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 | Household Toxin | Synthetic Toxin | PESTICIDE active ingredient | organic | insecticide | acaricide | Pesticide or Plant Growth Regulator Approved in Australia | Pesticide approved in USA (California) | Pesticide approved or pending approval in EU | Toxic and Dangerous to bees. Currently used in Australia as a pesticide | A Hazardous Substance that may be found in the Australian Workplace
- SUBSTANCE LINEAGE: Organic Compounds | Heterocyclic Compounds | Azoles | Pyrazoles | Phenylpyrazoles
- SYNONYMS: (RS)-5-amino-1-[2,6-dichloro-4-(trifluoromethyl)phenyl]-4- (trifluoromethylsulfinyl)-1H-pyrazole-3-carbonitrile | Fluocyanobenpyrazole | Termidor
- DESCRIPTION: Fipronil is a slow acting poison. When mixed with a bait it allows the poisoned insect time to return to the colony or haborage. In cockroaches the feces and carcass can contain sufficient residual pesticide to kill others in the same nesting site. In ants, the sharing of the bait among colony members assists in the spreading of the poison throughout the colony. With the cascading effect, the projected kill rate is about 95% in 3 days for ants and cockroaches. (L325)
- COMMENTS: Residues of this pesticide are tested for on Australian Foods | Pesticide approved in Australia Dangerous to bees. DO NOT apply where bees from managed hives are known to be foraging, and crops, weeds or cover crops are in flower at the time of spraying, or expected to flower within 28 days (7 days pasture and sorghum). Before spraying, notify beekeepers to move hives to a safe location with an untreated source of nectar, if there is potential for managed bees to be affected by the spray or spray drift. If an area has been sprayed inadvertently, in which the crop, weeds, or cover crop were in flower or subsequently came into flower, notify beekeepers in order to keep managed bees out of the area for at least 28 days (7days for pastures and sorghum) from the time of spraying. Where the owner of managed hives in the vicinity of a crop to be sprayed is not known, contact your State Department of Primary Industries/Agriculture, citing the registration number, for assistance in contacting the owner.
From Safe Work Australia and the Hazardous Substances Information System (HSIS) in Australia:
Toxic if inhaled. Toxic in contact with skin. Toxic 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: C12H4Cl2F6N4OS
- DATA SOURCES: DATA SOURCES: ARTICLE 4 | T3DB | PubChem | Consolidated Pesticide Information Dataset (CPI) from the USA EPA | Compendium of Pesticide Common Names | APVMA | DPR | EU Pesticides | 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
- POSSIBLE HEALTH CONSEQUENCES: | Organic nitriles are converted into cyanide ions through the action of cytochrome P450 enzymes in the liver. Cyanide is rapidly absorbed and distributed throughout the body. Cyanide is mainly metabolized into thiocyanate by either rhodanese or 3-mercaptopyruvate sulfur transferase. Cyanide metabolites are excreted in the urine. (L96)
- ACTION OF TOXIN: Fipronil blocks the passage of chloride ions through the GABA-regulated chloride channel, disrupting CNS activity. (T10) Organic nitriles decompose into cyanide ions both in vivo and in vitro. Consequently the primary mechanism of toxicity for organic nitriles is their production of toxic cyanide ions or hydrogen cyanide. Cyanide is an inhibitor of cytochrome c oxidase in the fourth complex of the electron transport chain (found in the membrane of the mitochondria of eukaryotic cells). It complexes with the ferric iron atom in this enzyme. The binding of cyanide to this cytochrome prevents transport of electrons from cytochrome c oxidase to oxygen. As a result, the electron transport chain is disrupted and the cell can no longer aerobically produce ATP for energy. Tissues that mainly depend on aerobic respiration, such as the central nervous system and the heart, are particularly affected. Cyanide is also known produce some of its toxic effects by binding to catalase, glutathione peroxidase, methemoglobin, hydroxocobalamin, phosphatase, tyrosinase, ascorbic acid oxidase, xanthine oxidase, succinic dehydrogenase, and Cu/Zn superoxide dismutase. Cyanide binds to the ferric ion of methemoglobin to form inactive cyanmethemoglobin. (L97) | Fipronil blocks the passage of chloride ions through the GABA-regulated chloride channel, disrupting CNS activity. (T10)
- TOXIN SITES OF ACTION IN CELL: "Membrane"
- Additional Exposure Routes:
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