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.
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 | Food Toxin | Synthetic Toxin | PESTICIDE active ingredient | Pesticide or Plant Growth Regulator Approved in Australia | Medication Approved in Australian (on the PBS) | Medication Approved in USA
- SUBSTANCE LINEAGE: Organic Compounds | Benzenoids | Benzene and Substituted Derivatives | Phenol Esters | Phenol Esters
- SYNONYMS: 2-(Acetyloxy)benzoate | 2-(Acetyloxy)benzoic acid | 2-Acetoxybenzenecarboxylic acid | 2-Acetoxybenzoate | 2-Acetoxybenzoic acid | 2-Carboxyphenyl acetate | Acenterine | Acetard | Aceticyl | Acetol | Acetonyl | Acetophen | Acetosal | Acetosalin | Acetylin | Acetylsalicylate | Acetylsalicylic acid | Acetylsalicylsaeure | Acetyonyl | Acetysal | Acetysalicylic acid | Acide 2-(acetyloxy)benzoique | Acide acétylsalicylique | ácido acetilsalicílico | Acidum acetylsalicylicum | Acylpyrin | Adiro | ASA | Asatard | Aspergum | Aspirdrops | Aspro | Azetylsalizylsaeure | Azetylsalizylsäure | Bayer Aspirin | Benaspir | Bialpirinia | Bufferin | Caprin | Cardioaspirina | Easprin | Ecolen | Ecotrin | Empirin | Endosprin | Endydol | Entrophen | Nu-seals | O-(Acetyloxy)benzoate | O-(Acetyloxy)benzoic acid | O-Acetoxybenzoate | O-Acetoxybenzoic acid | O-Acetylsalicylic acid | O-Carboxyphenyl acetate | Persistin | Pharmacin | Polopiryna | Premaspin | Rheumintabletten | Rhodine | Rhonal | Salcetogen | Saletin | Salicylic acid acetate | Salospir | Solprin | Solprin acid | Solpyron | St. Joseph Aspirin for Adults | Tasprin | Temperal | Toldex | Triaminicin
- DESCRIPTION: Acetylsalicylic acid (acetosal) or aspirin is only found in individuals who have consumed this drug. Acetylsalicylic acid is a drug in the family of salicylates, often used as an analgesic (against minor pains and aches), antipyretic (against fever), and anti-inflammatory. It has also an anticoagulant effect and is used in long-term low-doses to prevent heart attacks and cancer. It was isolated from meadowsweet (Filipendula ulmaria, formerly classified as Spiraea ulmaria) by German researchers in 1839. While their extract was somewhat effective, it also caused digestive problems such as irritated stomach and diarrhoea, and even death when consumed in high doses. In 1853, a French chemist named Charles Frederic Gerhardt neutralized salicylic acid by buffering it with sodium (sodium salicylate) and acetyl chloride, creating acetosalicylic anhydride. Gerhardt's product worked, but he had no desire to market it and abandoned his discovery. In 1897, researcher Arthur Eichengrun and Felix Hoffmann, a research assistant at Friedrich Bayer & Co. in Germany, derivatized one of the hydroxyl functional groups in salicylic acid with an acetyl group (forming the acetyl ester), which greatly reduced the negative effects. This was the first synthetic drug, not a copy of something that existed in nature, and the start of the pharmaceuticals industry. The name 'aspirin' is composed of a- (from the acetyl group) -spir- (from the plant genus Spiraea) and -in (a common ending for drugs at the time). It has also been stated that the name originated by another means. As referring to AcetylSalicylic and 'pir' in reference to one of the scientists who was able to isolate it in crystalline form, Raffaele Piria. Finally 'in' due to the same reasons as stated above. Salicylic acid (which is a naturally occurring substance found in many plants) can be acetylated using acetic anhydride, yielding aspirin and acetic acid as a byproduct. It is a common experiment performed in organic chemistry labs, and generally tends to produce low yields due to the relative difficulty of its extraction from an aqueous state. The trick to getting the reaction to work is to acidify with phosphoric acid and heat the reagents under reflux with a boiling water bath for between 40 minutes and an hour. Aspirin acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5).
- 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
- FORMULA: C9H8O4
- DATA SOURCES: DATA SOURCES: ARTICLE 4 | T3DB | PubChem | OEHHA | Compendium of Pesticide Common Names | APVMA | 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: Effects of overdose include: tinnitus, abdominal pain, hypokalemia, hypoglycemia, pyrexia, hyperventilation, dysrhythmia, hypotension, hallucination, renal failure, confusion, seizure, coma, and death.
- POSSIBLE HEALTH CONSEQUENCES: Might increase the risk of gastrointestinal bleeding; large doses of salicylate, a metabolite of aspirin, have been proposed to cause tinnitus; Reye's syndrome, a severe illness characterized by acute encephalopathy and fatty liver, can occur when children or adolescents are given aspirin for a fever or other illnesses or infections. [Wikipedia] | Acetylsalicylic acid is rapidly hydrolyzed primarily in the liver to salicylic acid, which is conjugated with glycine (forming salicyluric acid) and glucuronic acid and excreted largely in the urine. Half Life: The plasma half-life is approximately 15 minutes; that for salicylate lengthens as the dose increases: doses of 300 to 650 mg have a half-life of 3.1 to 3.2 hours; with doses of 1 gram, the half-life is increased to 5 hours and with 2 grams it is increased to about 9 hours.
- ACTION OF TOXIN: The analgesic, antipyretic, and anti-inflammatory effects of acetylsalicylic acid are due to actions by both the acetyl and the salicylate portions of the intact molecule as well as by the active salicylate metabolite. Acetylsalicylic acid directly and irreversibly inhibits the activity of both types of cyclooxygenase (COX-1 and COX-2) to decrease the formation of precursors of prostaglandins and thromboxanes from arachidonic acid. This makes acetylsalicylic acid different from other NSAIDS (such as diclofenac and ibuprofen) which are reversible inhibitors. Salicylate may competitively inhibit prostaglandin formation. Acetylsalicylic acid's antirheumatic (nonsteroidal anti-inflammatory) actions are a result of its analgesic and anti-inflammatory mechanisms; the therapeutic effects are not due to pituitary-adrenal stimulation. The platelet aggregation-inhibiting effect of acetylsalicylic acid specifically involves the compound's ability to act as an acetyl donor to cyclooxygenase; the nonacetylated salicylates have no clinically significant effect on platelet aggregation. Irreversible acetylation renders cyclooxygenase inactive, thereby preventing the formation of the aggregating agent thromboxane A2 in platelets. Since platelets lack the ability to synthesize new proteins, the effects persist for the life of the exposed platelets (7-10 days). Acetylsalicylic acid may also inhibit production of the platelet aggregation inhibitor, prostacyclin (prostaglandin I2), by blood vessel endothelial cells; however, inhibition prostacyclin production is not permanent as endothelial cells can produce more cyclooxygenase to replace the non-functional enzyme. | The analgesic, antipyretic, and anti-inflammatory effects of aspirin are due to actions by both the acetyl and the salicylate portions of the intact molecule as well as by the active salicylate metabolite. Aspirin directly and irreversibly inhibits the activity of both types of cyclo-oxygenase (COX-1 and COX-2) to decrease the formation of precursors of prostaglandins and thromboxanes from arachidonic acid. This makes aspirin different from other NSAIDS (such as diclofenac and ibuprofen) which are reversible inhibitors. Salicylate may competitively inhibit prostaglandin formation. Aspirin's antirheumatic (nonsteroidal anti-inflammatory) actions are a result of its analgesic and anti-inflammatory mechanisms; the therapeutic effects are not due to pituitary-adrenal stimulation. The platelet aggregation–inhibiting effect of aspirin specifically involves the compound's ability to act as an acetyl donor to the platelet membrane; the nonacetylated salicylates have no clinically significant effect on platelet aggregation. Aspirin affects platelet function by inhibiting the enzyme prostaglandin cyclooxygenase in platelets, thereby preventing the formation of the aggregating agent thromboxane A2. This action is irreversible; the effects persist for the life of the platelets exposed. Aspirin may also inhibit formation of the platelet aggregation inhibitor prostacyclin (prostaglandin I2) in blood vessels; however, this action is reversible.
- TOXIN SITES OF ACTION IN CELL: "Cytoplasm", "Extracellular"
- Additional Exposure Routes: For use in the temporary relief of various forms of pain, inflammation associated with various conditions (including rheumatoid arthritis, juvenile rheumatoid arthritis, systemic lupus erythematosus, osteoarthritis, and ankylosing spondylitis), and is also used to reduce the risk of death and/or nonfatal myocardial infarction in patients with a previous infarction or unstable angina pectoris. SEE MEDICATION SIDE EFFECTS
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