Toxno Substance Profile
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Substance Name

Dicamba
Identification Number: CASRN | 1918-00-9

  Substance Attributes


  • 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 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.

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 | Industrial/Workplace Toxin | Synthetic Toxin | PESTICIDE active ingredient | organic | herbicide | plant growth regulator | Pesticide or Plant Growth Regulator Approved in Australia | Pesticide approved in USA (California) | Pesticide approved or pending approval in EU | A Hazardous Substance that may be found in the Australian Workplace
  • SUBSTANCE LINEAGE: Organic Compounds | Organonitrogen Compounds | Nitrogen Mustard Compounds | | Chlorobenzenes
  • SYNONYMS: 2,5-Dichloro-6-methoxybenzoic acid | 2-Methoxy-3,6-dichlorobenzoic acid | 3,6-Dichloor-2-methoxy-benzoeizuur | 3,6-Dichlor-3-methoxy-benzoesaeure | 3,6-Dichloro-2-methoxybenzoic acid | 3,6-Dichloro-O-anisic acid | Acido (3,6-dicloro-2-metossi)-benzoico | Banex | Banlen | Banvel | Banvel 4S | Banvel 4ws | Banvel CST | Banvel d | Banvel herbicide | Banvel II herbicide | Brush buster | Compound b dicamba | Dianat | Dianate | Dicambe | Fallowmaster | Kyselina 3,6-dichlor-2-methoxybenzoova | MDBA | Mediben | Metambane | Tracker | Trooper | Velsicol 58-CS-11 | Velsicol compound r
  • DESCRIPTION: Dicamba is an herbicide used to control annual and perennial broadleaf weeds in grain crops and grasslands, and it is used to control brush and bracken in pastures. It will kill broadleaf weeds before and after they sprout. Legumes will be killed by dicamba. In combination with a phenoxyalkanoic acid or other herbicide, dicamba is used in pastures, range land, and non-crop areas (fence-rows, roadways and wastage) to control weeds. Brand names for formulations of this herbicide include Banvel, Oracle and Vanquish. (L371)
  • COMMENTS: Residues of this pesticide are tested for on Australian Foods | Pesticide approved in Australia

    From Safe Work Australia and the Hazardous Substances Information System (HSIS) in Australia:

    Harmful if swallowed. Causes serious eye damage. Harmful to aquatic life with long lasting effects | General 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.
  • toxin chemical structure pubchem
  • FORMULA: C15H24Cl3N4OPS
  • 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 | Safe Work Australia - Hazardous Substances Information System (HSIS)
  • LAST UPDATE: 28/04/2018

  Health Associations

Mostly focused on Health Implications of Long Term Exposure to this substance

  • SYMPTOMS: In addition to chloracne, CDD exposure causes skin rashes, discoloration, and excessive body hair. (L177)
  • POSSIBLE HEALTH CONSEQUENCES: Exposure to large amounts of CDDs causes chloracne, a severe skin disease with acne-like lesions that occur mainly on the face and upper body. CDDs may also cause liver damage and induce long-term alterations in glucose metabolism and subtle changes in hormonal levels. In addition, studies have shown that CDDs may disrupt the endocrine system and weaken the immune system, as well as cause reproductive damage and birth defects, central and peripheral nervous system pathology, thyroid disorders, endometriosis, and diabetes. 2,3,7,8-Tetrachlorodibenzo-p-dioxin is also a known human carcinogen. (L177, L178) | CDDs are absorbed through oral, inhalation, and dermal routes of exposure. CDDs are carried in the plasma by serum lipids and lipoproteins, distributing mainly to the liver and adipose tissue. CDDs are very slowly metabolized by the microsomal monooxygenase system to polar metabolites that can undergo conjugation with glucuronic acid and glutathione. They may increase the rate of their own metabolism by inducing CDDs induce both phase I and phase II enzymes. The major routes of excretion of CDDs are the bile and the feces, though smaller amounts are excreted in the urine and via lactation. (L177)
  • ACTION OF TOXIN: CDDs cause their toxic effects by binding to the aryl hydrocarbon receptor and subsequently altering the trascription of certain genes. The affinity for the Ah receptor depends on the structure of the specific CDD. The change in gene expression may result from the direct interaction of the Ah receptor and its heterodimer-forming partner, the aryl hydrocarbon receptor nuclear translocator, with gene regulatory elements or the initiation of a phosphorylation/dephosphorylation cascade that subsequently activates other transcription factors. The affected genes include several oncogenes, growth factors, receptors, hormones, and drug-metabolizing enzymes. The change in transcription/translation of these genes is believed to be the cause of most of the toxic effects of CDDs. This includes 2,3,7,8-tetrachlorodibenzo-p-dioxin's carcinogenicity is thought to be the result of its ability to alter the capacity of both exogenous and endogenous substances to damage the DNA by inducing CYP1A1- and CYP1A2-dependent drug-metabolizing enzymes. (L177) | Chlorinated dibenzo-p-dioxins cause their toxic effects by binding to the aryl hydrocarbon receptor and subsequently altering the trascription of certain genes. The affinity for the Ah receptor depends on the structure of the specific CDD. The change in gene expression may result from the direct interaction of the Ah receptor and its heterodimer-forming partner, the aryl hydrocarbon receptor nuclear translocator, with gene regulatory elements or the initiation of a phosphorylation/dephosphorylation cascade that subsequently activates other transcription factors. The affected genes include several oncogenes, growth factors, receptors, hormones, and drug-metabolizing enzymes. The change in transcription/translation of these genes is believed to be the cause of most of the toxic effects of CDDs. This includes 2,3,7,8-tetrachlorodibenzo-p-dioxin's carcinogenicity is thought to be the result of its ability to alter the capacity of both exogenous and endogenous substances to damage the DNA by inducing CYP1A1- and CYP1A2-dependent drug-metabolizing enzymes. (L177)
  • TOXIN SITES OF ACTION IN CELL: "Membrane"
  • Additional Exposure Routes: Dioxins occur as by-products from the manufacture of organochlorides, the bleaching of paper, chlorination by waste and drinking water treatment plants, municipal solid waste and industrial incinerators, and natural sources such as volcanoes and forest fires. (L177, L178)

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  Exposure Routes

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