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| Names | |
|---|---|
| Preferred IUPAC name 2-{[4-Chloro-6-(ethylamino)-1,3,5-triazin-2-yl]amino}-2-methylpropanenitrile | |
| Identifiers | |
3D model (JSmol) | |
| ChEBI | |
| ChEMBL | |
| ChemSpider | |
| ECHA InfoCard | 100.040.480 |
| RTECS number |
|
| UNII | |
| UN number | 2811, 2763 |
| |
| |
| Properties | |
| C9H13ClN6 | |
| Molar mass | 240.70 g·mol−1 |
| Appearance | White crystals |
| Density | 1.26 g/cm3 |
| Melting point | 168 °C (334 °F; 441 K) |
| 170 mg/L | |
| Hazards | |
| GHS labelling: | |
  | |
| Warning | |
| H302,H410 | |
| P264,P270,P273,P301+P312,P330,P391,P501 | |
Except where otherwise noted, data are given for materials in theirstandard state (at 25 °C [77 °F], 100 kPa). | |
Cyanazine is aherbicide that belongs to the group oftriazines. Cyanazine inhibitsphotosynthesis and is therefore used as aherbicide.[1]
Cyanazine is used as a herbicide to control annual grasses and broadleaf weeds. It belongs to the group oftriazineherbicides, just asatrazine. Thesepesticides work by inhibitingphotosynthesis. The majority of the cyanazine used is used forcorn. In 1985 this was 96% of the used cyanazine.[2] The Environmental Protection Agency (EPA) made a profile on the Health and Environmental effects of cyanazine in 1984.[3]In 1971 cyanazine was brought on the market under the names 'Bladex' and 'Fortol' by Shell. Cyanazine and the othertriazines have been among the group of most heavily usedherbicides in the mid-west and theUnited States of America.[4]In 2002 the European Union pesticides database disapproved the usage of cyanazine as a herbicide. It is classified as a teratogen on theHazardous Substance List, already in 1986.
Cyanazine is the common name for 2-chloro-4-(1-cyano-1-methylethyl-amino)-6-ethylamine-1,3,5-triazine. Themolecular formula for this compound isC
9H
13ClN
6,molecular weight is 240.695 g/mol. Cyanazine is a white or colourless crystalline solid. Themelting point is around 166.5-167.0 °C. ThelogP is 2.22.[clarification needed]
Cyanazine is not very reactive in neutral and slightly acidic/basic media, it ishydrolysed by strongacids and bases. It is stable toheat,light and tohydrolysis. It is also stable to UV irradiation under practical conditions.[3] Cyanazine candecompose on heating. This producescorrosive fumes ofhydrogen chloride,nitrogen oxides andcyanides.[5]
Cyanazine has one of the lowest rate constant ofreactivity withozone from differentpesticides.[6] Among four differentherbicide groups, cyanazine degrades the fastest in soil.[7]
Cyanazine is a chloro-1,3,5-triazine that is substituted at positions 6 and 4 by anethyl amino and anamino group respectively.[8] It can be prepared by reactingcyanuric chloride withethylamine and2-amino-2-methylpropionitrile.[9]
Cyanazine is available as a soluble concentrate, flowable concentrate, emulsifiable concentrate,wettable powder and granular product[10]
Cyanazine inhibitsphotosynthesis and is therefore used as aherbicide. It destroys unwantedvegetation, especially various types of weeds,grasses andwoody plants. The primary site of inhibition was on the reducing side ofphotosystem II. They inhibit theelectron transfer step between the primary electron acceptor (Q) and theplastoquinone pool of theelectron transport chain.[8]
Themetabolism pathways of cyanazine have been describe for differentanimal andplant species. Different studies showed that inanimal models (rats,dogs &cows) the cyanazine is quickly absorbed in theintestines. For the degradation of the absorbed cyanazine the following metabolic pathways are involved: de-alkylation & conjugation withglutathione, which results in differentmetabolites. After undergoing these metabolic pathways the metabolites leave the body in theurine andfeces. For example, inrats there were found sevenmetabolites inurine andfeces after oral intake of cyanazine. Another major route of degradation for cyanazine inmammals is N-De-ethylation, which leads to the yield of anethyl group. The freeethyl group will then by excreted by breathing.[11][12]In plants the following metabolic pathways are involvedhydrolysis, N-de-alkylation and conjugation withglutathione, resulting in differentmetabolites (shown in the figure below).[13]
Cyanazine is used as aherbicide to control annualgrasses and broadleaf weeds incorn,grain,sorghum,cotton andwheat fallow.
Cyanazine is used in the following doses: for preventing weeds, a dose of 0,14 kg/km2 – 0,54 kg/km2 is used. To treat existing weeds, 0.136 kg/km2 – 0,23 kg/km2 is used.[15]
Inanimals andalgae, theLD50/LC50/EC50 are as following:[16]
| Indicator | Species,intake route | Dose |
|---|---|---|
| LD50 | Rat, oral | 149 – 334 mg/kg |
| LD50 | Rat, dermal | >1200 mg/kg |
| LD50 | Rabbit, oral | 141 mg/kg |
| LD50 | Rabbit, dermal | <2000 mg/kg |
| LD50 | Quail, oral | 400 mg/kg |
| LD50 | Duck, oral | 750 mg/kg |
| LC50 | Channel catfish | 17.4 mg/L/96h |
| LC50 | Rainbow trout | 9.0 mg/L/96h |
| LC50 | Fathead Minnow | 16.3 – 21.3 mg/L/96h |
| EC50 | Freshwater green algae | 20 PPB |
| EC50 | Water flea | 49 PPM |
After repeated doses of 25 ppm cyanazine mixed inrat diets, notoxic effects were seen.[17]
Cyanazine was found topollute surface waters and drinking waters in multiplecountries inNorth America and ingroundwaters in theNetherlands. However, cyanazine or cyanazine degradation products have not been detected infood. Based on data from Canada and the Netherlands, intake fromdrinking water is around an estimate 0.2-0.3 μg/day. TheWorld Health Organization (WHO) set a maximum value of 0.198 μg/kg body weight, due to possibletoxic effects tohumans.[18]Furthermore, as seen in the table above, aquatic lifeforms are affected at a much lowerconcentration of cyanazine thanterrestrial animals. That, combined with the fact that cyanazine quickly washes out of thesoil to the surrounding waters, makes that theaquatic ecosystems are most compromised by cyanazine.
Triazineherbicides like cyanazine are extremelytoxic to certain types ofplants. This is why they are so effective in killing specific species of broadleaf weeds. Cyanazine will result in the dysfunction ofphotosystem II by binding important proteins which are required for this process. When this important step inphotosynthesis fails, a plant is not able to produce sugars which are crucial for its growth andmetabolism.
Contact with cyanazine may causedermatitis depending on the severity of the contact. Also, when high levels of cyanazine are being ingested,acute toxicity can occur.Inhalation of cyanazine fumes may lead to airway irritation.
Thecarcinogenic effects of cyanazine were unclear for a long time. However, it is not likely that thisherbicide will have anycarcinogenic effects on humans.[19] More research is needed to fully confirm that cyanazine is notcarcinogenic. This is why theUSEPA rated cyanazine as a group Cchemical; this means that it could becarcinogenic.
Research has shown thatatrazine is able to influence the LH andprolactin secretion of femalerats. Thesehormonal changes appear to be caused by an altered function of thepituitary.[20] As cyanazine belongs to the same class ofherbicides asatrazine, the effect on thehormonal status of rats by cyanazine could be the same. Cyanazine may also influenceGABAA-receptors in thebrain ofrats, depending on the dosage that is given. This can cause disruptions inGnRH-release.[21]
Cyanazine may causemalformations in theembryonal development of somespecies. InSilurana tropicalis, exposure totriazineherbicides like cyanazine may cause severe abnormalities.[22] It is unclear whether these effects could be seen in humans too. Also,eye defects inratfoetuses could be the effect oftoxic properties of cyanazine.[23]
Differenttriazineherbicides appear to have a synergistic effect on specificanimal species. In the case of cyanazine,atrazine can cause effects on non-target species like Chironomus tentans.Atrazine is able to influence the activity ofP450 enzymes in midges and therefore cause increasedtoxicity of theseherbicides.[24]
