| Revision as of 01:16, 16 August 2011 editCheMoBot (talk | contribs)Bots141,565 edits Updating {{chembox}} (no changed fields - added verified revid - updated 'DrugBank_Ref', 'UNII_Ref', 'ChEMBL_Ref', 'ChEBI_Ref', 'KEGG_Ref', 'StdInChI_Ref', 'StdInChIKey_Ref') per [[Misplaced Pages:WikiProject Chemicals/Chembox validation|Chem/Drugbox valid |
Latest revision as of 08:41, 23 September 2024 edit JWBE (talk | contribs)Extended confirmed users10,129 edits removed Category:Propyl esters; added Category:Propyl compounds using HotCat |
| Line 1: |
Line 1: |
|
|
{{short description|Chemical compound}} |
|
{{chembox |
|
{{chembox |
|
| verifiedrevid = 443742327 |
|
|verifiedrevid=445074416 |
|
|ImageFile=Ethoprop.png |
|
|ImageFile=Ethoprophos.svg |
|
|ImageSize= |
|
|ImageSize=200px |
|
|
|ImageFile2=Ethoprophos.png |
|
|IUPACName=1-(ethoxy-propylsulfanylphosphoryl)sulfanylpropane |
|
|
|
|ImageSize2=200px |
|
|OtherNames= |
|
|
|
|PIN=''O''-Ethyl ''S'',''S''-dipropyl phosphorodithioate |
| ⚫ |
|Section1= {{Chembox Identifiers |
|
|
|
|OtherNames=Ethoprophos, Prophos, Mocap |
| ⚫ |
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}} |
|
|
⚫ |
|Section1={{Chembox Identifiers |
|
⚫ |
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}} |
|
| ChemSpiderID = 3173 |
|
| ChemSpiderID = 3173 |
|
|
| EINECS = 236-152-1 |
|
| InChI = 1/C8H19O2PS2/c1-4-7-12-11(9,10-6-3)13-8-5-2/h4-8H2,1-3H3 |
|
| InChI = 1/C8H19O2PS2/c1-4-7-12-11(9,10-6-3)13-8-5-2/h4-8H2,1-3H3 |
|
| InChIKey = VJYFKVYYMZPMAB-UHFFFAOYAE |
|
| InChIKey = VJYFKVYYMZPMAB-UHFFFAOYAE |
| Line 16: |
Line 20: |
|
| CASNo_Ref = {{cascite|correct|CAS}} |
|
| CASNo_Ref = {{cascite|correct|CAS}} |
|
| CASNo=13194-48-4 |
|
| CASNo=13194-48-4 |
|
| PubChem=3289 |
|
| PubChem=3289 |
|
|
| RTECS = TE4025000 |
| ⚫ |
| ChEBI_Ref = {{ebicite|correct|EBI}} |
|
|
|
| UNNumber = 3018 |
|
|
| UNII = 765Y5683OQ |
|
|
| UNII_Ref = {{fdacite|correct|FDA}} |
|
⚫ |
| ChEBI_Ref = {{ebicite|correct|EBI}} |
|
| ChEBI = 38665 |
|
| ChEBI = 38665 |
|
|
| ChEMBL = 1894994 |
|
|
| KEGG = C18687 |
|
| SMILES = O=P(SCCC)(OCC)SCCC |
|
| SMILES = O=P(SCCC)(OCC)SCCC |
|
| MeSHName= |
|
| MeSHName= |
|
}} |
|
}} |
|
|Section2= {{Chembox Properties |
|
|Section2={{Chembox Properties |
|
|
| C=8 | H=19 | O=2 | P=1 | S=2 |
|
| Formula=C<sub>8</sub>H<sub>19</sub>O<sub>2</sub>PS<sub>2</sub> |
|
|
|
| Appearance=Colourless to yellow clear liquid |
|
| MolarMass=242.339 |
|
|
⚫ |
| Density=1.069 g/ml |
|
| Appearance= |
|
|
|
| MeltingPt=<-70 °C (-94 °F, 203 K) |
| ⚫ |
| Density= |
|
|
|
| BoilingPt=244.3 °C (471.7 °F, 517.5 K) (decomposes) |
|
| MeltingPt= |
|
|
|
| Odour = ]-like |
|
| BoilingPt= |
|
|
|
| VaporPressure = 78 mPa (20 °C), 128 mPa (25 °C) |
|
| Solubility= |
|
|
|
| Solubility=1.3-1.4 mg/L (water) |
|
}} |
|
|
|Section3= {{Chembox Hazards |
|
}}|Section3={{Chembox Hazards |
|
| MainHazards=Toxic |
|
| MainHazards=Toxic |
|
| FlashPt= |
|
| FlashPt=141 °C |
|
|
| AutoignitionPtC =280 |
|
| Autoignition= |
|
|
|
| GHSPictograms = {{GHS08}}{{GHS09}} |
|
|
| GHSSignalWord = Danger |
|
|
| HPhrases = {{H-phrases|301|310|317|330|410}} |
|
|
| PPhrases = {{P-phrases|260|261|262|264|270|271|272|273|280|284|301+310|302+350|302+352|304+340|310|320|321|322|330|333+313|361|363|391|403+233|405|501}} |
|
}} |
|
}} |
|
}} |
|
}} |
|
|
|
|
|
|
'''Ethoprophos''' (or '''ethoprop''') is an ] with the formula C<sub>8</sub>H<sub>19</sub>O<sub>2</sub>PS<sub>2</sub>.<ref name=":1" /> It is a clear yellow to colourless liquid that has a characteristic ]-like odour. It is used as an ] and ]<ref>{{Cite thesis|title=Effect and mode of action of some systemic nematicides|url=https://library.wur.nl/WebQuery/wurpubs/423038|publisher=Veenman|date=1975|place=Wageningen|first=J. A.|last=Bunt}}</ref> and it is an ].<ref>{{Cite web|url=https://www.cdpr.ca.gov/docs/risk/rcd/ethoprop.pdf|title=Ethoprop Risk Characterization Document|date=31 October 1995|website=www.cdpr.ca.gov|access-date=26 February 2019}}</ref> |
|
'''Ethoprop''' is an ] ] used as an ]. |
|
|
|
|
|
|
|
== Synthesis == |
|
{{Insecticides}} |
|
|
|
Ethoprop can be synthesised by reacting ] with two equivalents of ] and one equivalent of ]. A second pathway is reacting ''n''-propylmercaptan and sodium ethoxide with ] to yield ethoxy-bis(propylsulfanyl)phosphane, which can then be oxidized by ] to yield the product.<ref>{{Cite book|url=https://books.google.com/books?id=-9cHDi8OOO4C&q=ethoprophos+synthesis|title=Pesticide Synthesis Handbook|last=Unger|first=Thomas A.|date=1996-12-31|publisher=William Andrew|isbn=9780815518532|language=en}}</ref> |
|
{{Cholinergics}} |
|
|
|
|
|
{{organic-compound-stub}} |
|
|
|
:]{{clear-left}} |
|
|
|
|
|
:]{{clear-left}} |
|
|
|
|
|
== Applications == |
|
|
|
|
|
Ethoprop is used as an ] against soil insects like ] and as a ]. It is used on different crops, ranging from potatoes, bananas, and sugarcane to ornamental plants and tobacco.<ref name=":1" /> Most of the ethoprop used in the United States is applied to potatoes. In the period of 1987 to 1996, an estimated total of 691,000 pounds (313,400 kg) of the pesticide were used on field crops and vegetables.<ref name=":0">{{Cite web|url=https://archive.epa.gov/pesticides/reregistration/web/pdf/ethoprop_red.pdf|title=Reregistration Eligibility Decision for Ethoprop|date=2006|website=archive.epa.gov|access-date=26 February 2019}}</ref> |
|
|
|
|
|
== Toxicology == |
|
|
|
|
|
=== Mechanism of action === |
|
|
When an organism is exposed to ethoprophos either via the oral, dermal or inhalation routes, it primarily inhibits carboxyl ester hydrolases, specifically ] (AChE). This enzyme is important in degradation of the neurotransmitter ] (ACh). Inactivation of AChE takes place by ] of ] hydroxyl group at the active site of AChE. Later, phosphorylation is followed by one of the following scenarios:<ref name=":2">{{Cite news|first=Kenneth D. |last=Katz|date=2019-02-04|title=Organophosphate Toxicity: Practice Essentials, Background, Pathophysiology|url=https://emedicine.medscape.com/article/167726-overview|work=Medscape}}</ref> |
|
|
|
|
|
* endogenous hydrolysis of the phosphorylated enzyme by ] or ]; |
|
|
* reaction by a strong ] such as ] (2-PAM); |
|
|
* irreversible binding and permanent enzyme inactivation (also called aging). |
|
|
|
|
|
When AChE is inactivated, ACh accumulates in the nervous system, which then results in overstimulation of ] and ] receptors.<ref name=":2" /> |
|
|
|
|
|
Another target of ethoprophos is ] acetylcholinesterase. The only known location of this enzyme is on the outside of erythrocyte membranes. However, physiological functions of this AChE type are not completely known.<ref>{{Cite journal|last1=Igisu|first1=H.|last2=Matsumura|first2=H.|last3=Matsuoka|first3=M.|date=1994-09-01|title=|journal=Journal of UOEH|volume=16|issue=3|pages=253–262|issn=0387-821X|pmid=7938978|doi=10.7888/juoeh.16.253|doi-access=free}}</ref> |
|
|
|
|
|
In cases of exposure to ethoprophos, symptoms may include vomiting, nausea, diarrhea, ], abdominal cramps, ], muscular weakness, bronchial hypersecretion, anxiety, confusion and convulsions. In case of ethoprophos poisoning, a combination of ] and ] (2-PAM) is the most effective antidote.<ref name=":1" /> |
|
|
|
|
|
Additionally, ethoprophos is thought to be likely carcinogenic due to the occurrence of different types of tumors in rats after exposure to the compound. Dietary exposure (the most common route of exposure to ethoprophos) is so low, however, that there is a low risk for the general U.S. population.<ref name=":0" /> |
|
|
|
|
|
=== Metabolism === |
|
|
In mammals, metabolism usually proceeds by removal of one or both of the ] groups and subsequent ]. In rats, metabolism is independent of sex, dose, ], or repeated administration, and no parent compound is detectable in faeces or urine. The main metabolite in humans is EPPA, shown below, which can be used as a ] for ethoprophos. The dealkylated metabolites have similar toxic effects to the parent compound.<ref name=":1">{{Cite journal|last1=Arena|first1=Maria|last2=Auteri|first2=Domenica|last3=Barmaz|first3=Stefania|last4=Brancato|first4=Alba|last5=Brocca|first5=Daniela|last6=Bura|first6=Laszlo|last7=Cabrera|first7=Luis Carrasco|last8=Chiusolo|first8=Arianna|last9=Civitella|first9=Consuelo|date=2018|title=Peer review of the pesticide risk assessment of the active substance ethoprophos|journal=EFSA Journal|language=en|volume=16|issue=10|pages=e05290|doi=10.2903/j.efsa.2018.5290|pmid=32625701|pmc=7009744|issn=1831-4732}}</ref> |
|
|
] |
|
|
|
|
|
=== Distribution & Excretion === |
|
|
In tested animals, ethoprophos is widely distributed throughout the body, with the highest concentrations in the lungs, kidneys, and liver. In blood, it is mostly associated to cells instead of being in the plasma. Excretion mainly proceeds through the urine (~60%), but faecal excretion (~10%) and expired air (~15%) are also important routes. Intravenously dosed animals showed limited biliary excretion (~8%).<ref name=":1" /> |
|
|
|
|
|
=== Effects on animals === |
|
|
Experiments carried out on ethoprophos have shown that the toxin affects animals in various manners. Short-term toxicity effects in rabbits and mice, exposed through different routes include inhibition of ] and brain ]. While experiments on dogs gave rise to cellular ] as well.<ref name=":1" /> Acute toxicity studies on rats, in turn have resulted in more effects being observed, namely narcotic, ] and respiratory. The latter was shown to be expressed after a delay of 4 days and linked to an increase in lung weight.<ref>{{Cite journal|last1=Verschoyle|first1=R. D.|last2=Cabral|first2=J. R. P.|date=1982-12-01|title=Investigation of the acute toxicity of some trimethyl and triethyl phosphorothioates with particular reference to those causing lung damage|journal=Archives of Toxicology|language=en|volume=51|issue=3|pages=221–231|doi=10.1007/BF00348854|s2cid=44188825 |issn=1432-0738}}</ref> Studies carried out with extended exposure of ethoprophos in mice gave the same results as research on short-term exposure had, but in rats a fall in ] concentrations was also observed.<ref name=":1" /> On the other hand, a long-term exposure experiment conducted on dogs found that the toxin led to mild liver toxicity.<ref name=":0" /> |
|
|
|
|
|
Furthermore, exposure to ethoprophos was found to affect reproduction as well. Parental toxicity in rats resulted in a drop in their body weight and food consumption. Moreover, abortion cases increased, leading to a reduction of litter sizes. On the other hand, offspring toxicity led to a decrease in body weight gain and rise in postnatal mortality.<ref name=":1" /> |
|
|
|
|
|
Ethoprophos is considered to pose a low risk to mammals exposed to contaminated water as well as mammals feeding on contaminated fish. It is, however, extremely toxic to bees under direct exposure and also to birds which are exposed to the toxin through dietary routes. These involve ingestion of seeds or worms including residues of contaminated soil.<ref name=":1" /> Finally, a study showed that ethoprophos, along with 4 other active substances, was responsible for 40% of the utilized pesticides in Costa Rica, yet they contributed to more than three quarters of the aquatic toxicity.<ref>{{Cite journal|last=Humbert|first=Sébastien|date=January 2007|title=Toxicity assessment of the main pesticides used in Costa Rica|journal=Agriculture, Ecosystems & Environment|volume=118|issue=1–4|pages=183–190|doi=10.1016/j.agee.2006.05.010}}</ref> Thus, it has also been concluded to be highly toxic to aquatic species.<ref name=":1" /> |
|
|
|
|
|
=== Exposure === |
|
|
When orally exposed to ethoprophos, absorption is fast and extensive: the time it takes to reach peak blood levels is below 1 hour and more than 90% of the substance is absorbed.<ref name=":2" /> Short-term dermal exposure to liquid ethoprophos was tested in rabbits in a 21 day long study. The dermal ]L was 0.1 mg/kg/day and the researchers found that there was ] inhibition in plasma, ] and in the brain at a dose of 1.0 mg/kg/day. The short-term dermal exposure to granular ethoprophos was also studied. This study was conducted with rats and lasted for 28 days. In this case, a dermal NOAEL of 20 mg/kg/day was found. Acetylcholinesterase inhibition in plasma happened at a dose of 100 mg/kg/day. For short-term inhalation, a study was done with dogs and it lasted for 90 days. The results showed a NOAEL of 0.025 mg/kg/day and the acetylcholinesterase inhibition in plasma occurred at a dose of 0.075 mg/kg/day. No information about intermediate and long term exposure via dermal and inhalation routes is known at this moment. When rats were chronically exposed to ethoprophos with a dose of 2.81 x 10^-2 mg/kg/day, a number of rats developed malignant adrenal ]. For granular products, inhalation exposure is considered to be the main risk. In the case of liquid products dermal exposure is considered to be the main risk.<ref name=":0" /> |
|
|
|
|
|
==References== |
|
|
{{Reflist}} |
|
|
|
|
| ⚫ |
] |
|
|
] |
|
] |
|
] |
|
] |
|
|
] |
|
|
|
|
⚫ |
] |
|
] |
|
|
|
] |