Cause mutations to Genetic material like DNA, RNA or mitochondrial DNA
Negative impact on brain and nervous system.
Interferes with fertility
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.
Soluble in Water
This substance easily dissolves in water. As such it can be easily transported via waterways. Not really a nastiness attribute, but this feature helps rapidly spread other nastiness attributes this substance may have.
Volatile - Evaporates easily
This substance easily enters the air we breath. Not really a nastiness attribute, but this feature helps rapidly spread other nastiness attributes this substance may have.
These attributes are ONLY based on peer-reviewed evidence. See link to Data Sources below. Everyone benefits from knowing this stuff. Please Share.
- CATEGORIES: Chemicals used in hydraulic fracturing fluids | Chemicals detected in flowback and produced water - collectively referred to as - hydraulic fracturing wastewater | Household Toxin | Industrial/Workplace Toxin | Food Toxin | Natural Toxin | Indirect Additives Used in Food Contact Substances | PESTICIDE active ingredient | Pesticide approved in USA (California) | A Hazardous Substance that may be found in the Australian Workplace
- SUBSTANCE LINEAGE: Inorganic Compounds | Homogeneous Non-metal Compounds | Homogeneous Other Non-metal Compounds | | Other Non-metal Hydrides
- SYNONYMS: Ammonia anhydrous | Ammonia water | Anhydrous ammonia | Azane | Liquid ammonia | NH(3) | NH3 | Spirit of hartshorn
- DESCRIPTION: Has been used in CSG, Hydraulic Fracturing Operations (Fracking) as - Foamer, scale inhibitor, unknown, fracturing | Ammonia is a colorless alkaline gas with a characteristic sharp smell. Ammonia is one of the most abundant nitrogen-containing compounds in the atmosphere. It is an irritant with a characteristic pungent odor, which is widely used in industry. Inasmuch as ammonia is highly soluble in water and, upon inhalation, is deposited in the upper airways, occupational exposures to ammonia have commonly been associated with sinusitis, upper airway irritation, and eye irritation. Acute exposures to high levels of ammonia have also been associated with diseases of the lower airways and interstitial lung. Ammonia has been shown to be a neurotoxin that predominantly affects astrocytes. Disturbed mitochondrial function and oxidative stress, factors implicated in the induction of the mitochondrial permeability transition, appear to be involved in the mechanism of ammonia neurotoxicity. Ammonia is formed in nearly all tissues and organs of the vertebrate organism; it is the most common endogenous neurotoxic compounds. Ammonia can affect the glutamatergic and GABAergic neuronal systems, the two prevailing neuronal systems of the cortical structures. Ammonia is well recognized to be central in the pathogenesis of hepatic encephalopathy and has been of importance to generations dating back to the early Egyptians. The gut produces ammonia which is metabolized in the liver and almost all organ systems are involved in ammonia metabolism. Colonic bacteria produce ammonia by splitting urea and other amino acids, however this does not explain hyperammonemia and hepatic encephalopathy. The alternative explanation is that hyperammonemia is the result of intestinal breakdown of amino acids, especially glutamine. The intestines have significant glutaminase activity, predominantly located in the enterocytes. On the other hand, this organ has only a little glutamine synthetase activity, making it a major glutamine-consuming organ. In addition to the intestine, the kidney is an important source of blood ammonia in patients with liver disease. Ammonia is also taken up by the muscle and brain in hepatic coma, and there is confirmation that ammonia is metabolized in muscle. The excessive formation of ammonia in the brains of Alzheimer's disease patients has been demonstrated, and it has been shown that some Alzheimer's disease patients exhibit elevated blood ammonia concentrations. Ammonia is the most important natural modulator of lysosomal protein processing: there is evidence for the involvement of aberrant lysosomal processing of beta-amyloid precursor protein (beta-APP) in the formation of amyloid deposits. Inflammatory processes and activation of microglia are widely believed to be implicated in the pathology of Alzheimer's disease. Ammonia is able to affect the characteristic functions of microglia, such as endocytosis, and cytokine production. Based on these facts, an ammonia-based hypothesis for Alzheimer's disease has been suggested. (A7717, A7718, A7719, A7720, A7721).
From Safe Work Australia and the Hazardous Substances Information System (HSIS) in Australia:
Flammable gas. Toxic if inhaled. Causes severe skin burns and eye damage. Very toxic to aquatic life | 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: H3N
- DATA SOURCES: DATA SOURCES: ARTICLE 4 | T3DB | PubChem | Article-Colborn-2010 | FracFocus | EPA in USA | US HOUSE OF REPRESENTATIVES | FDA Indirect Food Additives | DPR | 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: Acute exposure leads to irritation and burning at the site of exposure. (L958) Symptoms include cough, chest pain (severe), chest tightness, difficulty breathing and wheezing, tearing and burning of eyes, temporary blindness, throat pain (severe), mouth pain, lip swelling, heart and blood, rapid, weak pulse, collapse and shock. Chronic exposure: Symptoms of hyperammonia include: lethargy, irritability, poor feeding, vomiting and seizures. Signs and symptoms of late-onset hyperammonemia (later in life) may include intermittent ataxia, intellectual impairment, failure to thrive, gait abnormality, behavior disturbances, epilepsy, recurrent Reye syndrome and protein avoidance.
- POSSIBLE HEALTH CONSEQUENCES: Acute exposure to high levels of ammonia in air may be irritating to skin, eyes, throat, and lungs and cause coughing and burns. Lung damage and death may occur after exposure to very high concentrations of ammonia. Swallowing concentrated solutions of ammonia can cause burns in mouth, throat, and stomach. Splashing ammonia into eyes can cause burns and even blindness. (L958) Chronically high levels of ammonia in the blood are associated with nearly 20 different inborn errors of metabolism including: 3-Hydroxy-3-Methylglutaryl-CoA Lyase Deficiency, Argininemia, Argininosuccinic Aciduria, Beta-Ketothiolase Deficiency, Biotinidase deficiency, Carbamoyl Phosphate Synthetase Deficiency, Carnitine-acylcarnitine translocase deficiency, Citrullinemia Type I, Hyperinsulinism-Hyperammonemia Syndrome, Hyperornithinemia-hyperammonemia-homocitrullinuria syndrome, Isovaleric Aciduria, Lysinuric Protein Intolerance, Malonic Aciduria, Methylmalonic Aciduria, Methylmalonic Aciduria Due to Cobalamin-Related Disorders, Propionic acidemia, Pyruvate carboxylase deficiency and Short Chain Acyl CoA Dehydrogenase Deficiency (SCAD Deficiency). Hyperammonemia is one of the metabolic derangements that contribute to hepatic encephalopathy. | Ammonia can be absorbed by inhalation and oral routes exposure, and also to a much lesser extent through the skin and eyes. Most of the inhaled ammonia is retained in the upper respiratory tract and is subsequently eliminated in expired air, while ingested ammonia is readily absorbed in the intestinal tract. Ammonia that reaches the circulation is widely distributed to all body compartments although substantial first pass metabolism occurs in the liver where it is transformed into urea and glutamine. Ammonia or ammonium ion reaching the tissues is taken up by glutamic acid, which participates in transamination and other reactions. Ammonia is mainly excreted in the urine. (L958)
- ACTION OF TOXIN: The topical damage caused by ammonia is probably due mainly to its alkaline properties. Its high water solubility allows it to dissolve in moisture on the mucous membranes, skin, and eyes, forming ammonium hydroxide. Ammonium hydroxide causes saponification of cell membrane lipids, resulting in cell disruption and death. Additionally, it extracts water from the cells and initiates an inflammatory response, which further damages the surrounding tissues. Excess circulating levels of ammonia (hyperammonemia) can cause serious neurological effects. This is thought to involve the alteration of glutamate metabolism in the brain and resultant increased activation of NMDA receptors, which causes decreased protein kinase C-mediated phosphorylation of Na+/K+ ATPase, increased activity of Na+/K+ ATPase, and depletion of ATP. Ammonia can chemically interact with an internal thiolester bond of complement 3 (C3). This causes a conformation change in C3, which activates the alternative complement pathway, causing the release of chemoattractants and the assembly of the membrane attack complex of complement. The altered C3 can also bind directly to phagocyte complement receptors, which causes the release of toxic oxygen species. (L958) | Ammonia can chemically interact with an internal thiolester bond of complement 3 (C3). This causes a conformation change in C3, which activates the alternative complement pathway, causing the release of chemoattractants and the assembly of the membrane attack complex of complement. The altered C3 can also bind directly to phagocyte complement receptors, which causes the release of toxic oxygen species. (L958)
- TOXIN SITES OF ACTION IN CELL: "Cytoplasm", "Extracellular"
- Additional Exposure Routes: Ammonia is used directly on farm crops, and is also a precursor to foodstuffs and fertilizers. It is also found in many household and industrial cleaners. (L958)
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