Negative impact on brain and nervous system.
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.
Serious Acute Effects
This is a serious nasty substance. Effects are Acute (seen immediately). Substances in this category may be FATAL or acutely toxic if inhaled, skin contact or swallowed. See further details.
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.
Toxic to Bees
Bees pollinate plants. No pollination no plants. No plants no food. We go hungry or starve.
These attributes are ONLY based on peer-reviewed evidence. See link to Data Sources below. Everyone benefits from knowing this stuff. Please Share.
- CATEGORIES: Pesticide | Food Toxin | Synthetic Toxin | PESTICIDE active ingredient | organic | insecticide | Pesticide or Plant Growth Regulator Approved in Australia | Highly Toxic and Dangerous to bees. Currently used in USA | Australia as a pesticide | A Hazardous Substance that may be found in the Australian Workplace
- SUBSTANCE LINEAGE: Organic Compounds | Organophosphorus Compounds | Organothiophosphorus Compounds | Organic Thiophosphoric Acids and Derivatives | Thiophosphate Triesters
- SYNONYMS: 4-Methylmercapto-3-methylphenyl dimethyl thiophosphate | Mercaptophos | MPP | O,O-Dimethyl O-4-(methylmercapto)-3-methylphenyl phosphorothioate | O,O-Dimethyl O-4-methylthio-m-tolyl phosphorothioate | O,O-Dimethyl O-[3-methyl-4-(methylsulfanyl)phenyl] thiophosphate | O,O-Dimethyl-O-4-(methylmercapto)-3-methylphenyl thiophosphate | Phosphorothioic acid | O,O-dimethyl O-(3-methyl-4-(methylthio)phenyl) ester
- DESCRIPTION: Fenthion is an organophosphate used primarily as an insecticide and secondarily as an avicide and acaricide. It was used extensively preharvest on sugar cane, rice, field corn, beets, pome and stone fruit, citrus fruits, pistachio, cotton, olives, coffee, cocoa, vegetables, and vines. However, fenthion no longer has Food and Drug Administration approval because of an excess number of poisoning related deaths (occur mostly by ingestion). Fenthion is neurotoxic. (L1682) (L1683)
- COMMENTS: Residues of this pesticide are tested for on Australian Foods | Pesticide approved in Australia Dangerous to bees. DO NOT spray any plants in flower where bees are foraging.
From Safe Work Australia and the Hazardous Substances Information System (HSIS) in Australia:
Suspected of causing genetic defects. Toxic if inhaled. Harmful in contact with skin. Harmful if swallowed. Causes damage to organs through prolonged or repeated exposure. Very toxic to aquatic life with long lasting effects | Chronic Health Hazard Environmental Hazard Acutely Toxic | 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: C10H15O3PS2
- DATA SOURCES: DATA SOURCES: T3DB | PubChem | Consolidated Pesticide Information Dataset (CPI) from the USA EPA | Compendium of Pesticide Common Names | APVMA | Rural Industries Research and Development Corporation; Honeybee pesticide poisoning: a risk management tool for Australian farmers and beekeepers 2012 | Beekeeping -Department of Entomology - PROTECTING HONEY BEES FROM PESTICIDES, Christian H. Krupke et al.; www.extension.purdue.edu | Safe Work Australia - Hazardous Substances Information System (HSIS)
- LAST UPDATE: 28/04/2018
Mostly focused on Health Implications of Long Term Exposure to this substance
- SYMPTOMS: The symptoms after inhalation and skin contact are: dizziness, nausea, vomiting, sweating, pupillary constriction, muscle cramp, excessive salivation, laboured breathing, convulsions, unconsciousness. The same symptoms occur after ingestion, with additionally abdominal cramps, diarrhoea, nausea and vomiting. In case of eye contact, blurred vision occurs. (L1681)
- POSSIBLE HEALTH CONSEQUENCES: Acute exposure to cholinesterase inhibitors can cause a cholinergic crisis characterized by severe nausea/vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Increasing muscle weakness is a possibility and may result in death if respiratory muscles are involved. Accumulation of ACh at motor nerves causes overstimulation of nicotinic expression at the neuromuscular junction. When this occurs symptoms such as muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis can be seen. When there is an accumulation of ACh at autonomic ganglia this causes overstimulation of nicotinic expression in the sympathetic system. Symptoms associated with this are hypertension, and hypoglycemia. Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur. Certain reproductive effects in fertility, growth, and development for males and females have been linked specifically to organophosphate pesticide exposure. Most of the research on reproductive effects has been conducted on farmers working with pesticides and insecticdes in rural areas. In females menstrual cycle disturbances, longer pregnancies, spontaneous abortions, stillbirths, and some developmental effects in offspring have been linked to organophosphate pesticide exposure. Prenatal exposure has been linked to impaired fetal growth and development. Neurotoxic effects have also been linked to poisoning with OP pesticides causing four neurotoxic effects in humans: cholinergic syndrome, intermediate syndrome, organophosphate-induced delayed polyneuropathy (OPIDP), and chronic organophosphate-induced neuropsychiatric disorder (COPIND). These syndromes result after acute and chronic exposure to OP pesticides. | Metabolism of organophosphates occurs principally by oxidation, by hydrolysis via esterases and by reaction with glutathione. Demethylation and glucuronidation may also occur. Oxidation of organophosphorus pesticides may result in moderately toxic products. In general, phosphorothioates are not directly toxic but require oxidative metabolism to the proximal toxin. The glutathione transferase reactions produce products that are, in most cases, of low toxicity. Paraoxonase (PON1) is a key enzyme in the metabolism of organophosphates. PON1 can inactivate some organophosphates through hydrolysis. PON1 hydrolyzes the active metabolites in several organophosphates insecticides as well as, nerve agents such as soman, sarin, and VX. The presence of PON1 polymorphisms causes there to be different enzyme levels and catalytic efficiency of this esterase, which in turn suggests that different individuals may be more susceptible to the toxic effect of organophosphate exposure.
- ACTION OF TOXIN: Fenthion is a cholinesterase or acetylcholinesterase (AChE) inhibitor. A cholinesterase inhibitor (or 'anticholinesterase') suppresses the action of acetylcholinesterase. Because of its essential function, chemicals that interfere with the action of acetylcholinesterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses, followed by muscle spasms and ultimately death. Nerve gases and many substances used in insecticides have been shown to act by binding a serine in the active site of acetylcholine esterase, inhibiting the enzyme completely. Acetylcholine esterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholine esterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop. Among the most common acetylcholinesterase inhibitors are phosphorus-based compounds, which are designed to bind to the active site of the enzyme. The structural requirements are a phosphorus atom bearing two lipophilic groups, a leaving group (such as a halide or thiocyanate), and a terminal oxygen. | Fenthion inhibits acetylcholinesterase.
- TOXIN SITES OF ACTION IN CELL: "Membrane"
- Additional Exposure Routes: The general population is not likely to be exposed to large amounts of fenthion. Occupational exposure to fenthion occurs through dermal contact and inhalation of dust and sprays, especially to workers applying the compound as an insecticide. Because fenthion has been detected in American foods, exposure to the general population can occur through consumption of foods containing fenthion residues. (L1682)
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