Toxno Substance Profile
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Substance Name

L-Lactic acid
Identification Number: CASRN | 79-33-4

  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.

These attributes are ONLY based on peer-reviewed evidence. See link to Data Sources below. Everyone benefits from knowing this stuff. Please Share.



  • CATEGORIES: Chemical used in hydraulic fracturing fluids | Household Toxin | Industrial/Workplace Toxin | Food Toxin | Natural Toxin | Animal Toxin | PESTICIDE active ingredient | Inert Pesticide Ingredient USA - Food Use Permitted | Pesticide approved in USA (California)
  • SUBSTANCE LINEAGE: Organic Compounds | Organic Acids and Derivatives | Hydroxy Acids and Derivatives | Alpha Hydroxy Acids and Derivatives | Alpha Hydroxy Acids and Derivatives
  • SYNONYMS: (+)-Lactate | (+)-Lactic acid | (alpha)-Lactate | (alpha)-Lactic acid | (S)-(+)-2-Hydroxypropanoate | (S)-(+)-2-Hydroxypropanoic acid | (S)-2-hydroxy-Propanoate | (S)-2-hydroxy-Propanoic acid | (S)-2-Hydroxypropanoate | (S)-2-Hydroxypropanoic acid | (S)-2-Hydroxypropionate | (S)-2-Hydroxypropionic acid | (S)-Lactate | (S)-Lactic acid | 1-Hydroxyethane 1-carboxylate | 1-Hydroxyethane 1-carboxylic acid | 1-Hydroxyethanecarboxylate | 1-Hydroxyethanecarboxylic acid | 2-Hydroxypropanoate | 2-Hydroxypropanoic acid | 2-Hydroxypropionate | a-Hydroxypropanoate | a-Hydroxypropanoic acid | a-Hydroxypropionate | a-Hydroxypropionic acid | alpha-Hydroxypropanoate | alpha-Hydroxypropanoic acid | alpha-Hydroxypropionate | alpha-Hydroxypropionic acid | L-(+)- Lactic acid | L-2-Hydroxypropanoate | L-2-Hydroxypropanoic acid | L-Lactate | Lactate | Lactic acid | Milk acid | Sarcolactic acid
  • DESCRIPTION: Has been used in CSG, Hydraulic Fracturing Operations (Fracking) as - Unknown | Lactic acid plays a role in several biochemical processes and is produced in the muscles during intense activity. Lactate measurement in the critically ill has been traditionally used to stratify patients with poor outcome. However, plasma lactate levels are the result of a finely tuned interplay of factors that affect the balance between its production and its clearance. When the oxygen supply does not match its consumption, organisms such as man who are forced to produce ATP for their integrity adapt in many different ways up to the point when energy failure occurs. Lactate, being part of the adaptive response, may then be used to assess the severity of the supply/demand imbalance. In such a scenario, the time to intervention becomes relevant: early and effective treatment may allow the cell to revert to a normal state, as long as the oxygen machinery (i.e. mitochondria) is intact. Conversely, once the mitochondria are deranged, energy failure occurs even in the presence of normoxia. The lactate increase in critically ill patients may therefore be viewed as an early marker of a potentially reversible state. A number of studies have demonstrated that malignant transformation is associated with an increase in glycolytic flux and in anaerobic and aerobic cellular lactate excretion. Using quantitative bioluminescence imaging in various primary carcinomas in patients (uterine cervix, head and neck, colorectal region) at first diagnosis of the disease, lactate concentrations in tumors in vivo could be relatively low or extremely high (up to 40 micromol/g) in different individual tumors or within the same lesion. In all tumor entities investigated, high molar concentrations of lactate were correlated with a high incidence of distant metastasis already in an early stage of the disease. Low lactate tumors (< median of approximately 8 micromol/g) were associated with both a longer overall and disease free survival compared to high lactate lesions (lactate > approximately 8 micromol/g). Lactate dehydrogenase was found to be upregulated in most of these tumors compared to surrounding normal tissue. (A3333, A3334).
  • COMMENTS:
  • toxin chemical structure pubchem
  • FORMULA: C3H6O3
  • DATA SOURCES: DATA SOURCES: ARTICLE 4 | T3DB | PubChem | FracFocus | EPA in USA | US HOUSE OF REPRESENTATIVES | DPR | EPA USA - Pesticide Inerts
  • LAST UPDATE: 28/04/2018

  Health Associations

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

  • SYMPTOMS:
  • POSSIBLE HEALTH CONSEQUENCES: Chronically high levels of Lactic acid are associated with at least a dozen inborn errors of metabolism including: 2-Methyl-3-hydroxybutyryl CoA dehydrogenase deficiency, Biotinidase deficiency, Fructose-1,6-diphosphatase deficiency, Glycogen Storage Disease Type 1A (GSD1A) or Von Gierke Disease, Glycogenosis, Type IB, Glycogenosis, Type IC, Glycogenosis, Type VI. Hers disease, Lactic Acidemia, Leigh Syndrome, Methylmalonate Semialdehyde Dehydrogenase Deficiency, Pyruvate Decarboxylase E1 Component Deficiency, Pyruvate dehydrogenase complex deficiency, Pyruvate dehydrogenase deficiency, Short Chain Acyl CoA Dehydrogenase Deficiency (SCAD Deficiency). |
  • ACTION OF TOXIN: Accumulation of L-lactic acid in the body has been shown to be toxic. At times of lactic acidosis, when excess intracellular lactate is released into the blood, maintenance of electroneutrality of the blood requires that a cation be released into the blood, as well. This can reduce blood pH. Lactate may exert a strong action over GABAergic networks in the developing brain, making them more inhibitory than it was previously assumed, acting either through better support of metabolites, or alterations in base intracellular pH levels, or both. (Wikipedia) |
  • TOXIN SITES OF ACTION IN CELL: "Cytoplasm", "Extracellular", "Mitochondria"
  • Additional Exposure Routes:

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  Exposure Routes

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