Toxno Substance Profile
Evidence-based data. We have more than 25,000 profiles on Toxno.
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Substance Name

2-Methyl-4-chlorophenoxyacetic acid
Identification Number: CASRN | 94-74-6

  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 | Industrial/Workplace Toxin | Synthetic Toxin | PESTICIDE active ingredient | organic | herbicide | 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 | Benzenoids | Benzene and Substituted Derivatives | Phenoxyacetic Acid Derivatives | Phenoxyacetic Acid Derivatives
  • SYNONYMS: ((4-chloro-O-Tolyl)oxy)acetic acid | (2-Methyl-4-chlorophenoxy)acetic acid | (4-chloro-2-Methylphenoxy)acetic acid | (4-chloro-O-Cresoxy)acetic acid | (4-chloro-O-Toloxy)acetic acid | 2,4-MCPA | 2-(4-chloro-2-Methylphenoxy)acetic acid | 2-Methyl-4-chlorophenoxyacetate | 2-Methyl-4-chlorophenoxymethylacetic acid | 2-Methyl-4-chlorphenoxyessigsaeure | 4-chloro-2-Methylphenoxyacetic acid | 4-chloro-O-Cresoxyacetic acid | 4-chloro-O-Toloxyacetic acid | 4-chloro-O-Tolyloxyacetic acid | Acetic acid | {[(4-chloro-O-tolyl)oxy]-} | Acme mcpa amine 4 | Agrichem MCPA-25 | 50 | Agricorn 500 | Agritox | Agritox 50 | Agroxon | Agroxone | Agroxone 50 | Albar-m | Anicon kombi | Anicon m | Atlas mcpa | B-selektonon m | Banvel m | BH mcpa | BH MCPA 75 | Bordermaster | Brominal m and plus | Campbell's MCPA 25 | 50 | Caswell No. 557C | Cekherbex | Chafer MCPA 675 | Chiptox | chloro-(O-Cresoxy)acetic acid | chloro-(O-Tolyloxy)acetic acid | Chwastox | Chwastox 30 | Chwastox extra | Chwastox f | CMP acetate | Cornox-m | Ded-weed | Dicopur-m | Dicotex | Dikotes | Dikotex | Dow MCP amine weed killer | Emcepan | Empal | Farmon MCPA 50 | FBC mcpa | FLUID 4 | Hedapur M 52 | Hedarex m | Hedonal | Hedonal m | Herbicide m | Hormotuho | Hornotuho | Kilsem | Kilsem4k-2m | Krezone | Legumex DB | Leuna m | Leyspray | Linormone | MCP | MCP ester | MCPA | Mcpa | Mcpa ester | Mcpa solution | Mecpa | Mephanac | Metaxon | Methoxone | Methyl chlorophenoxy acetic acid | Methylchlorophenoxyacetic acid | MSS MCPA 50 | Netazol | Okultin m | Phenoxylene 50 | Phenoxylene plus | Phenoxylene super | Power mcpa | Raphone | Razol dock killer | Rhomenc | Rhomene | Rhonox | Selektonon m | Seppic MMD | Shamrox | Soviet technical herbicide 2M-4C | Star mcpa | Trasan | U 46 M-FLUID | Ustinex | Vacate | Verdone | Vesakontuho mcpa | Weed-rhap | Weedar | Weedar mcpa | Weedar mcpa concentrate | Weedone | Weedone mcpa ester | WLN: QV1OR DG B1 | Zelan | [(4-Chloro-O-tolyl)oxy]acetic acid | {[(4-chloro-O-tolyl)oxy]acetic} acid
  • DESCRIPTION: 2-methyl-4-chlorophenoxyacetic acid or MCPA is a powerful, selective, widely used phenoxy herbicide. It controls broadleaf weeds, including thistle and dock, in cereal crops and pasture. It is selective for plants with broad leaves, and this includes most deciduous trees. Clovers are tolerant at moderate application levels. It is currently classified as a restricted use pesticide in the United States.
  • 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 skin irritation. Causes serious eye damage. Very toxic to aquatic life with long lasting effects | Environmental Hazard 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: C9H9ClO3
  • DATA SOURCES: DATA SOURCES: 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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