Chlorpyrifos: Difference between revisions

From Wikipedia, the free encyclopedia
Browse history interactively
← Previous editNext edit →
Content deleted Content added
VisualWikitext
E.Thorsos (talk | contribs)
176 edits
m →‎Manufacture and use: Adjusted language about restrictions on use. Will add an extensive section on chlorpyrifos regulation soon.
E.Thorsos (talk | contribs)
176 edits
→‎Effects on aquatic life and bees: Renamed section; added information known acute aquatic events and bee exposure/effects.
Line 687: Line 687:
}}</ref> In at least one study, nicotine appeared to enhance chlorpyrifos detoxification.<ref name= Lee2010/>
}}</ref> In at least one study, nicotine appeared to enhance chlorpyrifos detoxification.<ref name= Lee2010/>


==Effects on aquatic life and bees==
==Effects on wildlife==
===Aquatic life===
⚫
Chlorpyrifos is highly toxic to amphibians, and a recent study by the [[United States Geological Survey]] found that its main breakdown product in the environment, chlorpyrifos [[Oxon (chemical)|oxon]], is even more toxic to these animals.<ref>[http://www.sciencedaily.com/releases/2007/06/070623213748.htm Breakdown Products Of Widely Used Pesticides Are Acutely Lethal To Amphibians, Study Finds], ''Science Daily'', June 25, 2007. Retrieved July 2, 2006.</ref>
Among freshwater aquatic organisms, [[crustacean]]s and [[insect]]s appear to be more sensitive to acute exposure than are fish or the aquatic life stages of [[amphibian]]s, although little data may exist for amphibians.<ref name=Giddings2014>{{Cite book
| volume = 231
| pages = 119–162
| last = Giddings
| first = Jeffrey
| coauthors = W. Martin Williams, Keith Solomon, John Giesy
| title = Ecological Risk Assessment for Chlorpyrifos in Terrestrial and Aquatic Systems in the United States
| chapter = Risks to Aquatic Organisms from Use of Chlorpyrifos in the United States - Springer
| series = Reviews of Environmental Contamination and Toxicology, Continuation of Residue Reviews
| accessdate = 2014-08-05
| date = 2014
| chapterurl = http://link.springer.com/chapter/10.1007/978-3-319-03865-0_5/fulltext.html
⚫
}}</ref> A study by the [[United States Geological Survey]] suggested that the main breakdown product of chlorpyrifos in the environment, chlorpyrifos [[Oxon (chemical)|oxon]], is more toxic to amphibians than chlorpyrifos.<ref>[http://www.sciencedaily.com/releases/2007/06/070623213748.htm Breakdown Products Of Widely Used Pesticides Are Acutely Lethal To Amphibians, Study Finds], ''Science Daily'', June 25, 2007. Retrieved July 2, 2006.</ref> Aquatic insects and animals appear to absorb chlorpyrifos directly from water rather than ingesting it with their [[diet]] or through contact with [[sediment]].<ref name=Giddings2014 />


When concentrated chlorpyrifos has been released into various rivers, it has killed insects, shrimp, and/or fish. In Britain, the rivers [[River Roding | Roding]] (1985), [[River Ouse, Sussex | Ouse]] (2001), Wey (2002 & 2003), and [[River Kennet | Kennet]] (2013) all experienced insect, shrimp, and/or fish kills as a result of small releases of concentrated chlorpyrifos.<ref>{{cite news|title=Ban on domestic sale of insecticide welcomed by fisheries groups|url=http://www.fishupdate.com/news/archivestory.php/aid/20089/Ban_on_domestic_sale_of_insecticide_welcomed_by_fisheries_groups.html|accessdate=5 August 2014|publisher=FishUpdate.com|date=28 August, 2013}}</ref> 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.<ref>{{cite news|last1=Case|first1=Philip|title=Domestic source 'likely' cause of Kennet pollution|url=http://www.fwi.co.uk/articles/01/10/2013/141331/domestic-source-39likely39-cause-of-kennet-pollution.htm|publisher=Farmers Weekly|date=01 October 2013}}</ref> The pesticide entered the River Kennet from the Marlborough Water Treatment Works. Subsequently, freshwater shrimp, caddis fly, and mayfly in the river were killed downstream.
The substance is very toxic for aquaculture fish<ref>[http://npic.orst.edu/factsheets/chlorptech.pdf Chlorpyrifos Technical Fact Sheet], ''National Pesticide Information Center'', August, 2009. Retrieved July 1, 2013.</ref>and [[bee]]s.

===Bees===
{{Main|Pesticide toxicity to 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.<ref name=Christensen2009 /> 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.<ref>{{cite web|last1=Washington State Department of Agriculture|title=Bee Kill Prevention for Tree Fruits|url=http://agr.wa.gov/Pestfert/Pesticides/docs/BeeKillPreventionTreeFruits.pdf|accessdate=5 August 2014}}</ref>

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.<ref name=Sanchez-Bayo2014>{{Cite journal
| doi = 10.1371/journal.pone.0094482
| volume = 9
| issue = 4
| pages = –94482
| last = Sanchez-Bayo
| first = Francisco
| coauthors = Koichi Goka
| title = Pesticide Residues and Bees – A Risk Assessment
| journal = PLoS ONE
| accessdate = 2014-08-05
| date = 2014-04-09
| url = http://dx.doi.org/10.1371/journal.pone.0094482
}}</ref> 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.<ref name=Sanchez-Bayo2014 />

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.<ref>{{Cite journal
| doi = 10.1371/journal.pone.0077547
| issn = 1932-6203
| volume = 9
| issue = 1
| pages = –77547
| last = Zhu
| first = Wanyi
| coauthors = Daniel R Schmehl, Christopher A Mullin, James L Frazier
| title = Four common pesticides, their mixtures and a formulation solvent in the hive environment have high oral toxicity to honey bee larvae
| journal = PloS one
| date = 2014
| pmid = 24416121
| pmc = PMC3885384
}}</ref> 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.<ref name=Williamson2013>{{Cite journal
| doi = 10.3389/fphys.2013.00013
| volume = 4
| pages = 13
| last = Williamson
| first = Sally M.
| coauthors = Christopher Moffat, Martha Gomersall, Nastja Saranzewa, Christopher Connolly, Geraldine A. Wright
| title = Exposure to acetylcholinesterase inhibitors alters the physiology and motor function of honeybees
| journal = Invertebrate Physiology
| accessdate = 2014-08-05
| date = 2013
| url = http://journal.frontiersin.org/Journal/10.3389/fphys.2013.00013/full
}}</ref> Chlorpyrifos oxon appears to particularly inhibit acetylcholinesterase in bee gut tissue as opposed to head tissue.<ref name=Williamson2013 /> Other organophosphate pesticides have impaired bee learning and memory of smells in the laboratory.<ref>{{Cite journal
| doi = 10.1242/jeb.083931
| issn = 0022-0949, 1477-9145
| volume = 216
| issue = 10
| pages = 1799–1807
| last = Williamson
| first = Sally M.
| coauthors = Geraldine A. Wright
| title = Exposure to multiple cholinergic pesticides impairs olfactory learning and memory in honeybees
| journal = The Journal of Experimental Biology
| accessdate = 2014-02-18
| date = 2013-05-15
| url = http://jeb.biologists.org/content/216/10/1799
| pmid = 23393272
}}</ref>


==Exposure==
==Exposure==

Revision as of 21:30, 5 August 2014

Chlorpyrifos
Names
IUPAC name
O,O-Diethyl O-3,5,6-trichloropyridin-2-yl phosphorothioate
Other names
Brodan, Detmol UA, Dowco 179, Dursban, Empire, Eradex, Lorsban, Paqeant, Piridane, Scout, Stipend and Tricel.
Identifiers
3D model (JSmol)
ChEBI
ChEMBL
ChemSpider
ECHA InfoCard 100.018.969 Edit this at Wikidata
KEGG
UNII
  • InChI=1S/C9H11Cl3NO3PS/c1-3-14-17(18,15-4-2)16-9-7(11)5-6(10)8(12)13-9/h5H,3-4H2,1-2H3 checkY
    Key: SBPBAQFWLVIOKP-UHFFFAOYSA-N checkY
  • InChI=1/C9H11Cl3NO3PS/c1-3-14-17(18,15-4-2)16-9-7(11)5-6(10)8(12)13-9/h5H,3-4H2,1-2H3
    Key: SBPBAQFWLVIOKP-UHFFFAOYAG
  • Clc1c(OP(=S)(OCC)OCC)nc(Cl)c(Cl)c1
Properties
C9H11Cl3NO3PS
Molar mass 350.59 g/mol
Appearance colourless crystals[1]
Density 1.398 g/cm3 (43.5 °C)
Melting point 42 °C[2]
2 mg/L (25 °C)
log P 4.96 (octanol/water)[3]
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
checkY verify (what is checkY☒N ?)

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.[4] In agriculture, it remains "one of the most widely used organophosphate insecticides", according to the United States Environmental Protection Agency (EPA).[5]

Manufacture and use

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.[6] The crops with the most intense chlorpyrifos use are cotton, corn, almonds, and fruit trees including oranges, bananas and apples.[7]

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

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]

History

First registered in 1965 and marketed by Dow Chemical under the tradenames Dursban, Lorsban and Renoban, chlorpyrifos was a well known home and garden insecticide, and at one time it was one of the most widely used household pesticides in the US.

In 1995, Dow was fined US$732,000 for not sending the EPA reports it had received on 249 chlorpyrifos poisoning incidents.

Facing impending regulatory action by the EPA,[12] Dow agreed to withdraw registration of chlorpyrifos for almost all use (except child-proof containerized insect baits) in homes and other places where children could be exposed, and severely restricted its use on crops. These changes took effect on Dec 31, 2001.[5][13] It is still widely used in agriculture, and Dow continues to market Dursban for home use in developing countries. Dow's sales literature claimed Dursban has "an established record of safety regarding humans and pets."[14]

In 2003, Dow agreed to pay US$2 million – the largest penalty ever in a pesticide case – 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".[15]

On July 31, 2007, a coalition of farmworker and advocacy groups filed a lawsuit against the EPA seeking to end agricultural use of chlorpyrifos. The suit claims that the continued use of chlorpyrifos poses an unnecessary risk to farmworkers and their families.[16] The suit was still pending as of August 2012.[4]

In August 2007, Dow's Indian offices were raided by Indian authorities for allegedly bribing officials to allow chlorpyrifos to be sold in the country.[17]

In 2008, the National Marine Fisheries Service (NMFS) imposed 1000 ft buffer zones around salmon habitat to protect endangered salmon and steelhead species. Aerial applications of chlorpyrifos will be prohibited within these zones.[18]

Health effects

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

Infants and children are more susceptible than adults to effects from low exposure to chlorpyrifos. Early-life low-level exposure in children has been associated with changes in childhood and later in life, including lower birth weight;[19] increased rates of attention deficit hyperactivity disorder (ADHD) and pervasive developmental disorder at age 3;[20][21] and poorer memory, lower IQ, and delays in motor development at age 7.[22] MRI brain scans of children exposed to chlorpyrifos from residential use at levels too low to show acute symptoms demonstrated enlargements in brain regions involved in attention, language comprehension, social cognition, the reward system, and emotion.[23] These MRIs also demonstrated that several brain structures – the right inferior parietal lobule and the supramarginal gyrus, which are involved in language, empathy, mathematics, and sensory interpretation – in these exposed children did not show expected sex differences.[23] In another portion of the brain – the medial superior frontal gyrus, involved in social cognition – sex differences were reversed.

In experiments with animals, short-term low-dose exposure to chlorpyrifos early in life can result in lasting neurological changes, with larger effects on emotional processing and cognition than on motor skills.[20] Such rats can also exhibit behaviors consistent with depression and reduced anxiety.[20][24] In rats, low-level exposure during development to chlorpyrifos has its greatest neurotoxic effects during a window in which sex differences in the brain develop, leading to sex-specific responses to exposure.[25] After exposure during this period, there are reductions or reversals of normal rat male-female differences.[25][26]

Early-life exposure to low levels of chlorpyrifos may also affect the immune system and metabolism. Rats exposed immediately after birth to chlorpyrifos showed reduced T-cell production as adults.[27] Male, but not female, rats exposed to chlorpyrifos in utero and through their mother’s milk gained extra weight after weaning, likely due to a doubling of fatty tissues.[28] Further, adult male, but not female, rats that had been exposed to low doses of chlorpyrifos immediately after birth had high cholesterol and triglycerides.[29]

In several studies, children who produce low levels of the enzyme paraoxonase 1 (PON1), or whose mothers show low levels of PON1 activity, and who were also exposed to chlorpyrifos in utero or otherwise early in life exhibited smaller head circumference at birth, reduced mental development,[30] and higher body fat, higher blood pressure, and pre-diabetic metabolic indicators.[31]

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.[32]

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.[33][34]

A 2011 study on the neurotoxic effects of chlorpyrifos showed that chlorpyrifos and its more toxic metabolite, chlorpyrifos oxon, altered firing rates in the locus coeruleus. These results indicate that the pesticide may be involved in Gulf War Syndrome and other neurodegenerative disorders.[35]

Acute health effects

For acute effects, the World Health Organization classifies chlorpyrifos as Class II: moderately toxic.[36] 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.[37]

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.[38]

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.[38]

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.[39] Poisoning may be due to occupational or accidental exposure or intentional self-harm. Precise numbers of chlorpyrifos poisonings globally are not available.[40] 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.[39][40][41]

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.[42]

Treatment

Poisoning by chlorpyrifos and other organophosphate pesticides has been treated with atropine and simultaneously with oximes such as pralidoxime.[43] 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.[43] A small randomized controlled trial supported the use of higher doses of pralidoxime rather than lower doses.[44] 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.[45]

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.[46][47][48] Thai investigators have come to no conclusion as to what caused the deaths,[49] but maintain that chlorpyrifos was not responsible and that the deaths were not linked.[50]

Mechanisms of toxicity

Chlorpyrifos affects the nervous system and development through several mechanisms. Primarily chloryrifos interferes with the enzyme acetylcholinesterase. Chlorpyrifos also affects neurotransmitters, enzymes, and cell signaling pathways at doses below those that substantially inhibit acetylcholinesterase. The mechanisms for these effects remain to be fully characterized.[51]

Acetylcholine neurotransmission

Chlorpyrifos and other organophosphate pesticides interfere with signaling from the neurotransmitter acetylcholine.[38] One metabolite of chlorpyrifos, chlorpyrifos-oxon, binds permanently to the enzyme acetylcholinesterase, preventing this enzyme from deactivating acetylcholine in the synapse.[38][52] 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.[25] This mechanism is well established for acute chlorpyrifos poisoning and also some lower-dose health impacts. It is also the primary insecticidal mechanism.

Broad-spectrum effects

One study looked for changes in the expression of 252 genes in rats related to known developmental outcomes from exposure to low doses of chlorpyrifos.[53] Chlorpyrifos exposure for several days immediately after birth led to substantial changes in transcription of genes that affect growth and differentiation of neurons, development of glia and myelin, programmed cell death by apoptosis, cAMP cell signaling, oxidative stress, and neuronal damage by overstimulation. Exposure also altered genes involved in the neurotransmission pathways of acetylcholine, serotonin, norepinephrine, and dopamine, including neurotransmitter synthesis, storage, and membrane receptors.[53]

Serotonin

Low doses of chlorpyrifos have also been observed to enhance, in cell cultures and in developing rats, production of receptors and transporters in the serotonin signaling pathway.[54][55] In rats, exposure during critical prenatal and postnatal developmental windows can permanently increase gene expression in this pathway later in life and also increase serotonin removal from the synapse.[56] Parallel results indicate that, in adulthood, rats exposed to chlorpyrifos during these periods exhibit signs of depression.[24] The study authors propose that chlorpyrifos may reduce the responsiveness of postsynaptic cells to serotonin, resulting in compensatory increased serotonin activity in the presynaptic cells.[56] In rats, the serotonin pathway is most sensitive to chlorpyrifos exposure during late gestation and immediately after birth, which is also when rat brains develop sex-specific differences.[25] Exposure to chlorpyrifos during this window leads to sex-specific impacts, with greater effects on male rats than on female rats; outside of this window effects are similar regardless of sex.

CREB-binding protein

Low doses of chlorpyrifos and several of its metabolites (chlorpyrifos-oxon and trichloropyridinol) have, in neural cell cultures, phosphorylated and activated the Ca2+/cAMP response element binding protein, which instigates transcription of many transcription factors important to development.[57]

Other enzymes

In an in vivo study of mouse brain tissue, chlorpyrifos-oxon inhibited several enzymes that, like acetylcholinesterase, are in the serine hydrolase enzyme family, including monoacylglycerol lipase (MAGL), fatty acid amide hydrolase (FAAL), and hormone-sensitive lipase (HSL).[58] MAGL and FAAH are endocannabinoid enzymes, and reduced FAAH activity in mice results in decreased sensitivity to pain and anxiety. The effects of MAGL and HSL inhibition are less well understood. Both enzymes are involved in mobilizing stored fats.[58]

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.[30] 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.[30] 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.[30] 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.[30]

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.[59] 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.[60] 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.[61] 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.[62][63][64] In at least one study, nicotine appeared to enhance chlorpyrifos detoxification.[62]

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.[65] A study by the United States Geological Survey suggested that the main breakdown product of chlorpyrifos in the environment, chlorpyrifos oxon, is more toxic to amphibians than chlorpyrifos.[66] Aquatic insects and animals appear to absorb chlorpyrifos directly from water rather than ingesting it with their diet or through contact with sediment.[65]

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.[67] 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.[68] The pesticide entered the River Kennet from the Marlborough Water Treatment Works. Subsequently, freshwater shrimp, caddis fly, and mayfly in the river were killed downstream.

Bees

Main article: Pesticide toxicity to 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.[38] 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.[69]

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.[70] 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.[70]

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.[71] 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.[72] Chlorpyrifos oxon appears to particularly inhibit acetylcholinesterase in bee gut tissue as opposed to head tissue.[72] Other organophosphate pesticides have impaired bee learning and memory of smells in the laboratory.[73]

Exposure

A body burden study conducted by the Centers for Disease Control and Prevention found TCPy, a metabolite specific to chlorpyrifos, in the urine of 91% of people tested.[74] An independent analysis of the CDC data claims that Dow has contributed 80% of the chlorpyrifos body burden of people living in the US.[75] A 2008 study found dramatic drops in the urinary levels of chlorpyrifos metabolites when children switched from conventional to organic diets.[76]

Air monitoring studies conducted by the California Air Resources Board (CARB) have documented chlorpyrifos in the air of California communities.[77] 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.[78][79] Recent air monitoring studies in Washington and Lindsay, CA have yielded comparable results.[80][81] 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,[82] but a follow-up biomonitoring study in Lindsay, CA has shown that people there have higher than normal chlorpyrifos levels in their bodies.[83][84]

A study of the effects of chlorpyrifos on humans exposed over time showed that people exposed to high levels have autoimmune antibodies that are common in people with autoimmune disorders. There is a strong correlation to chronic illness associated with autoimmune disorders after exposure to chlorpyrifos.[85]

Before it was banned from residential use in the US, chlorpyrifos was detected in 100% of personal indoor air samples and 70% of umbilical-cord blood collected from pregnant women 18–35 years old who self-identified as African American or Dominican and living in New York City public housing.[86]

See also

References

  1. ^ a b Muller, Franz, ed. (2000). Agrochemicals: Composition, Production, Toxicology, Applications. Toronto: Wiley-VCH. p. 541. ISBN 3-527-29852-5.
  2. ^ Lide, David R. (1998). Handbook of Chemistry and Physics (87 ed.). Boca Raton, FL: CRC Press. pp. 3–126. ISBN 0-8493-0594-2.
  3. ^ Sangster J; LOGKOW Databank. Sangster Res. Lab., Montreal Quebec, Canada (1994)
  4. ^ a b "Common Insecticide May Harm Boys' Brains More Than Girls". Scientific American. August 21, 2012.
  5. ^ a b "Reregistration Eligibility Decision for Chlorpyrifos" (PDF). July 31, 2006.
  6. ^ The Dow Chemical Company. "Chlorpyrifos and Responsible Use". Retrieved July 24, 2014.
  7. ^ "NASS Agricultural Chemical Database". Pestmanagement.info. Retrieved November 20, 2011.
  8. ^ U.S. EPA (2002). "Interim Reregistration Eligibility Decision for Chlorpyrifos" (PDF). Retrieved July 24, 2014.
  9. ^ Grube, A. (2011). Pesticide Industry Sales and Usage Report: 2006 and 2007 Market Estimates (PDF) (Report). U.S. EPA. Retrieved July 24, 2014. {{cite report}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  10. ^ http://www.cdms.net/ldat/ld0AT004.pdf
  11. ^ http://www.farmoz.com.au/label/farmoz/STRIKE_OUT_500WP_16103844.pdf
  12. ^ EPA administrator's announcement, June 9, 2000
  13. ^ EPA's Chlorpyrifos Page (archived on archive.org)
  14. ^ "Bhopal.net". Bhopal.net. June 8, 2000. Retrieved November 20, 2011.
  15. ^ "Dow AgroSiences agrees to pay $2M to state over pesticide ads". The Business Review. December 15, 2003.
  16. ^ Press Release: Lawsuit Challenges EPA on Deadly Pesticide, EarthJustice, July 31, 2007.
  17. ^ CBI raids Dow Chemical's Indian subsidiary for graft. Monsters and Critics, August 21, 2007.
  18. ^ "Federal Government Announces Plan to Protect Salmon from Pesticides". Earthjustice. November 18, 2008.
  19. ^ Whyatt, Robin M. (2004-07). "Prenatal insecticide exposures and birth weight and length among an urban minority cohort". Environmental Health Perspectives. 112 (10): 1125–1132. doi:10.1289/ehp.6641. ISSN 0091-6765. PMC 1247388. PMID 15238288. Retrieved 2014-07-07. {{cite journal}}: Check date values in: |date= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)CS1 maint: PMC format (link)
  20. ^ a b c Timofeeva, Olga A. (2010). "Lasting Behavioral Consequences of Organophosphate Pesticide Exposure During Development". Hayes' Handbook of Pesticide Toxicology (Third Edition). New York: Academic Press. pp. 837–846. ISBN 978-0-12-374367-1. {{cite book}}: |access-date= requires |url= (help); External link in |chapterurl= (help); Unknown parameter |chapterurl= ignored (|chapter-url= suggested) (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |editors= ignored (|editor= suggested) (help)
  21. ^ Rauh, Virginia A. (December 1, 2006). "Impact of prenatal chlorpyrifos exposure on neurodevelopment in the first 3 years of life among inner-city children". Pediatrics. 118 (6): –1845-e1859. doi:10.1542/peds.2006-0338. ISSN 1098-4275 0031-4005, 1098-4275. PMID 17116700. Retrieved July 21, 2014. {{cite journal}}: Check |issn= value (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  22. ^ Rauh, Virginia (April 21, 2011). "Seven-Year Neurodevelopmental Scores and Prenatal Exposure to Chlorpyrifos, a Common Agricultural Pesticide". Environmental Health Perspectives. 119 (8): 1196–1201. doi:10.1289/ehp.1003160. ISSN 0091-6765. Retrieved August 29, 2013. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  23. ^ a b Rauh, Virginia A. (May 15, 2012). "Brain anomalies in children exposed prenatally to a common organophosphate pesticide". Proceedings of the National Academy of Sciences. 109 (20): 7871–7876. doi:10.1073/pnas.1203396109. ISSN 1091-6490 0027-8424, 1091-6490. PMID 22547821. Retrieved April 8, 2014. {{cite journal}}: Check |issn= value (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  24. ^ a b Aldridge, Justin E. (2005-05). "Developmental exposure of rats to chlorpyrifos leads to behavioral alterations in adulthood, involving serotonergic mechanisms and resembling animal models of depression". Environmental Health Perspectives. 113 (5): 527–531. doi:10.1289/ehp.7867. ISSN 0091-6765. PMC 1257542. PMID 15866758. Retrieved 2014-07-02. {{cite journal}}: Check date values in: |date= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)CS1 maint: PMC format (link)
  25. ^ a b c d Connors, Susan L. (2008-03). "Fetal Mechanisms in Neurodevelopmental Disorders". Pediatric Neurology. 38 (3): 163–176. doi:10.1016/j.pediatrneurol.2007.10.009. ISSN 0887-8994. Retrieved 2014-07-10. {{cite journal}}: Check date values in: |date= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  26. ^ Levin, Edward D. (2001). "Persistent behavioral consequences of neonatal chlorpyrifos exposure in rats". Developmental Brain Research. 130: 83–89. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  27. ^ Navarro, H. A (October 24, 2001). "Neonatal chlorpyrifos administration elicits deficits in immune function in adulthood: a neural effect?". Developmental Brain Research. 130 (2): 249–252. doi:10.1016/S0165-3806(01)00254-1. ISSN 0165-3806. Retrieved July 21, 2014. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  28. ^ Lassiter, T. Leon (2008-03). "Rats gain excess weight after developmental exposure to the organophosphorothionate pesticide, chlorpyrifos". Neurotoxicology and Teratology. 30 (2): 125–130. doi:10.1016/j.ntt.2007.10.004. ISSN 0892-0362. Retrieved 2014-07-09. {{cite journal}}: Check date values in: |date= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  29. ^ Slotkin, Theodore A. (2005-10). "Developmental exposure of rats to chlorpyrifos elicits sex-selective hyperlipidemia and hyperinsulinemia in adulthood". Environmental Health Perspectives. 113 (10): 1291–1294. doi:10.1289/ehp.8133. ISSN 0091-6765. PMC 1281268. PMID 16203236. Retrieved 2014-07-21. {{cite journal}}: Check date values in: |date= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)CS1 maint: PMC format (link)
  30. ^ a b c d e Costa, Lucio G. (May 10, 2013). "Paraoxonase 1 (PON1) as a genetic determinant of susceptibility to organophosphate toxicity". Toxicology. Emerging health issues from chronic pesticide exposure: Innovative methodologies and effects on molecular cell and tissue level. 307: 115–122. doi:10.1016/j.tox.2012.07.011. ISSN 0300-483X. Retrieved July 9, 2014. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  31. ^ Andersen, Helle R. (May 15, 2012). "Paraoxonase 1 polymorphism and prenatal pesticide exposure associated with adverse cardiovascular risk profiles at school age". PLoS ONE. 7 (5): –36830. doi:10.1371/journal.pone.0036830. Retrieved July 9, 2014. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)CS1 maint: unflagged free DOI (link)
  32. ^ Hoppin, Jane A (March 1, 2002). "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. doi:10.1164/ajrccm.165.5.2106074. ISSN 1073-449X. Retrieved June 3, 2014. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  33. ^ "Lung Cancer in the Agricultural Health Study (IA)" http://aghealth.nci.nih.gov/pdfs/IALungCancer2006.pdf
  34. ^ Lee, Won Jin (December 1, 2004). "Cancer incidence among pesticide applicators exposed to chlorpyrifos in the Agricultural Health Study". Journal of the National Cancer Institute. 96 (23): 1781–1789. doi:10.1093/jnci/djh324. ISSN 1460-2105 0027-8874, 1460-2105. PMID 15572760. Retrieved July 21, 2014. {{cite journal}}: Check |issn= value (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  35. ^ Cao, Jun-li , Varnell, Andrew, and Cooper, Donald.(2011) Gulf War Syndrome: A role for organophosphate induced plasticity of locus coeruleus neurons. Available from Nature Precedings <http://hdl.handle.net/10101/npre.2011.6057.1> (2011)
  36. ^ World Health Organization (2010). The WHO Recommended Classification of Pesticides by Hazard and Guidelines to Classification 2009 (Report). World Health Organization. Retrieved July 9, 2014.
  37. ^ "Chlorpyrifos". Pmep.cce.cornell.edu. Retrieved November 20, 2011.
  38. ^ a b c d e Christensen, K. (2009). "Chlorpyrifos Technical Fact Sheet". National Pesticide Information Center. Retrieved July 3, 2014. {{cite web}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  39. ^ a b Eddleston, M. (November 1, 2000). "Patterns and problems of deliberate self‐poisoning in the developing world". QJM. 93 (11): 715–731. doi:10.1093/qjmed/93.11.715. ISSN 1460-2393 1460-2725, 1460-2393. PMID 11077028. Retrieved July 9, 2014. {{cite journal}}: Check |issn= value (help)
  40. ^ a b Gunnell, David (December 21, 2007). "The global distribution of fatal pesticide self-poisoning: Systematic review". BMC Public Health. 7: 357. doi:10.1186/1471-2458-7-357. ISSN 1471-2458. PMC 2262093. PMID 18154668. Retrieved July 9, 2014. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link)
  41. ^ Eddleston, Michael (October 28, 2005). "Differences between organophosphorus insecticides in human self-poisoning: a prospective cohort study". The Lancet. 366 (9495): 1452–1459. doi:10.1016/S0140-6736(05)67598-8. ISSN 0140-6736. Retrieved July 7, 2014. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  42. ^ Stone, David L (April 20, 2009). "Longitudinal trends in organophosphate incidents reported to the National Pesticide Information Center, 1995-2007". Environmental Health. 8: 18. doi:10.1186/1476-069X-8-18. ISSN 1476-069X. PMC 2673208. PMID 19379510. Retrieved July 9, 2014. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link)
  43. ^ a b Buckley, Nick A (2011). "Oximes for acute organophosphate pesticide poisoning". Cochrane Database of Systematic Reviews. John Wiley & Sons, Ltd. ISBN 1465-1858. {{cite book}}: |access-date= requires |url= (help); Check |isbn= value: length (help); External link in |chapterurl= (help); Unknown parameter |chapterurl= ignored (|chapter-url= suggested) (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  44. ^ Pawar, Kirti S (December 22, 2006). "Continuous pralidoxime infusion versus repeated bolus injection to treat organophosphorus pesticide poisoning: a randomised controlled trial". The Lancet. 368 (9553): 2136–2141. doi:10.1016/S0140-6736(06)69862-0. ISSN 0140-6736. Retrieved July 9, 2014. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  45. ^ Eddleston, Michael (2009-06). "Pralidoxime in acute organophosphorus insecticide poisoning--A randomised controlled trial". PLoS Medicine. 6 (6). doi:10.1371/journal.pmed.1000104. ISSN 1549-1277. PMC 2696321. PMID 19564902. Retrieved 2014-07-09. {{cite journal}}: Check date values in: |date= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link)
  46. ^ "Toxin 'likely' cause of Sarah Carter's death". stuff.co.nz. Retrieved May 8, 2011.
  47. ^ "Sarah Carter's likely cause of death – insecticide". 3 News.
  48. ^ "Thailand death cover-up suspected". NZ Herald Online. May 9, 2011.
  49. ^ Hayden Donnell (May 11, 2011). "Thai experts: Bed bug spray didn't kill Kiwi tourist". The New Zealand Herald. Retrieved May 11, 2011.
  50. ^ "Thais deny tourists' deaths linked". Dominion Post. May 26, 2011. Retrieved May 26, 2011.
  51. ^ Slotkin, Theodore A (July 15, 2004). "Cholinergic systems in brain development and disruption by neurotoxicants: nicotine, environmental tobacco smoke, organophosphates". Toxicology and Applied Pharmacology. 198 (2): 132–151. doi:10.1016/j.taap.2003.06.001. ISSN 0041-008X. Retrieved August 12, 2013.
  52. ^ Flaskos, John (February 25, 2012). "The developmental neurotoxicity of organophosphorus insecticides: A direct role for the oxon metabolites". Toxicology Letters. 209 (1): 86–93. doi:10.1016/j.toxlet.2011.11.026. ISSN 0378-4274. Retrieved July 3, 2014.
  53. ^ a b Slotkin, Theodore A. (May 30, 2007). "Comparative developmental neurotoxicity of organophosphates in vivo: Transcriptional responses of pathways for brain cell development, cell signaling, cytotoxicity and neurotransmitter systems". Brain Research Bulletin. 72 (4–6): 232–274. doi:10.1016/j.brainresbull.2007.01.005. ISSN 0361-9230. Retrieved July 3, 2014. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  54. ^ Slotkin, Theodore A. (December 1, 2008). "Developmental neurotoxicants target neurodifferentiation into the serotonin phenotype: Chlorpyrifos, diazinon, dieldrin and divalent nickel". Toxicology and Applied Pharmacology. 233 (2): 211–219. doi:10.1016/j.taap.2008.08.020. ISSN 0041-008X. Retrieved July 3, 2014. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  55. ^ Aldridge, Justin E. (2005-08). "Alterations in central nervous system serotonergic and dopaminergic synaptic activity in adulthood after prenatal or neonatal chlorpyrifos exposure". Environmental Health Perspectives. 113 (8): 1027–1031. doi:10.1289/ehp.7968. ISSN 0091-6765. PMC 1280344. PMID 16079074. Retrieved 2014-07-03. {{cite journal}}: Check date values in: |date= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)CS1 maint: PMC format (link)
  56. ^ a b Cite error: The named reference Aldridge2005b was invoked but never defined (see the help page).
  57. ^ Schuh, Rosemary A. (July 15, 2002). "Noncholinesterase mechanisms of chlorpyrifos neurotoxicity: Altered phosphorylation of Ca2+/cAMP response rlement binding protein in cultured neurons". Toxicology and Applied Pharmacology. 182 (2): 176–185. doi:10.1006/taap.2002.9445. ISSN 0041-008X. Retrieved July 2, 2014. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  58. ^ a b Casida, John E. (September 25, 2008). "Organophosphate-sensitive lipases modulate brain lysophospholipids, ether lipids and endocannabinoids". Chemico-Biological Interactions. Proceedings of the IX International Meeting on Cholinesterases. 175 (1–3): 355–364. doi:10.1016/j.cbi.2008.04.008. ISSN 0009-2797. Retrieved July 2, 2014. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  59. ^ Slotkin, Theodore A. (2013-05). "Prenatal dexamethasone augments the sex-selective developmental neurotoxicity of chlorpyrifos: Implications for vulnerability after pharmacotherapy for preterm labor". Neurotoxicology and Teratology. 37: 1–12. doi:10.1016/j.ntt.2013.02.002. ISSN 0892-0362. Retrieved 2014-07-10. {{cite journal}}: Check date values in: |date= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  60. ^ Slotkin, Theodore A. (2014-01). "Prenatal dexamethasone, as used in preterm labor, worsens the impact of postnatal chlorpyrifos exposure on serotonergic pathways". Brain Research Bulletin. 100: 44–54. doi:10.1016/j.brainresbull.2013.10.014. ISSN 0361-9230. Retrieved 2014-07-21. {{cite journal}}: Check date values in: |date= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  61. ^ Levin, Edward D. (2014-01). "Prenatal dexamethasone augments the neurobehavioral teratology of chlorpyrifos: Significance for maternal stress and preterm labor". Neurotoxicology and Teratology. 41: 35–42. doi:10.1016/j.ntt.2013.10.004. ISSN 0892-0362. Retrieved 2014-07-21. {{cite journal}}: Check date values in: |date= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  62. ^ a b Lee, Sookwang (March 30, 2010). "Effect of in vivo nicotine exposure on chlorpyrifos pharmacokinetics and pharmacodynamics in rats". Chemico-Biological Interactions. 184 (3): 449–457. doi:10.1016/j.cbi.2010.01.024. ISSN 0009-2797. Retrieved July 21, 2014. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  63. ^ Billauer-Haimovitch, Hana (December 28, 2009). "Reversal of chlorpyrifos neurobehavioral teratogenicity in mice by nicotine administration and neural stem cell transplantation". Behavioural Brain Research. 205 (2): 499–504. doi:10.1016/j.bbr.2009.08.006. ISSN 0166-4328. Retrieved July 21, 2014. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  64. ^ Qiao, Dan (December 30, 2003). "Nicotine is a developmental neurotoxicant and neuroprotectant: stage-selective inhibition of DNA synthesis coincident with shielding from effects of chlorpyrifos". Developmental Brain Research. Role of Prenatal Drugs of Abuse on Neuronal Development. 147 (1–2): 183–190. doi:10.1016/S0165-3806(03)00222-0. ISSN 0165-3806. Retrieved July 21, 2014. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  65. ^ a b Giddings, Jeffrey (2014). "Risks to Aquatic Organisms from Use of Chlorpyrifos in the United States - Springer". Ecological Risk Assessment for Chlorpyrifos in Terrestrial and Aquatic Systems in the United States. Reviews of Environmental Contamination and Toxicology, Continuation of Residue Reviews. Vol. 231. pp. 119–162. {{cite book}}: |access-date= requires |url= (help); External link in |chapterurl= (help); Unknown parameter |chapterurl= ignored (|chapter-url= suggested) (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  66. ^ Breakdown Products Of Widely Used Pesticides Are Acutely Lethal To Amphibians, Study Finds, Science Daily, June 25, 2007. Retrieved July 2, 2006.
  67. ^ "Ban on domestic sale of insecticide welcomed by fisheries groups". FishUpdate.com. 28 August, 2013. Retrieved 5 August 2014. {{cite news}}: Check date values in: |date= (help)
  68. ^ Case, Philip (01 October 2013). "Domestic source 'likely' cause of Kennet pollution". Farmers Weekly. {{cite news}}: Check date values in: |date= (help)
  69. ^ Washington State Department of Agriculture. "Bee Kill Prevention for Tree Fruits" (PDF). Retrieved August 5, 2014.
  70. ^ a b Sanchez-Bayo, Francisco (April 9, 2014). "Pesticide Residues and Bees – A Risk Assessment". PLoS ONE. 9 (4): –94482. doi:10.1371/journal.pone.0094482. Retrieved August 5, 2014. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)CS1 maint: unflagged free DOI (link)
  71. ^ Zhu, Wanyi (2014). "Four common pesticides, their mixtures and a formulation solvent in the hive environment have high oral toxicity to honey bee larvae". PloS one. 9 (1): –77547. doi:10.1371/journal.pone.0077547. ISSN 1932-6203. PMC 3885384. PMID 24416121. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link)
  72. ^ a b Williamson, Sally M. (2013). "Exposure to acetylcholinesterase inhibitors alters the physiology and motor function of honeybees". Invertebrate Physiology. 4: 13. doi:10.3389/fphys.2013.00013. Retrieved August 5, 2014. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)CS1 maint: unflagged free DOI (link)
  73. ^ Williamson, Sally M. (May 15, 2013). "Exposure to multiple cholinergic pesticides impairs olfactory learning and memory in honeybees". The Journal of Experimental Biology. 216 (10): 1799–1807. doi:10.1242/jeb.083931. ISSN 1477-9145 0022-0949, 1477-9145. PMID 23393272. Retrieved February 18, 2014. {{cite journal}}: Check |issn= value (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  74. ^ CDC Third National Exposure Report[dead link]
  75. ^ ""Chemical Trepass," Pesticide Action Network North America, 2004". Panna.org. November 3, 2011. Retrieved November 20, 2011.
  76. ^ Lu, Chensheng; Dana B. Barr; Melanie A. Pearson; Lance A. Waller (2008). "Dietary Intake and Its Contribution to Longitudinal Organophosphorus Pesticide Exposure in Urban/Suburban Children". Environ. Health Perspect. (116): 537–542. doi:10.1289/ehp.10912. PMC 2290988. PMID 18414640.
  77. ^ "CARB Chlorpyrifos Monitoring Studies". Cdpr.ca.gov. Retrieved November 20, 2011.
  78. ^ "S Lee et al., Environmental Health Perspectives, 2002, 110, 1175–1184". Ehponline.org. doi:10.1289/ehp.021101175. Retrieved November 20, 2011.
  79. ^ S Kegley et al., "Secondhand Pesticides", Pesticide Action Network North America, 2003[dead link]
  80. ^ C Dansereau et al., "Poisons on the Wind", Farm Worker Pesticide Project, 2006[dead link]
  81. ^ S Kegley et al., "Drift Catching In Lindsay, California", Pesticide Action Network North America, 2006[dead link]
  82. ^ Hansen, Heather (January 18, 2007). "Heather Hansen, "Proper Pest Management Keeps Washington Fruit Crop Healthy", Seattle Post Intellegencer, Jan 19, 2007". Seattlepi.com. Retrieved November 20, 2011.
  83. ^ "Douglas Fischer, "Toxins permeate Central Valley town", ''Tri-Valley Herald'', May 15th, 2007". Origin.insidebayarea.com. Retrieved November 20, 2011.
  84. ^ "Californians For Pesticide Reform, ''Airborne Poisons: Pesticides in Our Air, and in Our Bodies'', May 16th, 2007" (PDF). Retrieved November 20, 2011.
  85. ^ Thrasher, PhD, Jack D. (2002). "Immunological Abnormalities in Humans Chronically Exposed to Chlorpyrifos". Archives of Environmental Health, 2002, 57:181–187. 2002 (57): 181–187. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  86. ^ Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1289/ehp.5768, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1289/ehp.5768 instead.

External links

Retrieved from "https://en.wikipedia.org/w/index.php?title=Chlorpyrifos&oldid=620011194"