before chlorpyrifos was restricted from residential use in the U.S., data from 1999-2000 in the national NHANES study detected the metabolite TCPy in 91% of human urine samples tested.[48] In samples collected between 2007 and 2009 from families living in Northern California, TCPy was found in 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.[48] 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.[49]

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 United States to excrete levels of the metabolite TCPy in their urine that are 5 to 10 times greater than levels in the general population.[50][51][52]

Air monitoring studies conducted by the California Air Resources Board (CARB) have documented chlorpyrifos in the air of California communities.[53] Analyses of the CARB data indicate that children living in areas of high chlorpyrifos use are often exposed to levels of the insecticide that exceed levels considered acceptable by the EPA.[54][55] Advocacy groups monitored air samples in Washington and Lindsay, CA, in 2006 with comparable results.[56][57] Grower and pesticide industry groups have argued that the air levels documented in these studies are not high enough to cause significant exposure or adverse effects,[58] but a follow-up biomonitoring study in Lindsay, CA, has shown that people there have higher than normal chlorpyrifos levels in their bodies.[59][60]

Effects on wildlife

Aquatic life

Among freshwater aquatic organisms, crustaceans and insects appear to be more sensitive to acute exposure than are fish or the aquatic life stages of amphibians, although little data may exist for amphibians.[61] Aquatic insects and animals appear to absorb chlorpyrifos directly from water rather than ingesting it with their diet or through contact with sediment.[61]

When concentrated chlorpyrifos has been released into various rivers, it has killed insects, shrimp, and/or 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.[62] 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.[63]


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.[23] Guidelines for the State of Washington indicate that chlorpyrifos products should not be applied to flowering plants such as fruit trees within 4–6 days of blooming to prevent bees from directly contacting the residue.[64]

Risk assessments have primarily considered acute exposure, but more recently researchers have begun to investigate the effects on bees of chronic exposure to low levels of chlorpyrifos through residue in pollen and components of bee hives.[65] A review of studies in the U.S., 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 combined high toxicity to bees and prevalence in pollen and honey, bees are considered to have higher risk from chlorpyrifos exposure via their diet than from many other pesticides.[65]

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.[66] 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.[67] Chlorpyrifos oxon appears to particularly inhibit acetylcholinesterase in bee gut tissue as opposed to head tissue.[67] Other organophosphate pesticides have impaired bee learning and memory of smells in the laboratory.[68]


International law

Chlorpyrifos is not yet regulated under any international law or treaty. Organizations such as PANNA and the NRDC have argued 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.[69]

Outside the United States

Chlorpyrifos is restricted from termite control in Singapore as of 2009[70] and from residential use in South Africa as of 2010.[71]

In 2010, India barred Dow from commercial activity for 5 years[72] after India’s Central Bureau of Investigation found Dow guilty of bribing Indian officials in 2007 to allow the sale of chlorpyrifos.[73]

United States

In the United States, several laws directly or indirectly regulate the use of pesticides including chlorpyrifos. 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).[74]

Chlorpyrifos may be sold in restricted-use products for certified pesticide applicators to use in agriculture and other settings such as golf courses or mosquito control.[75] It may also be sold in ant and roach baits with childproof packaging.[76] 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.[77]


The use of chlorpyrifos in agriculture can leave chemical residue on food commodities. The FFDCA requires the 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.[78][79] These tolerances limit the amount of chlorpyrifos that can be applied to crops. The Food and Drug Administration (FDA) enforces pesticide tolerances established by the EPA and determines “action levels” for the unintended drift of pesticide residues onto crops without tolerances.[80]

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.[81] Chlorpyrifos and its metabolites have approximately 112 tolerances pertaining to food products and supplies.[79][82] In 2006, to reduce children’s exposure, the EPA amended the chlorpyrifos tolerance on apples, grapes and tomatoes, reducing the grape and apple tolerances to 0.01 ppm and eliminating the tolerance on tomatoes.[79] Chlorpyrifos is not allowed on crops such as spinach, squash, carrots, and tomatoes; any chlorpyrifos residue on these crops may represent chlorpyrifos misuse or spray drift.[79]

Food handling establishments, places where food products are held, processed, prepared or served, are also 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.[82] Food items are to be removed or protected during treatment. Food handling establishment tolerances may be modified or exempted under FFDCA sec. 408.[83]

Regulation in 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 Clean Water Act Amendments of 1977 and 1978.[84] The regulation is inclusive of all chlorpyrifos isomers and hydrates in any solution or mixture. EPA has not yet set a drinking water regulatory standard for chlorpyrifos but has established a federal drinking water guideline of 2 ug/L.[85]

In 2009, in order to protect threatened salmon and steelhead under the Clean Water Act and the Endangered Species Act, the 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 toxicity to fish in addition to the standard labeling requirements for all chlorpyrifos-based products.[86] Manufacturers declined to add these limitations.[87] In February 2013 in Dow AgroSciences vs NMFS, the 4th U.S Circuit Court of Appeals vacated EPA’s order for these labeling requirements.[88] 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.[89] These buffers will remain until the EPA makes a permanent decision in consultation with the National Marine Fisheries Service.[90]

Reporting Releases and Spills

The Emergency Planning and Community Right-to-Know Act (EPCRA) designates the chemicals that facilities must report to the Toxics Release Inventory (TRI), based on EPA assessments. Chlorpyrifos is not on the list of chemicals that need to be reported to TRI. Yet, it is on the list of hazardous substances under the Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA), which is also known as the Superfund Act. Therefore, in the event that chlorpyrifos is spilled or released into the environment, in an amount equal to or greater than its reportable quantity of 1 lb or 0.454 kg, facilities are required to notify the National Response Center (NRC) immediately at their toll free number, (800) 424-8802.[91]

In 1995, Dow paid a $732,000 EPA penalty for not sending reports it had received on 249 chlorpyrifos poisoning incidents.[92]

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.[93]

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 from JSH Farms, and the property owner suffered from eye and skin irritation.[94]

Under U.S. 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.[95] Other states are reviewing chlorpyrifos following the federal government’s recommendations for pesticide surveillance.

In 2003, Dow agreed to pay $2 million to the state of New York, in response to a lawsuit filed by the Attorney General to end Dow's illegal 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 listing chlorpyrifos under California’s Prop 65.[99]

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

See also


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  3. ^ Sangster J; LOGKOW Databank. Sangster Res. Lab., Montreal Quebec, Canada (1994)
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  10. ^ Grube, Arthur; Donaldson, David; Kiely, Timothy; Wu, La (2011). Pesticide Industry Sales and Usage Report: 2006 and 2007 Market Estimates (PDF) (Report). U.S. EPA. Retrieved 2014-07-24. 
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  14. ^ a b c d Timofeeva, Olga A.; Levin, Edward D. (2010). "Lasting Behavioral Consequences of Organophosphate Pesticide Exposure During Development". In R. Krieger (ed.). Hayes' Handbook of Pesticide Toxicology (Third Edition). New York: Academic Press. pp. 837–846. ISBN 978-0-12-374367-1. 
  15. ^ Muñoz-Quezada, Maria Teresa; Lucero, Boris A.; Barr, Dana B.; Steenland, Kyle; Levy, Karen; Ryan, P. Barry; Iglesias, Veronica; Alvarado, Sergio; Concha, Carlos; Rojas, Evelyn; Vega, Catalina (2013-12). "Neurodevelopmental effects in children associated with exposure to organophosphate pesticides: A systematic review". NeuroToxicology 39: 158–168. ISSN 0161-813X. PMC 3899350. PMID 24121005. doi:10.1016/j.neuro.2013.09.003. Retrieved 2014-01-17.  Check date values in: |date= (help)
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  17. ^ a b Slotkin, T. A. (2011-04). "Does early-life exposure to organophosphate insecticides lead to prediabetes and obesity?". Reproductive Toxicology. Prenatal Programming and Toxicity II (PPTOX II): Role of Environmental Stressors in the Developmental Origins of Disease 31 (3): 297–301. ISSN 0890-6238. PMC 3025269. PMID 20850519. doi:10.1016/j.reprotox.2010.07.012. Retrieved 2014-08-06.  Check date values in: |date= (help)
  18. ^ Hoppin, Jane A.; Umbach, David M.; London, Stephanie J.; Alavanja, Michael C. R.; Sandler, Dale P. (2002-03-01). "Chemical predictors of wheeze among farmer pesticide applicators in the Agricultural Health Study". American Journal of Respiratory and Critical Care Medicine 165 (5): 683–689. ISSN 1073-449X. PMID 11874814. doi:10.1164/ajrccm.165.5.2106074. Retrieved 2014-06-03. 
  19. ^ "Lung Cancer in the Agricultural Health Study (IA)"
  20. ^ Lee, Won Jin; Blair, Aaron; Hoppin, Jane A.; Lubin, Jay H.; Rusiecki, Jennifer A.; Sandler, Dale P.; Dosemeci, Mustafa; Alavanja, Michael C. R. (2004-12-01). "Cancer incidence among pesticide applicators exposed to chlorpyrifos in the Agricultural Health Study". Journal of the National Cancer Institute 96 (23): 1781–1789. ISSN 0027-8874. PMID 15572760. doi:10.1093/jnci/djh324. Retrieved 2014-07-21. 
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