Cause mutations to Genetic material like DNA, RNA or mitochondrial DNA
Negative impact on brain and nervous system.
Interferes with fertility
Known to effect development of fetus.
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 specific organs
Can damage liver, kidney, lungs, heart or gut. Ironically liver, kidneys and gut are the main detoxifications systems.
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: Chemical Found in Air near CSG Operations | Pit Chemicals | Household Toxin | Industrial/Workplace Toxin | Pollutant | Airborne Pollutant | Food Toxin | Natural Toxin | CSG Fracking BTEX Chemicals | A Hazardous Substance that may be found in the Australian Workplace
- SUBSTANCE LINEAGE: Organic Compounds | Benzenoids | Benzene and Substituted Derivatives | | Toluenes
- SYNONYMS: 1,4-Dimethylbenzene | 1,4-Dimethylbenzol | 1,4-xylene | 4-methyltoluene | p-dimethylbenzene | p-Methyltoluene | P-Xylene | p-Xylol | para-xylene
- DESCRIPTION: Has been used in CSG, Hydraulic Fracturing Operations (Fracking) as - Unknown | p-Xylene is an aromatic hydrocarbon based on benzene with two methyl substituents with the chemical formula C8H10 or C6H4(CH3)2. The p stands for para, identifying the location of the methyl groups as across from one another. Overexposure of p-xylene in humans can cause headache, fatigue, dizziness, listlessness, confusion, irritability, gastrointestinal disturbances including nausea and loss of appetite, flushing of the face, and a feeling of increased body heat. p-Xylene vapor exposure over the recommended exposure limit of 100 parts per million (ppm) can cause irritation to eye, nose, and throat and possible chest tightening and an abnormal gait.
- COMMENTS: This Chemical is in the category of VOC and is found in Air near CSG Operations
From Safe Work Australia and the Hazardous Substances Information System (HSIS) in Australia:
Flammable liquid and vapour. Harmful if inhaled. Harmful in contact with skin. Causes skin irritation | 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.
- FORMULA: C8H10
- DATA SOURCES: DATA SOURCES: ARTICLE 4 | T3DB | PubChem | TEDX | US HOUSE OF REPRESENTATIVES | Article-Colborn-Air | 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: Inhalation and ingestion can lead to dizziness, drowsiness, headache, and nausea. Burning sensations and abdominal pain can also result from ingestion. Dermal and eye exposure can cause skin dryness, redness, and pain. Conjunctivitis, dermatitis, respiratory tract irritation, dyspnea, anorexia, vomiting, fatigue, vertigo, incoordination, irritation, gangrene and anemia are other symptoms following xylene poisoning. (A579)
- POSSIBLE HEALTH CONSEQUENCES: Acute exposure to cholinesterase inhibitors can cause a cholinergic crisis characterized by severe nausea/vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Increasing muscle weakness is a possibility and may result in death if respiratory muscles are involved. Accumulation of ACh at motor nerves causes overstimulation of nicotinic expression at the neuromuscular junction. When this occurs symptoms such as muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis can be seen. When there is an accumulation of ACh at autonomic ganglia this causes overstimulation of nicotinic expression in the sympathetic system. Symptoms associated with this are hypertension, and hypoglycemia. Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur. Certain reproductive effects in fertility, growth, and development for males and females have been linked specifically to organophosphate pesticide exposure. Most of the research on reproductive effects has been conducted on farmers working with pesticides and insecticdes in rural areas. In females menstrual cycle disturbances, longer pregnancies, spontaneous abortions, stillbirths, and some developmental effects in offspring have been linked to organophosphate pesticide exposure. Prenatal exposure has been linked to impaired fetal growth and development. Neurotoxic effects have also been linked to poisoning with OP pesticides causing four neurotoxic effects in humans: cholinergic syndrome, intermediate syndrome, organophosphate-induced delayed polyneuropathy (OPIDP), and chronic organophosphate-induced neuropsychiatric disorder (COPIND). These syndromes result after acute and chronic exposure to OP pesticides. | Xylenes are well absorbed by the inhalation and oral routes, and to a much lesser extent by dermal route. Xylene is rapidly distributed throughout the body via the systemic circulation. Its metabolites are excreted in urine. Methylhippuric acid, the primary metabolite of xylenes, is formed from conjugation with glycine and oxidation of a methyl group. Xylenol is a minor metabolite obtained from aromatic hydroxylation of xylene. Other minor metabolites found in urine include methylbenzyl alcohol and glucuronic acid conjugates of the oxidized xylene. In humans, hepatic microsomal CYP2E1 is the primary enzyme involved in metabolisation of xylene to methylbenzylalcohol, intermediate in the methylhippuric acid pathway. Unmetabolized xylene is also found in urine, and can also be exhalated. (L165)
- ACTION OF TOXIN: p-Xylene is a cholinesterase or acetylcholinesterase (AChE) inhibitor. A cholinesterase inhibitor (or 'anticholinesterase') suppresses the action of acetylcholinesterase. Because of its essential function, chemicals that interfere with the action of acetylcholinesterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses, followed by muscle spasms and ultimately death. Nerve gases and many substances used in insecticides have been shown to act by binding a serine in the active site of acetylcholine esterase, inhibiting the enzyme completely. Acetylcholine esterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholine esterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop. Among the most common acetylcholinesterase inhibitors are phosphorus-based compounds, which are designed to bind to the active site of the enzyme. The structural requirements are a phosphorus atom bearing two lipophilic groups, a leaving group (such as a halide or thiocyanate), and a terminal oxygen. | Certain metabolites of xylene have been shown to inhibit pulmonary mixed-function oxidases. (A117)
- TOXIN SITES OF ACTION IN CELL: "Membrane"
- Additional Exposure Routes: Xylene is used as a solvent and in the printing, rubber, and leather industries. It is also used as a cleaning agent, a thinner for paint, and in paints and varnishes. It is found in small amounts in airplane fuel and gasoline. Exposure to xylene may occur from breathing it in contaminated air, drinking or eating xylene-contaminated water or food, and through dermal and eye contact with xylene containing products. (L165, L165)
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