Known to effect development of fetus.
Metabolic Interference or Disruption
Interferes with human metabolism. This can be a very serious thing. Some of these interference mechanics are well established. However, often long term effects and health consequences remain largely unknown. Additionally an emerging area of concern and one that is not currently studied, is the combined synergistic effects these metabolically disrupting chemicals have on human health.
Metabolic interference happens when the substance produces highly reactive and often damaging intermediates during detoxification or when the substance binds to specific enzymes, important structural groups on molecules, receptors and membranes or targets DNA or mimics key nutrients.
Exposure Produces Health Symptoms
Symptoms maybe short term or long term depending on the exposure duration and intensity and effects areas like Cardiovascular, Gastrointestinal, Cognition, Fatigue. A substance with this attribute may cause an allergic skin reaction, serious eye irritation, allergy or asthma symptoms or breathing difficulties if inhaled.
Toxic to specific organs
Can damage liver, kidney, lungs, heart or gut. Ironically liver, kidneys and gut are the main detoxifications systems.
Toxic to Wildlife
May kill plants, fish, birds or other animals and insects or may be very toxic to aquatic life with long lasting effects. This then effects delicate environmental ecology and food supply in ways we don't fully understand yet.
Has known Side Effects
This is often the result of long or short term medication use. The same medication can have a range of side effects ranging from none at all to totally debilitating symptoms within different individuals. Reasons for this include individual genetics, individual detoxification capacity, nutrition status, duration of use and total number of medications being taken.
It becomes very difficult to establish clear causes of symptoms when multiple medications are being taken at once.
See SIDE EFFECTS LINKOUT at end of this profile.
These attributes are ONLY based on peer-reviewed evidence. See link to Data Sources below. Everyone benefits from knowing this stuff. Please Share.
- CATEGORIES: Medication or Drug | Pesticide | Food Toxin | Synthetic Toxin | PESTICIDE active ingredient | organic | rodenticide | Pesticide or Plant Growth Regulator Approved in Australia | Pesticide approved in USA (California) | A Hazardous Substance that may be found in the Australian Workplace | Medication Approved in Australian (on the PBS)
- SUBSTANCE LINEAGE: Organic Compounds | Phenylpropanoids and Polyketides | Coumarins and Derivatives | Hydroxycoumarins | Homoisoflavones
- SYNONYMS: (phenyl-1 acetyl-2 ethyl) 3-hydroxy-4 coumarin | (phenyl-1 acetyl-2 ethyl) 3-hydroxy-4 coumarine | (S)-4-hydroxy-3-(3-oxo-1-phenylbutyl)-2-benzopyrone | 1-(4'-Hydroxy-3'-coumarinyl)-1-phenyl-3-butanone | 200 Coumarin | 3-(1'-Phenyl-2'-acetylethyl)-4-hydroxycoumarin | 3-(Acetonylbenzyl)-4-hydroxycoumarin | 3-(alpha-Acetonylbenzyl)-4-hydroxycoumarin | 3-(alpha-Phenyl-beta-acetylaethyl)-4-hydroxycumarin | 3-(alpha-Phenyl-beta-acetylethyl)-4-hydroxycoumarin | 4-Hydroxy-3- (3-oxo-1-fenyl-butyl) cumarine | 4-Hydroxy-3- (3-oxo-1-phenyl-butyl)-cumarin | 4-Hydroxy-3-(3-oxo-1-fenyl-butyl) cumarine | 4-Hydroxy-3-(3-oxo-1-phenyl-butyl)-cumarin | 4-Hydroxy-3-(3-oxo-1-phenylbutyl)-2H-1-benzopyran-2-one | 4-Hydroxy-3-(3-oxo-1-phenylbutyl)-2H-chromen-2-one | 4-Hydroxy-3-(3-oxo-1-phenylbutyl)coumarin | 4-Idrossi-3- (3-oxo-)-fenil-butil)-cumarine | 4-Idrossi-3-(3-oxo-)-fenil-butil)-cumarine | 4-Idrossi-3-(3-oxo-1-fenil-butil)-cumarine | 4oh-coumarin deriv. | Arab rat death | Arab rat deth | Athrombin-k | Athrombine-k | Brumolin | Co-rax | Compound 42 | Coumadin | Coumafen | Coumafene | Coumaphen | Coumaphene | Coumarins | Coumefene | Cov-R-tox | D-Con | delta-Con | Dethmor | Dethnel | Dicusat e | DL-3-(alpha-acetonylbenzyl)-4-hydroxycoumarin | Eastern states duocide | Fasco fascrat powder | Frass-ratron | Jantoven | Killgerm sewarin p | Kumader | Kumadu | Kumatox | Kypfarin | Latka 42 | Lawarin | Liqua-tox | Maag rattentod cum | Mar-frin | Marevan | Martin'S mar-frin | Maveran | Mouse pak | Place-pax | Prothromadin | Rat & mice bait | Rat and mice bait | Rat-a-way | Rat-alpha-way | Rat-b-gon | Rat-beta-gon | Rat-gard | Rat-kill | Rat-mix | Rat-O-cide #2 | Rat-O-cide no. 2 | Rat-ola | Rat-trol | Ratorex | Ratox | Ratoxin | Ratron | Ratron g | Rats-no-more | Ratten-koederrohr | Rattenstreupulver neu schacht | Rattenstreupulver new schacht | Rattentraenke | Rattunal | RAX | RCR grey squirrel killer concentrate | Ro-deth | Rodafarin | Rodafarin c | Rodex | Rodex blox | Rosex | Rough & ready mouse mix | Rough and ready mouse mix | Sakarat | Sewarin | Solfarin | Sorexa plus | Spray-trol brand roden-trol | Temus w | Tox-hid | Twin light rat away | Vampirinip II | Vampirinip III | Waran | Warfant | Warfarin sodium | Zoocoumarin
- DESCRIPTION: Warfarin is an anticoagulant drug normally used to prevent blood clot formation as well as migration. Although originally marketed as a pesticide (d-Con, Rodex, among others), Warfarin has since become the most frequently prescribed oral anticoagulant in North America. Warfarin has several properties that should be noted when used medicinally, including its ability to cross the placental barrier during pregnancy which can result in fetal bleeding, spontaneous abortion, preterm birth, stillbirth, and neonatal death. Additional adverse effects such as necrosis, purple toe syndrome, osteoporosis, valve and artery calcification, and drug interactions have also been documented with warfarin use. Warfarin does not actually affect blood viscosity, rather, it inhibits vitamin-k dependent synthesis of biologically active forms of various clotting factors in addition to several regulatory factors.
- COMMENTS: Residues of this pesticide are NOT tested for on Australian Foods even though the Pesticide is approved in Australia. This is partly so because this pesticide is not usually used around food agriculture. | Pesticide approved in Australia
From Safe Work Australia and the Hazardous Substances Information System (HSIS) in Australia:
May damage the unborn child . Causes damage to organs through prolonged or repeated exposure . Harmful to aquatic life with long lasting effects | Chronic Health Hazard | A Hazardous Substance that may be found in the Australian Workplace. Check with your employer or health and safety officer. Stay informed and become aware of the dangers that surround you. This chemical is included on the list of recognised hazardous chemicals from the Safe Work Australia - Hazardous Substances Information System (HSIS) that is based on the Globally Harmonised System of Classification and Labelling of Chemicals (GHS)
Work Health and Safety (WHS) Regulations are the basis for hazardous chemicals regulations in Commonwealth, State and Territory jurisdictions in Australia. Under the model WHS Regulations, manufacturers and importers of substances, mixtures and articles supplied for use in workplaces are required to determine whether they are hazardous to health and safety before supply. The model WHS Regulations mandate that the hazards of a chemical as determined by the Globally Harmonised System of Classification and Labelling of Chemicals (GHS) must be included in safety data sheets and on labels. There are transitional arrangements in place for moving to the GHS-based system.
The GHS Hazardous Chemical Information List contains chemicals classified by an authoritative source (such as the European Commission or NICNAS) in accordance with the Globally Harmonized System of Classification and Labelling of Chemicals (the GHS). This list contains the vast majority of chemicals currently in HSIS. This list and its detail are regularly updated by Work Safe Australia. The model Work Health and Safety (WHS) Regulations require chemicals to be classified in accordance with the Globally Harmonised System of Classification and Labelling of Chemicals (GHS). However transitional arrangements allow use of classification information in HSIS derived from the Approved Criteria until the 31 December 2016.
- FORMULA: C19H16O4
- DATA SOURCES: DATA SOURCES: T3DB | PubChem | OEHHA | Consolidated Pesticide Information Dataset (CPI) from the USA EPA | Compendium of Pesticide Common Names | APVMA | DPR | Safe Work Australia - Hazardous Substances Information System (HSIS) | Drugbank | Australian Approved Medications PBS | USA FDA APPROVED DRUG PRODUCTS
- LAST UPDATE: 28/04/2018
Mostly focused on Health Implications of Long Term Exposure to this substance
- SYMPTOMS: LD50=374 (orally in mice)
- POSSIBLE HEALTH CONSEQUENCES: Hemorrhage is the most prevalent adverse effect of oral anticoagulant therapy. The incidence of bleeding complications is related to the duration and range of therapy. (L1151) | Metabolized stereo- and regio-selectively by hepatic microsomal enzymes. S-warfarin is predominantly metabolized by cytochrome P450 (CYP) 2C9 to yield the 6- and 7-hydroxylated metabolites. R-warfarin is metabolized by CYP1A1, 1A2, and 3A4 to yield 6-, 8-, and 10-hydroxylated metabolites. Hydroxylated metabolites may be further conjugated prior to excretion into bile and urine. UGT1A1 appears to be responsible for producing the 6-O-glucuronide of warfarin, with a possibly contribution from UGT1A10. Five UGT1As may be involved in the formation of 7-O-glucuronide warfarin. S-warfarin has higher potency than R-warfarin and genetic polymorphisms in CYP2C9 may dramatically decrease clearance of and increase toxicity of the medication. In man, the dextrowarfarin enantiomorph is metabolized by side chain reduction to a secondary alcohol, whereas levowarfarin is metabolized by oxidation of the ring, primarily to 7-hydroxywarfarin. These inactive metabolic products are to some extent conjugated with glucuronic acid, undergo an enterohepatic circulation, & are ultimately excreted in urine & stool. (A613) Route of Elimination: The elimination of warfarin is almost entirely by metabolism. Very little warfarin is excreted unchanged in urine. The metabolites are principally excreted into the urine; and to a lesser extent into the bile. Half Life: R-warfarin t1/2=37-89 hours; S-warfarin t1/2=21-43 hours.
- ACTION OF TOXIN: Warfarin inhibits vitamin K reductase, resulting in depletion of the reduced form of vitamin K (vitamin KH2). As vitamin K is a cofactor for the carboxylation of glutamate residues on the N-terminal regions of vitamin K-dependent proteins, this limits the gamma-carboxylation and subsequent activation of the vitamin K-dependent coagulant proteins. The synthesis of vitamin K-dependent coagulation factors II, VII, IX, and X and anticoagulant proteins C and S is inhibited. Depression of three of the four vitamin K-dependent coagulation factors (factors II, VII, and X) results in decreased prothrombin levels and a decrease in the amount of thrombin generated and bound to fibrin. This reduces the thrombogenicity of clots. | Warfarin inhibits vitamin K reductase, resulting in depletion of the reduced form of vitamin K (vitamin KH2). As vitamin K is a cofactor for the carboxylation of glutamate residues on the N-terminal regions of vitamin K-dependent proteins, this limits the gamma-carboxylation and subsequent activation of the vitamin K-dependent coagulant proteins. The synthesis of vitamin K-dependent coagulation factors II, VII, IX, and X and anticoagulant proteins C and S is inhibited. Depression of three of the four vitamin K-dependent coagulation factors (factors II, VII, and X) results in decresed prothrombin levels and a decrease in the amount of thrombin generated and bound to fibrin. This reduces the thrombogenicity of clots.
- TOXIN SITES OF ACTION IN CELL: "Membrane"
- Additional Exposure Routes: Warfarin is an anticoagulant drug and rodenticide derived from coumarin. As a drug it is used for the treatment of retinal vascular occlusion, pulmonary embolism, cardiomyopathy, atrial fibrillation and flutter, cerebral embolism, transient cerebral ischaemia, arterial embolism and thrombosis. (A308) SEE MEDICATION SIDE EFFECTS
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