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Ramset Chemset Injection Reo 502
ITW Australia Pty Ltd (Ramset)
Chemwatch Hazard Alert Code: Issue Date: 09/09/2015
Version No: 3.1.1.1
Print Date: 09/09/2015
Material Safety Data Sheet according to NOHSC and ADG requirements Initial Date: Not Available
SECTION 1 IDENTIFICATION OF THE SUBSTANCE / MIXTURE AND OF THE COMPANY / UNDERTAKING
Product name
Ramset Chemset Injection Reo 502 Product Code: REO502J, REO502J600 Proper shipping name
CORROSIVE LIQUID, BASIC, ORGANIC, N.O.S. (contains benzene-1,3-dimethanamine,N-aminoethylpiperazine and nonylphenol) Other means of
Relevant identified uses of the substance or mixture and uses advised against
Requires that the two parts be mixed by hand or mixer before use, in accordance with manufacturers directions. Mix only as much as is required. Do
Relevant identified uses
not return the mixed material to the original containers
Details of the supplier of the safety data sheet
Registered company name
ITW Australia Pty Ltd (Ramset) 1 Ramset Drive Chirnside Park 3116 VIC Australia 1300 780 063; +613 9727 6229 Emergency telephone number
Association / Organisation
1800 039 008 (24 hrs) Other emergency telephone
SECTION 2 HAZARDS IDENTIFICATION
Classification of the substance or mixture
HAZARDOUS SUBSTANCE. DANGEROUS GOODS. According to the Criteria of NOHSC, and the ADG Code.
CHEMWATCH HAZARD RATINGS
Harmful by inhalation, in contact with skin and if swallowed.
May cause SENSITISATION by inhalation and skin contact. Toxic to aquatic organisms, may cause long-term adverse effects in the aquatic environment. Risk Phrases
Risk of serious damage to eyes. Possible risk of impaired fertility. Possible risk of harm to the unborn child. Possible risk of irreversible effects.
1. Classified by Chemwatch; 2. Classification drawn from HSIS ; 3. Classification drawn from EC Directive 1272/2008 - Annex VI Page 2 of 18
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Relevant risk statements are found in section 2 Indication(s) of danger
Keep out of reach of children. Keep away from living quarters. Keep away from food, drink and animal feeding stuffs. When using do not eat or drink. When using do not smoke. Do not breathe gas/fumes/vapour/spray. In case of contact with eyes, rinse with plenty of water and contact Doctor or Poisons Information Centre. After contact with skin, wash immediately with detergent and plenty of water.
Do not empty into drains. This material and its container must be disposed of in a safe way. Wear suitable protective clothing. Wear suitable gloves. Wear eye/face protection. To clean the floor and all objects contaminated by this material, use water and detergent. In case of accident or if you feel unwell IMMEDIATELY contact Doctor or Poisons Information Centre (show label if possible). If swallowed, seek medical advice immediately and show this container or label.
Use only in well ventilated areas. Avoid exposure - obtain special instructions before use. Dispose of this material and its container at hazardous or special waste collection point. Use appropriate container to avoid environmental contamination.
Avoid release to the environment. Refer to special instructions/Safety data sheets. If swallowed, rinse mouth with water (only if the person is conscious).
Cumulative effects may result following exposure*. Limited evidence of a carcinogenic effect*.
SECTION 3 COMPOSITION / INFORMATION ON INGREDIENTS
See section below for composition of Mixtures bisphenol A/ diglycidyl ether polymer, high molecular weight ingredients determined not to be hazardous ingredients determined not to be hazardous The specific chemical identity and/or exact percentage (concentration) of composition has been withheld as a trade secret.
SECTION 4 FIRST AID MEASURES
Description of first aid measures
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If this product comes in contact with the eyes: Immediately hold eyelids apart and flush the eye continuously with running water. Eye Contact
Ensure complete irrigation of the eye by keeping eyelids apart and away from eye and moving the eyelids by occasionally lifting the upper and lower lids. Continue flushing until advised to stop by the Poisons Information Centre or a doctor, or for at least 15 minutes. Transport to hospital or doctor without delay. Removal of contact lenses after an eye injury should only be undertaken by skilled personnel. If skin or hair contact occurs: Immediately flush body and clothes with large amounts of water, using safety shower if available. Skin Contact
Quickly remove all contaminated clothing, including footwear. Wash skin and hair with running water. Continue flushing with water until advised to stop by the Poisons Information Centre. Transport to hospital, or doctor. If fumes or combustion products are inhaled remove from contaminated area. Lay patient down. Keep warm and rested. Prostheses such as false teeth, which may block airway, should be removed, where possible, prior to initiating first aid procedures. Apply artificial respiration if not breathing, preferably with a demand valve resuscitator, bag-valve mask device, or pocket mask as trained. Perform CPR ifnecessary. Transport to hospital, or doctor. Inhalation of vapours or aerosols (mists, fumes) may cause lung oedema. Corrosive substances may cause lung damage (e.g. lung oedema, fluid in the lungs). As this reaction may be delayed up to 24 hours after exposure, affected individuals need complete rest (preferably in semi-recumbent posture) and must be kept under medical observation even if no symptoms are (yet) manifested. Before any such manifestation, the administration of a spray containing a dexamethasone derivative or beclomethasone derivative may be considered. This must definitely be left to a doctor or person authorised by him/her.
(ICSC13719)
For advice, contact a Poisons Information Centre or a doctor at once.
Urgent hospital treatment is likely to be needed.
If swal owed do NOT induce vomiting.
If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain open airway and prevent aspiration.
Observe the patient carefully. Never give liquid to a person showing signs of being sleepy or with reduced awareness; i.e. becoming unconscious. Give water to rinse out mouth, then provide liquid slowly and as much as casualty can comfortably drink. Transport to hospital or doctor without delay. Indication of any immediate medical attention and special treatment needed
Treat symptomatically.
For acute or short-term repeated exposures to highly alkaline materials: Respiratory stress is uncommon but present occasionally because of soft tissue edema. Unless endotracheal intubation can be accomplished under direct vision, cricothyroidotomy or tracheotomy may be necessary. Oxygen is given as indicated. The presence of shock suggests perforation and mandates an intravenous line and fluid administration. Damage due to alkaline corrosives occurs by liquefaction necrosis whereby the saponification of fats and solubilisation of proteins allow deep penetration into the tissue. Alkalis continue to cause damage after exposure.
INGESTION: Milk and water are the preferred diluents No more than 2 glasses of water should be given to an adult.
Neutralising agents should never be given since exothermic heat reaction may compound injury. * Catharsis and emesis are absolutely contra-indicated.
* Activated charcoal does not absorb alkali.
* Gastric lavage should not be used.
Supportive care involves the following: Withhold oral feedings initially. If endoscopy confirms transmucosal injury start steroids only within the first 48 hours. Carefully evaluate the amount of tissue necrosis before assessing the need for surgical intervention. Patients should be instructed to seek medical attention whenever they develop difficulty in swallowing (dysphagia). Injury should be irrigated for 20-30 minutes. Eye injuries require saline. [Ellenhorn & Barceloux: Medical Toxicology] For acute or short term repeated exposures to phenols/ cresols: Phenol is absorbed rapidly through lungs and skin. [Massive skin contact may result in collapse and death]* [Ingestion may result in ulceration of upper respiratory tract; perforation of oesophagus and/or stomach, with attendant complications, may occur. Oesophageal stricture may occur.]* An initial excitatory phase may present. Convulsions may appear as long as 18 hours after ingestion. Hypotension and ventricular tachycardia that require vasopressor and antiarrhythmictherapy, respectively, can occur. Respiratory arrest, ventricular dysrhythmias, seizures and metabolic acidosis may complicate severe phenol exposures so the initial attention should be directed towards stabilisation ofbreathing and circulation with ventilation, intubation, intravenous lines, fluids and cardiac monitoring as indicated. [Vegetable oils retard absorption; do NOT use paraffin oils or alcohols. Gastric lavage, with endotracheal intubation, should be repeated until phenol odour is no longer detectable; follow with vegetable oil. A saline cathartic should then be given.]* ALTERNATIVELY: Activated charcoal (1g/kg) may be given. A cathartic should be given after oral activated charcoal. Severe poisoning may require slow intravenous injection of methylene blue to treat methaemoglobinaemia. [Renal failure may require haemodialysis.]* Most absorbed phenol is biotransformed by the liver to ethereal and glucuronide sulfates and is eliminated almost completely after 24 hours. [Ellenhorn and Barceloux: Medical Toxicology]*[Union Carbide] BIOLOGICAL EXPOSURE INDEX - BEI These represent the determinants observed in specimens collected from a healthy worker who has been exposed to the Exposure Standard (ES or TLV): 1. Total phenol in blood 250 mg/gm creatinine B: Background levels occur in specimens collected from subjects NOT exposed
NS: Non-specific determinant; also seen in exposure to other materials Page 4 of 18
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SECTION 5 FIREFIGHTING MEASURES
Water spray or fog. Alcohol stable foam. Dry chemical powder. Carbon dioxide. Special hazards arising from the substrate or mixture
Avoid contamination with oxidising agents i.e. nitrates, oxidising acids, chlorine bleaches, pool chlorine etc. as ignition may result Advice for firefighters
Alert Fire Brigade and tell them location and nature of hazard. Wear full body protective clothing with breathing apparatus. Prevent, by any means available, spillage from entering drains or water course. Use fire fighting procedures suitable for surrounding area. Do not approach containers suspected to be hot.
Cool fire exposed containers with water spray from a protected location.
If safe to do so, remove containers from path of fire.
Equipment should be thoroughly decontaminated after use.
Combustible. Slight fire hazard when exposed to heat or flame. Heating may cause expansion or decomposition leading to violent rupture of containers. On combustion, may emit toxic fumes of carbon monoxide (CO). May emit acrid smoke. Mists containing combustible materials may be explosive. Combustion products include: carbon dioxide (CO2), nitrogen oxides (NOx), other pyrolysis products typical of burning organic material May emit corrosivefumes.
SECTION 6 ACCIDENTAL RELEASE MEASURES
Personal precautions, protective equipment and emergency procedures
Drains for storage or use areas should have retention basins for pH adjustments and dilution of spills before discharge or disposal of material. Check regularly for spills and leaks. Small spills should be covered with inorganic absorbents and disposed of properly. Organic absorbents have been known to ignite when contaminated withamines in closed containers. Certain cellulosic materials used for spill cleanup such as wood chips or sawdust have shown reactivity with ethyleneamines andshould be avoided. Ethyleneamine leaks will frequently be identified by the odor (ammoniacal) or by the formation of a white, solid, waxy substance (aminecarbamates). Inorganic absorbents or water may be used to clean up the amine waste. Minor Spills
Clean up all spills immediately. Avoid breathing vapours and contact with skin and eyes. Control personal contact with the substance, by using protective equipment. Contain and absorb spill with sand, earth, inert material or vermiculite. Wipe up. Place in a suitable, labelled container for waste disposal. Clear area of personnel and move upwind. Alert Fire Brigade and tell them location and nature of hazard. Wear full body protective clothing with breathing apparatus. Prevent, by any means available, spillage from entering drains or water course. Consider evacuation (or protect in place). Stop leak if safe to do so. Major Spills
Contain spill with sand, earth or vermiculite. Collect recoverable product into labelled containers for recycling. Neutralise/decontaminate residue (see Section 13 for specific agent). Collect solid residues and seal in labelled drums for disposal. Wash area and prevent runoff into drains. After clean up operations, decontaminate and launder all protective clothing and equipment before storing and re-using. If contamination of drains or waterways occurs, advise emergency services. Personal Protective Equipment advice is contained in Section 8 of the SDS.
SECTION 7 HANDLING AND STORAGE
Precautions for safe handling
DO NOT allow clothing wet with material to stay in contact with skin
Avoid all personal contact, including inhalation.
Wear protective clothing when risk of exposure occurs. Use in a well-ventilated area. Avoid contact with moisture. Avoid contact with incompatible materials. When handling, DO NOT eat, drink or smoke.
Keep containers securely sealed when not in use. Avoid physical damage to containers. Always wash hands with soap and water after handling. Work clothes should be laundered separately. Launder contaminated clothing before re-use. Use good occupational work practice. Observe manufacturer's storage and handling recommendations contained within this MSDS.
Atmosphere should be regularly checked against established exposure standards to ensure safe working conditions are maintained. Page 5 of 18
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for bulk storages: If slight coloration of the ethyleneamine is acceptable, storage tanks may be made of carbon steel or black iron, provided they are free of rust and mill scale.
However, if the amine is stored in such tanks, color may develop due to iron contamination. If iron contamination cannot be tolerated, tanks constructed oftypes 304 or 316 stainless steel should be used. (Note: Because they are quickly corroded by amines, do not use copper, copper alloys, brass, or bronze intanks or lines.) This product should be stored under a dry inert gas blanket, such as nitrogen, to minimize contamination resulting from contact with air and water Store in original containers. Keep containers securely sealed.
Store in a cool, dry, well-ventilated area.
Store away from incompatible materials and foodstuff containers.
Protect containers against physical damage and check regularly for leaks.
Observe manufacturer's storage and handling recommendations contained within this MSDS.
DO NOT store near acids, or oxidising agents
No smoking, naked lights, heat or ignition sources.
Conditions for safe storage, including any incompatibilities
Lined metal can, lined metal pail/ can. Plastic pail. Polyliner drum. Packing as recommended by manufacturer. Check all containers are clearly labelled and free from leaks. For low viscosity materials Drums and jerricans must be of the non-removable head type. Where a can is to be used as an inner package, the can must have a screwed enclosure. For materials with a viscosity of at least 2680 cSt. (23 deg. C) and solids (between 15 C deg. and 40 deg C.): Removable head packaging; Cans with friction closures and low pressure tubes and cartridges may be used.
Where combination packages are used, and the inner packages are of glass, porcelain or stoneware, there must be sufficient inert cushioning material incontact with inner and outer packages unless the outer packaging is a close fitting moulded plastic box and the substances are not incompatible with theplastic.
is a strong base in aqueous solutions is incompatible wit strong oxidisers, organic anhydrides, acrylates, alcohols, aldehydes, alkylene oxides, substituted allyls, cellulose nitrate, cresols,caprolactam solution, epichlorohydrin, ethylene dichloride, isocyanates, ketones, glycols, nitrates, organic halides, phenols, vinyl acetate decomposes exothermically with maleic anhydride may increase the explosive sensitivity of nitromethane attacks aluminium, copper, magnesium, nickel, zinc, or their alloys, and galvanised steel Phenols are incompatible with strong reducing substances such as hydrides, nitrides, alkali metals, and sulfides. Avoid use of aluminium, copper and brass alloys in storage and process equipment. Heat is generated by the acid-base reaction between phenols and bases. Phenols are sulfonated very readily (for example, by concentrated sulfuric acid at room temperature), these reactions generate heat. Phenols are nitrated very rapidly, even by dilute nitric acid. Nitrated phenols often explode when heated. Many of them form metal salts that tend toward detonation by rather mild shock. Avoid oxidising agents, acids, acid chlorides, acid anhydrides, chloroformates. Avoid contact with copper, aluminium and their alloys. SECTION 8 EXPOSURE CONTROLS / PERSONAL PROTECTION
OCCUPATIONAL EXPOSURE LIMITS (OEL)
Australia Exposure Standards Australia Exposure Standards bisphenol A/ diglycidyl etherpolymer, high molecular Epoxy resin (EPON 1001) bisphenol A/ diglycidyl etherpolymer, high molecular Epoxy resin (EPON 1007) bisphenol A/ diglycidyl etherpolymer, high molecular Epoxy resin (EPON 820) bisphenol A/ diglycidyl etherpolymer, high molecular Epoxy resin ERL-2795 Bisphenol A; (4,4'-Isopropylidenediphenol) Aminoethylpiperazine, N- Nonyl phenol (mixed isomers) Nonyl phenol, 4- (branched) Benzyldimethylamine; (Dimethylbenzylamine, N,N-; BDMA) Page 6 of 18
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Revised IDLH
bisphenol A/ diglycidyl etherpolymer, high molecular Engineering controls are used to remove a hazard or place a barrier between the worker and the hazard. Well-designed engineering controls can be highlyeffective in protecting workers and will typically be independent of worker interactions to provide this high level of protection.
The basic types of engineering controls are:Process controls which involve changing the way a job activity or process is done to reduce the risk.
Enclosure and/or isolation of emission source which keeps a selected hazard "physically" away from the worker and ventilation that strategically "adds" and"removes" air in the work environment. Ventilation can remove or dilute an air contaminant if designed properly. The design of a ventilation system must matchthe particular process and chemical or contaminant in use.
Employers may need to use multiple types of controls to prevent employee overexposure. General exhaust is adequate under normal operating conditions. Local exhaust ventilation may be required in special circumstances. If risk of overexposureexists, wear approved respirator. Supplied-air type respirator may be required in special circumstances. Correct fit is essential to ensure adequate protection.
Provide adequate ventilation in warehouses and enclosed storage areas. Air contaminants generated in the workplace possess varying "escape" velocitieswhich, in turn, determine the "capture velocities" of fresh circulating air required to effectively remove the contaminant.
Type of Contaminant: 0.25-0.5 m/s (50-100 solvent, vapours, degreasing etc., evaporating from tank (in still air).
aerosols, fumes from pouring operations, intermittent container filling, low speed conveyer transfers, welding, spray drift, plating 0.5-1 m/s (100-200 acid fumes, pickling (released at low velocity into zone of active generation) direct spray, spray painting in shallow booths, drum filling, conveyer loading, crusher dusts, gas discharge (active generation into 1-2.5 m/s (200-500 zone of rapid air motion) grinding, abrasive blasting, tumbling, high speed wheel generated dusts (released at high initial velocity into zone of very high rapid 2.5-10 m/s (500-2000 Within each range the appropriate value depends on: Lower end of the range Upper end of the range 1: Room air currents minimal or favourable to capture 1: Disturbing room air currents 2: Contaminants of low toxicity or of nuisance value only.
2: Contaminants of high toxicity 3: Intermittent, low production.
3: High production, heavy use 4: Large hood or large air mass in motion 4: Small hood-local control only Simple theory shows that air velocity falls rapidly with distance away from the opening of a simple extraction pipe. Velocity generally decreases with the squareof distance from the extraction point (in simple cases). Therefore the air speed at the extraction point should be adjusted, accordingly, after reference todistance from the contaminating source. The air velocity at the extraction fan, for example, should be a minimum of 1-2 m/s (200-400 f/min) for extraction ofsolvents generated in a tank 2 meters distant from the extraction point. Other mechanical considerations, producing performance deficits within the extractionapparatus, make it essential that theoretical air velocities are multiplied by factors of 10 or more when extraction systems are installed or used.
Chemical goggles.
Full face shield may be required for supplementary but never for primary protection of eyes.
Contact lenses may pose a special hazard; soft contact lenses may absorb and concentrate irritants. A written policy document, describing the wearing oflenses or restrictions on use, should be created for each workplace or task. This should include a review of lens absorption and adsorption for the class of Eye and face protection
chemicals in use and an account of injury experience. Medical and first-aid personnel should be trained in their removal and suitable equipment should bereadily available. In the event of chemical exposure, begin eye irrigation immediately and remove contact lens as soon as practicable. Lens should be removedat the first signs of eye redness or irritation - lens should be removed in a clean environment only after workers have washed hands thoroughly. [CDC NIOSHCurrent Intelligence Bulletin 59], [AS/NZS 1336 or national equivalent] See Hand protection below Wear chemical protective gloves, e.g. PVC. Wear safety footwear or safety gumboots, e.g. Rubber When handling corrosive liquids, wear trousers or overalls outside of boots, to avoid spills entering boots. The material may produce skin sensitisation in predisposed individuals. Care must be taken, when removing gloves and other protective equipment, to avoidall possible skin contact. Contaminated leather items, such as shoes, belts and watch-bands should be removed and destroyed. The selection of suitable gloves does not only depend on the material, but also on further marks of quality which vary from manufacturer to manufacturer. Where Page 7 of 18
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the chemical is a preparation of several substances, the resistance of the glove material can not be calculated in advance and has therefore to be checked priorto the application.
The exact break through time for substances has to be obtained from the manufacturer of the protective gloves and.has to be observed when making a finalchoice.
Suitability and durability of glove type is dependent on usage. Important factors in the selection of gloves include: frequency and duration of contact,chemical resistance of glove material, glove thickness and Select gloves tested to a relevant standard (e.g. Europe EN 374, US F739, AS/NZS 2161.1 or national equivalent).
When prolonged or frequently repeated contact may occur, a glove with a protection class of 5 or higher (breakthrough time greater than 240 minutesaccording to EN 374, AS/NZS 2161.10.1 or national equivalent) is recommended.
When only brief contact is expected, a glove with a protection class of 3 or higher (breakthrough time greater than 60 minutes according to EN 374, AS/NZS2161.10.1 or national equivalent) is recommended.
Some glove polymer types are less affected by movement and this should be taken into account when considering gloves for long-term use.
Contaminated gloves should be replaced.
Gloves must only be worn on clean hands. After using gloves, hands should be washed and dried thoroughly. Application of a non-perfumed moisturiser isrecommended.
See Other protection below Overalls. PVC Apron. PVC protective suit may be required if exposure severe. Eyewash unit. Ensure there is ready access to a safety shower. GLOVE SELECTION INDEX
Type AK-P Filter of sufficient capacity. (AS/NZS 1716 & 1715, EN 143:2000 & 149:2001, ANSIZ88 or national equivalent) Glove selection is based on a modified presentation of the:
"Forsberg Clothing Performance Index".
Where the concentration of gas/particulates in the breathing zone, approaches or exceeds the The effect(s) of the following substance(s) are taken into account in the computer-
"Exposure Standard" (or ES), respiratory protection is required.
generated selection:
Degree of protection varies with both face-piece and Class of filter; the nature of protection Ramset Chemset Injection Reo 502 varies with Type of filter.
Powered Air
* CPI - Chemwatch Performance Index A: Best SelectionB: Satisfactory; may degrade after 4 hours continuous immersion C: Poor to Dangerous Choice for other than short term immersion NOTE: As a series of factors will influence the actual performance of the glove, a final
selection must be based on detailed observation. -* Where the glove is to be used on a short term, casual or infrequent basis, factors such as "feel" or convenience (e.g. disposability), may dictate a choice of gloves which might otherwise A(All classes) = Organic vapours, B AUS or B1 = Acid gasses, B2 = Acid gas or hydrogen be unsuitable following long-term or frequent use. A qualified practitioner should be consulted.
cyanide(HCN), B3 = Acid gas or hydrogen cyanide(HCN), E = Sulfur dioxide(SO2), G =Agricultural chemicals, K = Ammonia(NH3), Hg = Mercury, NO = Oxides of nitrogen, MB =Methyl bromide, AX = Low boiling point organic compounds(below 65 degC) SECTION 9 PHYSICAL AND CHEMICAL PROPERTIES
Information on basic physical and chemical properties
Supplied in a plastic coaxial tube - containing both parts. Part A is a white viscous liquid; not miscible with water. Part B is a black viscous liquid; not miscible Relative density (Water = 1)
n-octanol / water
pH (as supplied)
Melting point / freezing
point (°C)
Initial boiling point and
Molecular weight (g/mol)
boiling range (°C)
Flash point (°C)
Surface Tension (dyn/cm or
Upper Explosive Limit (%)
Lower Explosive Limit (%)
Volatile Component (%vol)
VOC = 0 g/l (mixed and hardened) Vapour pressure (kPa)
Gas group
Solubility in water (g/L)
pH as a solution (1%)
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Vapour density (Air = 1)
SECTION 10 STABILITY AND REACTIVITY
Unstable in the presence of incompatible materials.
Product is considered stable.
Hazardous polymerisation will not occur.
Possibility of hazardous
Conditions to avoid
SECTION 11 TOXICOLOGICAL INFORMATION
Information on toxicological effects
Inhalation of vapours or aerosols (mists, fumes), generated by the material during the course of normal handling, may be harmful.
Inhalation of epoxy resin amine hardeners (including polyamines and amine adducts) may produce bronchospasm and coughing episodes lasting several daysafter cessation of the exposure. Even faint traces of these vapours may trigger an intense reaction in individuals showing "amine asthma".
The compound causes intestinal irritation due to its caustic nature. Lower doses may cause impaired appetite, sluggish reaction to stimuli and reducedalertness. High doses may cause eye irritation, excessive tear secretion; difficulty in breathing; lung, liver and kidney damage. Death may also result. The above reflect the results of animal testing.
Inhaling corrosive bases may irritate the respiratory tract. Symptoms include cough, choking, pain and damage to the mucous membrane.
Inhalation hazard is increased at higher temperatures.
If phenols are absorbed via the lungs, systemic effects may occur affecting the cardiovascular and nervous systems. Inhalation can result in profuseperspiration, intense thirst, nausea, vomiting, diarrhoea, cyanosis, restlessness, stupor, falling blood pressure, hyperventilation, abdominal pain, anaemia,convulsions, coma, swelling and inflammation of the lung.
Accidental ingestion of the material may be harmful; animal experiments indicate that ingestion of less than 150 gram may be fatal or may produce seriousdamage to the health of the individual.
The material can produce chemical burns within the oral cavity and gastrointestinal tract following ingestion.
Ingestion of amine epoxy-curing agents (hardeners) may cause severe abdominal pain, nausea, vomiting or diarrhoea. The vomitus may contain blood andmucous.
Some phenol derivatives can cause damage to the digestive system. If absorbed, profuse sweating, thirst, nausea, vomiting, diarrhoea, cyanosis, restlessness,stupor, low blood pressure, gasping, abdominal pain, anaemia, convulsions, coma and lung swelling can happen followed by pneumonia.
Skin contact with the material may be harmful; systemic effects may result following absorption.
The material can produce chemical burns following direct contact with the skin.
Amine epoxy-curing agents (hardeners) may produce primary skin irritation and sensitisation dermatitis in predisposed individuals. Cutaneous reactionsinclude erythema, intolerable itching and severe facial swelling.
Undiluted benzene-1,3-dimethanamine�may be corrosive to the skin. Concentrated solution of the material produces severe reddening and irritation. Repeated Skin Contact
applications of a dilute concentration produce local swelling and redness, and skin sensitisation, which has been reported among workers in plasticsmanufacturing.
Phenol and its derivatives can cause severe skin irritation if contact is maintained, and can be absorbed to the skin affecting the cardiovascular and centralnervous system. Effects include sweating, intense thirst, nausea and vomiting, diarrhoea, cyanosis, restlessness, stupor, low blood pressure, hyperventilation,abdominal pain, anaemia, convulsions, coma, lung swelling followed by pneumonia.
Open cuts, abraded or irritated skin should not be exposed to this material The material can produce chemical burns to the eye following direct contact. Vapours or mists may be extremely irritating.
If applied to the eyes, this material causes severe eye damage.
Some phenol derivatives may produce mild to severe eye irritation with redness, pain and blurred vision. Permanent eye injury may occur; recovery may also becomplete or partial.
Repeated or prolonged exposure to corrosives may result in the erosion of teeth, inflammatory and ulcerative changes in the mouth and necrosis (rarely) of thejaw. Bronchial irritation, with cough, and frequent attacks of bronchial pneumonia may ensue.
Strong evidence exists that this substance may cause irreversible mutations (though not lethal) even following a single exposure.
Inhaling this product is more likely to cause a sensitisation reaction in some persons compared to the general population.
Skin contact with the material is more likely to cause a sensitisation reaction in some persons compared to the general population.
Ample evidence from experiments exists that there is a suspicion this material directly reduces fertility.
Based on experience with animal studies, exposure to the material may result in toxic effects to the development of the foetus, at levels which do not causesignificant toxic effects to the mother.
Laboratory (in vitro) and animal studies show, exposure to the material may result in a possible risk of irreversible effects, with the possibility of producingmutation.
Substance accumulation, in the human body, may occur and may cause some concern following repeated or long-term occupational exposure.
Long-term exposure to phenol derivatives can cause skin inflammation, loss of appetite and weight, weakness, muscle aches and pain, liver damage, dark urine, loss of nails, skin eruptions, diarrhoea, nervous disorders with headache, salivation, fainting, discolouration of the skin and eyes, vertigo and mental disorders, and damage to the liver and kidneys.
There has been some concern that this material can cause cancer or mutations but there is not enough data to make an assessment.
Solid phenol is highly toxic if swallowed, inhaled or on skin contact. Chronic phenol poisoning is very rarely reported, but symptoms include vomiting, difficulty inswallowing, diarrhoea, lack of appetite, headache, fainting, dizziness, dark urine, mental disturbances, possibly skin rash and death due to liver and kidneydamage may occur.
Repeated exposure of animals to phenol vapour at concentrations ranging from 26 to 52 ppm has produced respiratory, cardiovascular, liver, kidney and neurologic toxicity and may produce blood cancers in mice on oral exposure.
Inhalation of epoxy resin amine hardeners (including polyamines and amine adducts) may produce bronchospasm and coughing episodes lasting several daysafter cessation of the exposure. Even faint traces of these vapours may trigger an intense reaction in individuals showing "amine asthma".
Ramset Chemset Injection
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bisphenol A/ diglycidyl ether
polymer, high molecular
dermal (rat) LD50: >800 mg/kg Eye (rabbit): 100 mg - mild Oral (rat) LD50: 13447 mg/kg dermal (rat) LD50: >3100 mg/kg Eye (rabbit): 0.05 mg/24h SEVERE Inhalation (rat) LC50: 700 ppm/1hE Skin (rabbit): 0.75 mg/24h SEVERE Oral (rat) LD50: 987 mg/kg Dermal (rabbit) LD50: 3600 mg/kg Eye (rabbit): 0.25 mg/24h-SEVERE bisphenol A
Oral (rat) LD50: 1200 mg/kg Skin (rabbit): 250 mg open - mild Skin (rabbit): 500 mg/24h - mild Dermal (rabbit) LD50: 866 mg/kg Eye (rabbit): 20 mg/24h - mod Oral (rat) LD50: >1000 mg/kg Skin (rabbit): 0.1 mg/24h - mild Skin (rabbit): 5 mg/24h - SEVERE Dermal (rabbit) LD50: 2030.86 mg/kg Oral (rat) LD50: 1246 mg/kg Dermal (rabbit) LD50: 1494 mg/kg Eye (rabbit): 5 mg - SEVERE Inhalation (mouse) LC50: 1.8 mg/L/2hE Skin (rabbit): 500 mg/4h-SEVERE Inhalation (mouse) LC50: 2.052 mg/L4 h Inhalation (rat) LC50: ca.2.052 mg/L4 h Oral (rat) LD50: 270 mg/kg dermal (rat) LD50: 662.5 mg/kg Eye(rabbit): 100 mg rinse - mild Inhalation (rat) LC50: 0.316 mg/L/4H Eye(rabbit): 5 mg - SEVERE Oral (rat) LD50: 317 mg/kgE Skin(rabbit): 500 mg open -SEVERE Skin(rabbit): 500 mg/24hr - SEVERE 1. Value obtained from Europe ECHA Registered Substances - Acute toxicity 2.* Value obtained from manufacturer's SDS. Unless otherwise specified dataextracted from RTECS - Register of Toxic Effect of chemical Substances The following information refers to contact allergens as a group and may not be specific to this product. Contact allergies quickly manifest themselves as contact eczema, more rarely as urticaria or Quincke's oedema. The pathogenesis of contact eczemainvolves a cell-mediated (T lymphocytes) immune reaction of the delayed type. Other allergic skin reactions, e.g. contact urticaria, involve antibody- mediated immune reactions. The significance of the contact allergen is not simply determined by its sensitisation potential: the distribution of the substance and the opportunities for contact with it are equally important. A weakly sensitising substance which is widely distributed can be a moreimportant allergen than one with stronger sensitising potential with which few individuals come into contact. From a clinical point of view, substancesare noteworthy if they produce an allergic test reaction in more than 1% of the persons tested.
Allergic reactions involving the respiratory tract are usually due to interactions between IgE antibodies and allergens and occur rapidly. Allergicpotential of the allergen and period of exposure often determine the severity of symptoms. Some people may be genetically more prone than others, andexposure to other irritants may aggravate symptoms. Allergy causing activity is due to interactions with proteins.
Attention should be paid to atopic diathesis, characterised by increased susceptibility to nasal inflammation, asthma and eczema.
Exogenous allergic alveolitis is induced essentially by allergen specific immune-complexes of the IgG type; cell-mediated reactions (T lymphocytes) may be involved. Such allergy is of the delayed type with onset up to four hours following exposure.
Ramset Chemset Injection Reo
No significant acute toxicological data identified in literature search. The chemical structure of hydroxylated diphenylalkanes or bisphenols consists of two phenolic rings joined together through a bridging carbon. Thisclass of endocrine disruptors that mimic oestrogens is widely used in industry, particularly in plasticsBisphenol A (BPA) and some related compounds exhibit oestrogenic activity in human breast cancer cell line MCF-7, but there were remarkabledifferences in activity. Several derivatives of BPA exhibited significant thyroid hormonal activity towards rat pituitary cell line GH3, which releases growthhormone in a thyroid hormone-dependent manner. However, BPA and several other derivatives did not show such activity. Results suggest that the4-hydroxyl group of the A-phenyl ring and the B-phenyl ring of BPA derivatives are required for these hormonal activities, and substituents at the3,5-positions of the phenyl rings and the bridging alkyl moiety markedly influence the activities.
Bisphenols promoted cell proliferation and increased the synthesis and secretion of cell type-specific proteins. When ranked by proliferative potency, thelonger the alkyl substituent at the bridging carbon, the lower the concentration needed for maximal cell yield; the most active compound contained twopropyl chains at the bridging carbon. Bisphenols with two hydroxyl groups in the para position and an angular configuration are suitable for appropriatehydrogen bonding to the acceptor site of the oestrogen receptor.
Ethyleneamines are very reactive and can cause chemical burns, skin rashes and asthma-like symptoms. It is readily absorbed through the skin and maycause eye blindness and irreparable damage. As such, they require careful handling. In general, the low-molecular weight polyamines have beenpositive in the Ames assay (for genetic damage); however, this is probably due to their ability to chelate copper.
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The material may produce severe irritation to the eye causing pronounced inflammation. Repeated or prolonged exposure to irritants may produceconjunctivitis.
The material may cause severe skin irritation after prolonged or repeated exposure and may produce on contact skin redness, swelling, the productionof vesicles, scaling and thickening of the skin. Repeated exposures may produce severe ulceration.
Asthma-like symptoms may continue for months or even years after exposure to the material ceases. This may be due to a non-allergenic condition known as reactive airways dysfunction syndrome (RADS) which can occur following exposure to high levels of highly irritating compound. Key criteria for the diagnosis of RADS include the absence of preceding respiratory disease, in a non-atopic individual, with abrupt onset of persistent asthma-likesymptoms within minutes to hours of a documented exposure to the irritant. A reversible airflow pattern, on spirometry, with the presence of moderate tosevere bronchial hyperreactivity on methacholine challenge testing and the lack of minimal lymphocytic inflammation, without eosinophilia, have alsobeen included in the criteria for diagnosis of RADS. RADS (or asthma) following an irritating inhalation is an infrequent disorder with rates related tothe concentration of and duration of exposure to the irritating substance. Industrial bronchitis, on the other hand, is a disorder that occurs as result ofexposure due to high concentrations of irritating substance (often particulate in nature) and is completely reversible after exposure ceases. Thedisorder is characterised by dyspnea, cough and mucus production.
The following information refers to contact allergens as a group and may not be specific to this product. Contact allergies quickly manifest themselves as contact eczema, more rarely as urticaria or Quincke's oedema. The pathogenesis of contact eczemainvolves a cell-mediated (T lymphocytes) immune reaction of the delayed type. Other allergic skin reactions, e.g. contact urticaria, involve antibody- mediated immune reactions. The significance of the contact allergen is not simply determined by its sensitisation potential: the distribution of the substance and the opportunities for contact with it are equally important. A weakly sensitising substance which is widely distributed can be a moreimportant allergen than one with stronger sensitising potential with which few individuals come into contact. From a clinical point of view, substancesare noteworthy if they produce an allergic test reaction in more than 1% of the persons tested.
The chemical structure of hydroxylated diphenylalkanes or bisphenols consists of two phenolic rings joined together through a bridging carbon. Thisclass of endocrine disruptors that mimic oestrogens is widely used in industry, particularly in plasticsBisphenol A (BPA) and some related compounds exhibit oestrogenic activity in human breast cancer cell line MCF-7, but there were remarkabledifferences in activity. Several derivatives of BPA exhibited significant thyroid hormonal activity towards rat pituitary cell line GH3, which releases growthhormone in a thyroid hormone-dependent manner. However, BPA and several other derivatives did not show such activity. Results suggest that the4-hydroxyl group of the A-phenyl ring and the B-phenyl ring of BPA derivatives are required for these hormonal activities, and substituents at the3,5-positions of the phenyl rings and the bridging alkyl moiety markedly influence the activities.
Bisphenols promoted cell proliferation and increased the synthesis and secretion of cell type-specific proteins. When ranked by proliferative potency, thelonger the alkyl substituent at the bridging carbon, the lower the concentration needed for maximal cell yield; the most active compound contained twopropyl chains at the bridging carbon. Bisphenols with two hydroxyl groups in the para position and an angular configuration are suitable for appropriatehydrogen bonding to the acceptor site of the oestrogen receptor.
The material may produce severe irritation to the eye causing pronounced inflammation. Repeated or prolonged exposure to irritants may produceconjunctivitis.
The material may cause skin irritation after prolonged or repeated exposure and may produce on contact skin redness, swelling, the production of vesicles, scaling and thickening of the skin.
In mice, dermal application of bisphenol A diglycidyl ether (BADGE) (1, 10, or 100 mg/kg) for 13 weeks produced mild to moderate chronic activedermatitis. At the high dose, spongiosis and epidermal micro abscess formation were observed. In rats, dermal application of BADGE (10, 100, or 1000mg/kg) for 13 weeks resulted in a decrease in body weight at the high dose. The no-observable effect level (NOEL) for dermal exposure was 100 mg/kgfor both sexes. In a separate study, application of BADGE (same doses) five times per week for 13 weeks not only caused a decrease in body weightbut also produced chronic dermatitis at all dose levels in males and at >100 mg/kg in females (as well as in a satellite group of females given 1000mg/kg).
BISPHENOL A/ DIGLYCIDYL
Reproductive and Developmental Toxicity: BADGE (50, 540, or 750 mg/kg) administered to rats via gavage for 14 weeks (P1) or 12 weeks (P2)
ETHER POLYMER, HIGH
produced decreased body weight in all males at the mid dose and in both males and females at the high dose, but had no reproductive effects. The NOEL for reproductive effects was 750 mg/kg.
Carcinogenicity: IARC concluded that "there is limited evidence for the carcinogenicity of bisphenol A diglycidyl ether in experimental animals." Its
overall evaluation was "Bisphenol A diglycidyl ether is not classifiable as to its carcinogenicity to humans (Group 3).
In a lifetime tumourigenicity study in which 90-day-old C3H mice received three dermal applications per week of BADGE (undiluted dose) for 23
months, only one out of 32 animals developed a papilloma after 16 months. A retest, in which skin paintings were done for 27 months, however, produced
no tumours (Weil et al., 1963). In another lifetime skin-painting study, BADGE (dose n.p.) was also reported to be noncarcinogenic to the skin of C3H
mice; it was, however, weakly carcinogenic to the skin of C57BL/6 mice (Holland et al., 1979; cited by Canter et al., 1986). In a two-year bioassay, female
Fisher 344 rats dermally exposed to BADGE (1, 100, or 1000 mg/kg) showed no evidence of dermal carcinogenicity but did have low incidences of
tumours in the oral cavity (U.S. EPA, 1997).
Genotoxicity: In S. typhimurium strains TA100 and TA1535, BADGE (10-10,000 ug/plate) was mutagenic with and without S9; negative results were
obtained in TA98 and TA1537 (Canter et al., 1986; Pullin, 1977). In a spot test, BADGE (0.05 or 10.00 mg) failed to show mutagenicity in strains TA98
and TA100 (Wade et al., 1979). Negative results were also obtained in the body fluid test using urine of female BDF and ICR mice (1000 mg/kg
BADGE), the mouse host-mediated assay (1000 mg/kg), micronucleus test (1000 mg/kg), and dominant lethal assay ( 3000 mg/kg).
Immunotoxicity: Intracutaneous injection of diluted BADGE (0.1 mL) three times per week on alternate days (total of 8 injections) followed by a
three-week incubation period and a challenge dose produced sensitisation in 19 of 20 guinea pigs
-
Consumer exposure to BADGE is almost exclusively from migration of BADGE from can coatings into food. Using a worst-case scenario that
assumes BADGE migrates at the same level into all types of food, the estimated per capita daily intake for a 60-kg individual is approximately 0.16 ug/kgbody weight/day. A review of one- and two-generation reproduction studies and developmental investigations found no evidence of reproductive orendocrine toxicity, the upper ranges of dosing being determined by maternal toxicity. The lack of endocrine toxicity in the reproductive and developmentaltoxicological tests is supported by negative results from both in vivo and in vitro assays designed specifically to detect oestrogenic and androgenicproperties of BADGE. An examination of data from sub-chronic and chronic toxicological studies support a NOAEL of 50 mg/ kg/body weight day fromthe 90-day study, and a NOAEL of 15 mg/kg body weigh/day (male rats) from the 2-year carcinogenicity study. Both NOAELS are consideredappropriate for risk assessment. Comparing the estimated daily human intake of 0.16 ug/kg body weight/day with the NOAELS of 50 and 15 mg/kg bodyweight/day shows human exposure to BADGE from can coatings is between 250,000 and 100,000-fold lower than the NOAELs from the most sensitivetoxicology tests. These large margins of safety together with lack of reproductive, developmental, endocrine and carcinogenic effects supports thecontinued use of BADGE for use in articles intended to come into contact with foodstuffs.
for RTECS No: SL 6475000: (liquid grade) Equivocal tumourigen by RTECS criteria Somnolence, dyspnea, peritonitis The following information refers to contact allergens as a group and may not be specific to this product. Contact allergies quickly manifest themselves as contact eczema, more rarely as urticaria or Quincke's oedema. The pathogenesis of contact eczemainvolves a cell-mediated (T lymphocytes) immune reaction of the delayed type. Other allergic skin reactions, e.g. contact urticaria, involve antibody- mediated immune reactions. The significance of the contact allergen is not simply determined by its sensitisation potential: the distribution of the substance and the opportunities for contact with it are equally important. A weakly sensitising substance which is widely distributed can be a more important allergen than one with stronger sensitising potential with which few individuals come into contact. From a clinical point of view, substances are noteworthy if they produce an allergic test reaction in more than 1% of the persons tested.
Asthma-like symptoms may continue for months or even years after exposure to the material ceases. This may be due to a non-allergenic condition known as reactive airways dysfunction syndrome (RADS) which can occur following exposure to high levels of highly irritating compound. Key criteria for the diagnosis of RADS include the absence of preceding respiratory disease, in a non-atopic individual, with abrupt onset of persistent asthma-likesymptoms within minutes to hours of a documented exposure to the irritant. A reversible airflow pattern, on spirometry, with the presence of moderate to Page 11 of 18
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severe bronchial hyperreactivity on methacholine challenge testing and the lack of minimal lymphocytic inflammation, without eosinophilia, have alsobeen included in the criteria for diagnosis of RADS. RADS (or asthma) following an irritating inhalation is an infrequent disorder with rates related tothe concentration of and duration of exposure to the irritating substance. Industrial bronchitis, on the other hand, is a disorder that occurs as result ofexposure due to high concentrations of irritating substance (often particulate in nature) and is completely reversible after exposure ceases. Thedisorder is characterised by dyspnea, cough and mucus production.
Allergic reactions involving the respiratory tract are usually due to interactions between IgE antibodies and allergens and occur rapidly. Allergicpotential of the allergen and period of exposure often determine the severity of symptoms. Some people may be genetically more prone than others, andexposure to other irritants may aggravate symptoms. Allergy causing activity is due to interactions with proteins.
Attention should be paid to atopic diathesis, characterised by increased susceptibility to nasal inflammation, asthma and eczema.
Exogenous allergic alveolitis is induced essentially by allergen specific immune-complexes of the IgG type; cell-mediated reactions (T lymphocytes) may be involved. Such allergy is of the delayed type with onset up to four hours following exposure.
For benzene-1,3-dimethanamine (m-xylene-alpha,alpha'- diamine)The toxicity via oral administration and inhalation was tissue damage in the digestive and respiratory organs, respectively, which are the first contactsites. The chemical is corrosive to rat and mouse skin and a sensitiser in the guinea pig maximisation test.
In the 28-day repeated dose toxicity study [OECD TG 407], the chemical was given to rats by gavage at doses of 0, 10, 40, 150 and 600 mg/kg b.w/day.
One male and four females died, and salivation, low locomotor activity and piloerection were noted in the 600 mg/kg group. Furthermore, ulceration,acanthosis with hyperkeratosis and submucosal inflammation were observed in the forestomach. No adverse effects were observed in the 150 mg/kgand the lower dose groups.
A reproductive /developmental toxicity screening test [OECD TG 421] of rats by gavage at 50, 150 and 450 mg/kg b.w/day for at least 41 days resulted indeath in one male in the 150 mg/kg group, and three males and one female in the 450 mg/kg group. In almost all 450 mg/kg animals, the samehistopathological changes as the above 28-day study were observed in the forestomach. No adverse effects were found at 50 mg/kg b.w/day. Based onthis information, the NOAEL for repeated dose toxicity is considered to be 50 mg/kg b.w/day.
In the above reproductive/developmental toxicity screening test [OECD TG 421] the substance was administered from 14 days before mating to 20 daysafter mating in males and to day 3 of lactation in females. No adverse effects were observed in terms of copulation, fertility, delivery and nursing ofparents, and the viability, body weight and morphology of offspring. The NOAEL for reproductive/developmental toxicity (F1 offspring) was 450 mg/kgb.w/day.
The chemical was not mutagenic in bacteria [OECD TG 471 & 472]. It induced neither chromosomal aberrations in mammalian cells in vitro [OECDTG 473] nor micronuclei in mouse bone marrow in vivo [OECD TG 474].
In clinical observation of workers during the manufacturing process, the chemical appears to act as a gastrointestinal irritant. It has also been shown tocause contact sensitisation reactions in workers at concentrations equal to and below 0.1 mg/m3 The material may produce severe irritation to the eye causing pronounced inflammation. Repeated or prolonged exposure to irritants may produceconjunctivitis.
The material may cause severe skin irritation after prolonged or repeated exposure and may produce on contact skin redness, swelling, the productionof vesicles, scaling and thickening of the skin. Repeated exposures may produce severe ulceration.
The following information refers to contact allergens as a group and may not be specific to this product. Contact allergies quickly manifest themselves as contact eczema, more rarely as urticaria or Quincke's oedema. The pathogenesis of contact eczemainvolves a cell-mediated (T lymphocytes) immune reaction of the delayed type. Other allergic skin reactions, e.g. contact urticaria, involve antibody- mediated immune reactions. The significance of the contact allergen is not simply determined by its sensitisation potential: the distribution of the substance and the opportunities for contact with it are equally important. A weakly sensitising substance which is widely distributed can be a moreimportant allergen than one with stronger sensitising potential with which few individuals come into contact. From a clinical point of view, substancesare noteworthy if they produce an allergic test reaction in more than 1% of the persons tested.
Asthma-like symptoms may continue for months or even years after exposure to the material ceases. This may be due to a non-allergenic condition known as reactive airways dysfunction syndrome (RADS) which can occur following exposure to high levels of highly irritating compound. Key criteria for the diagnosis of RADS include the absence of preceding respiratory disease, in a non-atopic individual, with abrupt onset of persistent asthma-likesymptoms within minutes to hours of a documented exposure to the irritant. A reversible airflow pattern, on spirometry, with the presence of moderate tosevere bronchial hyperreactivity on methacholine challenge testing and the lack of minimal lymphocytic inflammation, without eosinophilia, have alsobeen included in the criteria for diagnosis of RADS. RADS (or asthma) following an irritating inhalation is an infrequent disorder with rates related tothe concentration of and duration of exposure to the irritating substance. Industrial bronchitis, on the other hand, is a disorder that occurs as result ofexposure due to high concentrations of irritating substance (often particulate in nature) and is completely reversible after exposure ceases. Thedisorder is characterised by dyspnea, cough and mucus production.
No significant acute toxicological data identified in literature search. The chemical structure of hydroxylated diphenylalkanes or bisphenols consists of two phenolic rings joined together through a bridging carbon. Thisclass of endocrine disruptors that mimic oestrogens is widely used in industry, particularly in plasticsBisphenol A (BPA) and some related compounds exhibit oestrogenic activity in human breast cancer cell line MCF-7, but there were remarkabledifferences in activity. Several derivatives of BPA exhibited significant thyroid hormonal activity towards rat pituitary cell line GH3, which releases growthhormone in a thyroid hormone-dependent manner. However, BPA and several other derivatives did not show such activity. Results suggest that the4-hydroxyl group of the A-phenyl ring and the B-phenyl ring of BPA derivatives are required for these hormonal activities, and substituents at the3,5-positions of the phenyl rings and the bridging alkyl moiety markedly influence the activities.
BISPHENOL A
Bisphenols promoted cell proliferation and increased the synthesis and secretion of cell type-specific proteins. When ranked by proliferative potency, thelonger the alkyl substituent at the bridging carbon, the lower the concentration needed for maximal cell yield; the most active compound contained twopropyl chains at the bridging carbon. Bisphenols with two hydroxyl groups in the para position and an angular configuration are suitable for appropriatehydrogen bonding to the acceptor site of the oestrogen receptor.
For bisphenol A (BPA)Following oral administration absorption of BPA is rapid and extensive while dermal absorption is limited. Extensive first pass metabolism occursfollowing absorption from the gastrointestinal tract with glucuronide conjugation being the major metabolic pathway. Bisphenol A is of low acute toxicity (rodent oral LD50 values from 3300-4100 mg/kg, a rabbit oral LD50 value 2230 mg/kg and a rat acute inhalation 6-hour LC50 value >170 mg/m3).
Bisphenol A is not a skin irritant, however, it is severely irritating to the eyes. BPA was negative in gene mutation and clastogenicity assays in culturedmammalian cells, as well as in a micronucleus test for clastogenicity in vivo; therefore, BPA is considered not to present a genotoxic concern forhuman health. BPA results in minimal effects on the liver and kidney (LOAEL from chronic exposure in the diet was 50 mg/kg/day). For reproductivetoxicity, data from a three-generation study in the rat, BPA was not a selective reproductive toxicant at doses ranging from 0.001 to 500 mg/kg/day. BPAis not a developmental toxicant in rats or mice.
Inconsistent findings are reported in the "low dose" literature for bisphenol A. The inherent challenge of conducting these types of studies may beexacerbated with bisphenol A because the endpoints of concern are endocrine-mediated and potentially impacted by factors that include phytoestrogencontent of the animal feed, extent of bisphenol A exposure from caging or water bottles, and the alleged sensitivity of the animal model to oestrogens.
High-dose studies are less susceptible to these types of influences because the toxicologic response should be more robust and less variable . Severallarge, robust, well designed studies with multiple dose groups using several strains of rats and mice have been conducted and none of these detectedany adverse reproductive effects at low to moderate dosage levels of BPA administered via the relevant route of human exposures. Further, none of thesestudies detected changes in prostate weight, age at puberty (rat), pathology or tumors in any tissue, or reproductive tract malformations.
Every chemical that produces low dose cellular and molecular alterations of endocrine function also produces a cascade of effects increasing inseverity resulting in clearly adverse alterations at higher doses, albeit the effects can be different from those seen at low doses. With these endocrinedisrupters, but not BPA, the low dose effects are often causally linked to the high-dose adverse effects of the chemical. This is true for androgens liketestosterone and trenbolone, estrogens like DES, 17beta-oestradiol and ethinyl oestradiol, xenoestrogens like methoxychlor and genistein, andantiandrogens like vinclozolin, for example. Hence, the failure of BPA to produce reproducible adverse effects via a relevant route of exposure, coupled Page 12 of 18
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with the lack of robustness of the many of the low dose studies (sample size, dose range, statistical analyses and experimental design, GLP) and the inability to reproduce many of these effects of any adverse effect strains the credibility of some of these study results.
The lack of reproducibility of the low dose effects, the absence of toxicity in those low-dose-affected tissues at high-doses, and the uncertain adversity ofthe reported effects lead to the conclusion that there is "minimal" concern for reproductive effects.
In contrast, the literature on bisphenol A effects on neural and behavioral response is more consistent with respect to the number of "positive"' studies although it should be noted that the high-dose studies that proved to be the most useful for evaluating reproductive effects did not adequately assessneural and behavioral responses. In addition, even though different investigators assessed different neural and behavioral endpoints, an expert Panelconcluded that the overall findings suggest that bisphenol A may be associated with neural changes in the brain and behavioral alterations related tosexual dimorphism in rodents. For this reason, the Panel expressed "some" concern for these effects even though it is not clear the reported effectsconstitute an adverse toxicological response. In summary:For pregnant women and foetuses, the Expert Panel has different levels of concern for the different developmental endpoints that may be susceptible tobisphenol A disruption, as follows: For neural and behavioral effects, the Expert Panel has some concern;For prostate effects, the Expert Panel has minimal concern;For the potential effect of accelerated puberty, the Expert Panel has minimal concern; andFor birth defects and malformations, the Expert Panel has negligible concern.
For infants and children, the Expert Panel has the following levels of concern for biological processes that might be altered by Bisphenol A, as follows: Some concern for neural and behavioral effects; and Minimal concern for the effect of accelerated puberty.
For adults, the Expert Panel has negligible concern for adverse reproductive effects following exposures in the general population to Bisphenol A. For
highly exposed subgroups, such as occupationally exposed populations, the level of concern is elevated to minimal.
NTP-CERHR Monograph on the Potential Human Reproductive and Developmental Effects of Bisphenol A
National Toxicology Program US Department of Health and Human Services September 2008 NTP Publication No 08-5994
The material may cause skin irritation after prolonged or repeated exposure and may produce on contact skin redness, swelling, the production of
vesicles, scaling and thickening of the skin.
The following information refers to contact allergens as a group and may not be specific to this product. Contact allergies quickly manifest themselves as contact eczema, more rarely as urticaria or Quincke's oedema. The pathogenesis of contact eczemainvolves a cell-mediated (T lymphocytes) immune reaction of the delayed type. Other allergic skin reactions, e.g. contact urticaria, involve antibody- mediated immune reactions. The significance of the contact allergen is not simply determined by its sensitisation potential: the distribution of the substance and the opportunities for contact with it are equally important. A weakly sensitising substance which is widely distributed can be a moreimportant allergen than one with stronger sensitising potential with which few individuals come into contact. From a clinical point of view, substancesare noteworthy if they produce an allergic test reaction in more than 1% of the persons tested.
Ethyleneamines are very reactive and can cause chemical burns, skin rashes and asthma-like symptoms. It is readily absorbed through the skin and maycause eye blindness and irreparable damage. As such, they require careful handling. In general, the low-molecular weight polyamines have beenpositive in the Ames assay (for genetic damage); however, this is probably due to their ability to chelate copper.
The material may produce moderate eye irritation leading to inflammation. Repeated or prolonged exposure to irritants may produce conjunctivitis.
The material may cause severe skin irritation after prolonged or repeated exposure and may produce on contact skin redness, swelling, the productionof vesicles, scaling and thickening of the skin. Repeated exposures may produce severe ulceration.
Asthma-like symptoms may continue for months or even years after exposure to the material ceases. This may be due to a non-allergenic condition known as reactive airways dysfunction syndrome (RADS) which can occur following exposure to high levels of highly irritating compound. Key criteria for the diagnosis of RADS include the absence of preceding respiratory disease, in a non-atopic individual, with abrupt onset of persistent asthma-likesymptoms within minutes to hours of a documented exposure to the irritant. A reversible airflow pattern, on spirometry, with the presence of moderate tosevere bronchial hyperreactivity on methacholine challenge testing and the lack of minimal lymphocytic inflammation, without eosinophilia, have alsobeen included in the criteria for diagnosis of RADS. RADS (or asthma) following an irritating inhalation is an infrequent disorder with rates related tothe concentration of and duration of exposure to the irritating substance. Industrial bronchitis, on the other hand, is a disorder that occurs as result ofexposure due to high concentrations of irritating substance (often particulate in nature) and is completely reversible after exposure ceases. Thedisorder is characterised by dyspnea, cough and mucus production.
for piperazine:Exposure to piperazine and its salts has clearly been demonstrated to cause asthma in occupational settings. No NOAEL can be estimated forrespiratory sensitisation (asthma).
Although the LD50 levels indicate a relatively low level of oral acute toxicity (LD50 1-5 g/kg bw), signs of neurotoxicity may appear in humans afterexposure to lower doses. Based on exposure levels of up to 3.4 mg/kg/day piperazine base and a LOAEL of 110 mg/kg, there is no concern for acute toxicityIn pigs, piperazine is readily absorbed from the gastrointestinal tract, and the major part of the resorbed compound is excreted as unchangedpiperazine during the first 48 hours. The principal route of excretion of piperazine and its metabolites is via urine, with a minor fraction recovered fromfaeces (16%). In humans the kinetics of the uptake and excretion of piperazine and its metabolites with urine appear to be roughly similar to that in thepig, and the nature and extent of conversion to metabolites has not been determined.
Piperazine has demonstrated a low acute toxicity (LD50 = 1-5 g/kg bw) by the oral, dermal, and subcutaneous route of administration to rodents,whereas adequate inhalation toxicity data have not been found. However, there are findings of EEG (electroencephalogram) changes in 37% of 89children administrated 90-130 mg/kg piperazine (two doses during one day), corroborated by a proposed GABA (gamma-aminobutyric acid) receptoragonism exerted by piperazine. Since clinical symptoms of neurotoxicity may occur after exposure to higher doses, a LOAEL of 110 mg/kg piperazinebase for acute neurotoxicity in humans after acute exposure is proposed.
Piperazine, as concentrated aqueous solution, has strongly irritating properties with regard to skin, and should be regarded as corrosive with respectto the eye. Exposure to piperazine and it salts has been demonstrated to cause allergic dermatitis as well as respiratory sensitisation in humans. Asshown by the LLNA, piperazine has a sensitising potential in animals. Although piperazine is clearly sensitising, no NOAEL can be set for this effectfrom the present database.
A NOAEL of 25 mg/kg/day of piperazine for liver toxicity in the beagle dog has been chosen after repeated exposure. A LOAEL of 30 mg/kg/day ofpiperazine for neurotoxicity is proposed based on documentation of (rare cases) of neurotoxicity from human clinical practice. Neurotoxicity alsoappears in other species (e.g., rabbits, dogs, cats, tigers, and horses), but not in rodents.
For reproductive effects of piperazine, there is a NOAEL of 125 mg/kg/day for effects on fertility, i.e., reduced pregnancy index, decreased number ofimplantation sites, and decreased litter sizes in rats. The teratogenic properties have been investigated in rats and rabbits in adequate studies. Inrabbit, such effects may be elicited at a dose level that is also toxic to the dam. The LOAEL is 94 mg/kg/day, and the NOAEL 42 mg/kg/day piperazinebase (maternal and embryotoxic). In the rat study, there were decreases in body weight of both dams and offspring at the top dose (2,100 mg/kg/daypiperazine base), but there were no signs of any malformations.
The genotoxic properties have been investigated both in vitro (in the Ames test, in a nonstandard study on Saccharomyces cervisiae and in Chinesehamster ovary cells) and in vivo, in a micronuclei assay on mice, all with negative results. There are no solid indications of a carcinogenic effect ofpiperazine, neither in animal studies, nor from the investigation on humans. In view of lack of genotoxic action, it appears unlikely that piperazine posesa carcinogenic risk.
There seems to be an additional cancer risk due to the formation of N-mononitrosopiperazine (NPZ) from piperazine. It is possible to calculate ahypothetical additional cancer risk posed by NPZ after exposure to piperazine, but the calculation would depend on several assumptions. We concludethat there seems to be an additional cancer risk due to the formation of NPZ from piperazine, and although it is difficult to estimate, it is probably small.
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Skin (rabbit) LD50: 2140 mg/kg Skin (rabbit): 500 mg(open)-mod Eye (rabbit): 0.5 mg (open)-SEVEREThe material may produce severe irritation to the eye causing pronounced inflammation. Repeated or prolonged exposure to irritants may produceconjunctivitis.
The material may cause severe skin irritation after prolonged or repeated exposure and may produce on contact skin redness, swelling, the productionof vesicles, scaling and thickening of the skin. Repeated exposures may produce severe ulceration.
Asthma-like symptoms may continue for months or even years after exposure to the material ceases. This may be due to a non-allergenic condition known as reactive airways dysfunction syndrome (RADS) which can occur following exposure to high levels of highly irritating compound. Key criteria for the diagnosis of RADS include the absence of preceding respiratory disease, in a non-atopic individual, with abrupt onset of persistent asthma-likesymptoms within minutes to hours of a documented exposure to the irritant. A reversible airflow pattern, on spirometry, with the presence of moderate tosevere bronchial hyperreactivity on methacholine challenge testing and the lack of minimal lymphocytic inflammation, without eosinophilia, have alsobeen included in the criteria for diagnosis of RADS. RADS (or asthma) following an irritating inhalation is an infrequent disorder with rates related tothe concentration of and duration of exposure to the irritating substance. Industrial bronchitis, on the other hand, is a disorder that occurs as result ofexposure due to high concentrations of irritating substance (often particulate in nature) and is completely reversible after exposure ceases. Thedisorder is characterised by dyspnea, cough and mucus production.
for nonylphenol: Nonylphenol was studied for oral toxicity in rats in a 28-day repeat dose toxicity test at doses of 0, 4, 15, 60 and 250 mg/kg/day. Changes suggesting renal dysfunction were mainly noted in both sexes given 250 mg/kg. Liver weights were increased in males given 60 mg/kg and in both sexes given 250 mg/kg group. Histopathologically, hypertrophy of the centrilobular hepatocytes was noted in both sexes given 250 mg/kg. Kidney weights were increased in males given 250 mg/kg and macroscopically, disseminated white spots, enlargement and pelvic dilatation were noted in females given 250 mg/kg. Histopathologically, the following lesions were noted in the 250 mg/kg group: basophilic change of the proximal tubules in both sexes, single cell necrosis of the proximal tubules, inflammatory cell infiltration in the interstitium and casts in females, basophilic change and dilatation of thecollecting tubules in both sexes, simple hyperplasia of the pelvic mucosa and pelvic dilatation in females. In the urinary bladder, simple hyperplasia wasnoted in both sexes given 250 mg/kg. In the caecum, macroscopic dilatation was noted in both sexes given 250 mg/kg. Almost all changes except thosein the kidney disappeared after a 14-day recovery period. The NOELs for males and females are considered to be 15 mg/kg/day and 60 mg/kg/day,respectively, under the conditions of the present study.
Nonylphenol was not mutagenic to Salmonella typhimurium, TA100, TA1535, TA98, TA1537 and Escherichia coli WP2 uvrA, with or without anexogeneous metabolic activation system.
Nonylphenol induced neither structural chromosomal aberrations nor polyploidy in CHL/IU cells, in the absence or presence of an exogenous metabolicactivation system.
These substances are intravenous anaesthetic agents. They have a very low level of acute toxicity; they may cause skin irritation.�Repeated exposure may irritate the stomach. There is no evidence of this group of substances causing mutation or adverse effects on reproduction. However, at highdoses, there may be reduction of newborn weight and reduced survival in early lactation period. Asthma-like symptoms may continue for months or even years after exposure to the material ceases. This may be due to a non-allergenic condition known as reactive airways dysfunction syndrome (RADS) which can occur following exposure to high levels of highly irritating compound. Key criteria for the diagnosis of RADS include the absence of preceding respiratory disease, in a non-atopic individual, with abrupt onset of persistent asthma-likesymptoms within minutes to hours of a documented exposure to the irritant. A reversible airflow pattern, on spirometry, with the presence of moderate tosevere bronchial hyperreactivity on methacholine challenge testing and the lack of minimal lymphocytic inflammation, without eosinophilia, have alsobeen included in the criteria for diagnosis of RADS. RADS (or asthma) following an irritating inhalation is an infrequent disorder with rates related tothe concentration of and duration of exposure to the irritating substance. Industrial bronchitis, on the other hand, is a disorder that occurs as result ofexposure due to high concentrations of irritating substance (often particulate in nature) and is completely reversible after exposure ceases. Thedisorder is characterised by dyspnea, cough and mucus production.
The material may produce severe irritation to the eye causing pronounced inflammation. Repeated or prolonged exposure to irritants may produceconjunctivitis.
The material may cause severe skin irritation after prolonged or repeated exposure and may produce on contact skin redness, swelling, the productionof vesicles, scaling and thickening of the skin. Repeated exposures may produce severe ulceration.
N, N-Dimethylbenzylamine was studied for oral toxicity in a 28 day repeat dose toxicity test. Mortalities of both males and females receiving 400 mg/kg were observed from week 2. Clinical observation revealed miosis in both sexes receiving 100 mg/kg and miosis and salivation in those receiving 200and 400 mg/kg. Body weight gain was suppressed in males receiving 400 mg/kg. Slight increases in total cholesterol were observed in males receiving 200 mg/kg. Pathological examination revealed no abnormalities attributable to the test substance treatment. The NOEL for repeat dose toxicityis considered to be 50 mg/kg/day for both sexes. N, N-Dimethylbenzylamine was not mutagenic to Salmonella typhimurium TA100, TA1535, TA98,TA1537 and Escherichia coli WP2 uvrA and with or without an exogeneous metabolic activation system. N, N-Dimethylbenzylamine induced structuralchromosomal aberrations with an exogeneous metabolic activation system.
The material may produce severe irritation to the eye causing pronounced inflammation. Repeated or prolonged exposure to irritants may produceconjunctivitis.
The material may cause severe skin irritation after prolonged or repeated exposure and may produce on contact skin redness, swelling, the productionof vesicles, scaling and thickening of the skin. Repeated exposures may produce severe ulceration.
Asthma-like symptoms may continue for months or even years after exposure to the material ceases. This may be due to a non-allergenic condition known as reactive airways dysfunction syndrome (RADS) which can occur following exposure to high levels of highly irritating compound. Key criteria for the diagnosis of RADS include the absence of preceding respiratory disease, in a non-atopic individual, with abrupt onset of persistent asthma-like symptoms within minutes to hours of a documented exposure to the irritant. A reversible airflow pattern, on spirometry, with the presence of moderate to
severe bronchial hyperreactivity on methacholine challenge testing and the lack of minimal lymphocytic inflammation, without eosinophilia, have also
been included in the criteria for diagnosis of RADS. RADS (or asthma) following an irritating inhalation is an infrequent disorder with rates related to
the concentration of and duration of exposure to the irritating substance. Industrial bronchitis, on the other hand, is a disorder that occurs as result of
exposure due to high concentrations of irritating substance (often particulate in nature) and is completely reversible after exposure ceases. The
disorder is characterised by dyspnea, cough and mucus production.
The substance is classified by IARC as Group 3:
NOT classifiable as to its carcinogenicity to humans.
Evidence of carcinogenicity may be inadequate or limited in animal testing.
Serious Eye
STOT - Single Exposure
Respiratory or Skin
STOT - Repeated Exposure
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– Data required to make classification available – Data available but does not fill the criteria for classification – Data Not Available to make classification SECTION 12 ECOLOGICAL INFORMATION
Toxic to aquatic organisms, may cause long-term adverse effects in the aquatic environment. Do NOT allow product to come in contact with surface waters or to intertidal areas below the mean high water mark. Do not contaminate water when cleaning equipment or disposing of equipment wash-waters.
Wastes resulting from use of the product must be disposed of on site or at approved waste sites.
For Alkylphenols:Environmental Fate: The alkylphenolics may be divided into three groups. Group I: Ortho-substituted mono-alkylphenols. Group II: Para-substituted mono-alkylphenols. Group III: Di- andtri-substituted mixed alkyl phenols. None of the alkylphenols will be ionized significantly at environmental or physiological pHs. Water solubility and vapor pressure decreases with increasing molecular weight and with increasing octanol/water partition coefficient (log Kow). A few lower molecular weight phenols will be present in significant quantities (>10%) in the air and water compartments.
Atmospheric Fate: Direct photolysis is not expected to be a significant route of loss for any of the alkylphenols; however, indirect photolysis (atmospheric oxidation) has been estimated for allsubstances.
Terrestrial Fate: The vast majority of the alkylphenols will be located in the soil compartment with a few exceptions. This is especially evident in the Group II and Group III materials.
Aquatic Fate: None of the alkylphenols are expected to be susceptible to abiotic hydrolysis under environmental conditions.
Ecotoxicity: The aquatic toxicities for the alkylphenols appear to be related to their degree of absorption in fats and increase basically in line with log Kow. It is reasonable to assume (whereexperimentally determined data are not available) that the toxicity of a particular alkylphenol will be comparable to that of another with like fat absorbability.
For bisphenol A and related bisphenols: In general, studies have shown that bisphenol A can affect growth, reproduction and development in aquatic organisms. Among freshwater organisms, fish appear to be the most sensitive species.
Evidence of endocrine-related effects in fish, aquatic invertebrates, amphibians and reptiles has been reported at environmentally relevant exposure levels lower than those required for acutetoxicity. There is a widespread variation in reported values for endocrine-related effects, but many fall in the range of 1 ug/L to 1 mg/LBisphenol A, its derivatives and analogues, can be released from polymers, resins and certain substances by metabolic productsAs an environmental contaminant, bisphenol A interferes with nitrogen fixation at the roots of leguminous plants associated with the bacterial symbiont Sinorhizobium meliloti. Despite a half-life inthe soil of only 1-10 days, its ubiquity makes it an important pollutant. According to Environment Canada, "initial assessment shows that at low levels, bisphenol A can harm fish and organisms overtime. Studies also indicate that it can currently be found in municipal wastewater." However, a study conducted in the United States found that 91-98% of bisphenol A may be removed from waterduring treatment at municipal water treatment plants.
A 2009 review of the biological impacts of plasticisers on wildlife published by the Royal Society with a focus on annelids (both aquatic and terrestrial), molluscs, crustaceans, insects, fish andamphibians concluded that bisphenol A has been shown to affect reproduction in all studied animal groups, to impair development in crustaceans and amphibians and to induce genetic aberrations.
A large 2010 study of two rivers in Canada found that areas contaminated with hormone-like chemicals including bisphenol A showed females made up 85 per cent of the population of a certain fish,while females made up only 55 per cent in uncontaminated areas.
Although abundant data are available on the toxicity of bisphenol-A (2,2-bis (4-hydroxydiphenyl)propane;(BPA) A variety of BPs were examined for their acute toxicity against Daphnia magna,mutagenicity, and oestrogenic activity using the Daphtoxkit (Creasel Ltd.), the umu test system, and the yeast two-hybrid system, respectively, in comparison with BPA. BPA was moderately toxic toD. magna (48-h EC50 was 10 mg/l) according to the current U.S. EPA acute toxicity evaluation standard, and it was weakly oestrogenic with 5 orders of magnitude lower activity than that of thenatural estrogen 17 beta-oestradiol in the yeast screen, while no mutagenicity was observed. All seven BPs tested here showed moderate to slight acute toxicity, no mutagenicity, and weakoestrogenic activity as well as BPA. Some of the BPs showed considerably higher oestrogenic activity than BPA, and others exhibited much lower activity. Bisphenol S (bis(4-hydroxydiphenyl)sulfone) and bis(4-hydroxyphenyl)sulfide) showed oestrogenic activity.
Biodegradation is a major mechanism for eliminating various environmental pollutants. Studies on the biodegradation of bisphenols have mainly focused on bisphenol A. A number ofBPA-degrading bacteria have been isolated from enrichments of sludge from wastewater treatment plants. The first step in the biodegradation of BPA is the hydroxylation of the carbon atom of amethyl group or the quaternary carbon in the BPA molecule. Judging from these features of the biodegradation mechanisms, it is possible that the same mechanism used for BPA is used tobiodegrade all bisphenols that have at least one methyl or methylene group bonded at the carbon atom between the two phenol groups. However, bisphenol F ([bis(4-hydroxyphenyl)methane; BPF),which has no substituent at the bridging carbon, is unlikely to be metabolised by such a mechanism. Nevertheless BPF is readily degraded by river water microorganisms under aerobicconditions. From this evidence, it was clear that a specific mechanism for biodegradation of BPF does exist in the natural ecosystem,Algae can enhance the photodegradation of bisphenols. The photodegradation rate of BPF increased with increasing algae concentration. Humic acid and Fe3+ ions also enhanced thephotodegradation of BPF. The effect of pH value on the BPF photodegradation was also important.
For Alkylphenols and their Ethoxylates, or Propoxylates (APE):Environmental fate: Alkylphenols are found everywhere in the environmental, when released. Releases are generally as wastes; they are extensively used throughout industry and in the home.
Alkylphenol ethoxylates are widely used surfactants in domestic and industrial products, which are commonly found in wastewater discharges and in sewage treatment plant effluents. Thesesubstances can �load� considerably in various environmental compartments.
Atmospheric Fate: Alkylphenols released to the atmosphere will exist in the vapor phase and are thought to be degraded by reaction with hydroxyl radicals, with a calculated half-life, for nonylphenol,of 0.3 days. However, emissions to the air will be limited.
Terrestrial Fate: These substances will adsorb to organic soil substances. Adsorption decreases as certain chains in the chemical get longer and increases if water is present.
Aquatic Fate: These substances will partition to the sediment if they are released to water. These substances are expected to undergo primary breakdown in oxygenated river water at a relativelyfast rate. Nonylphenols are susceptible to breakdown by sunlight in water. Light breakdown of with ethoxylated nonylphenol in water is much slower and is not expected to be an important fateprocess. The non-biological breakdown of these substances is negligible and biological breakdown of these substances does not readily take place. The half-life in surface water may be around 30days.
Ecotoxicology: There is concern that APE metabolites, (NP, OP, NPE1-3), can mimic natural hormones and that the levels of the substances present in the environment may be sufficient to disruptendocrine function in wildlife and humans. Organisms in different levels of the food chain may experience different responses to the natural hormone mimics found in these substances. Thesesubstances are not expected to be toxic to Daphnia magna water fleas; however, negative impacts on male fathead minnow reproduction have been noted. These substances may have a profoundnegative affect on reproduction in adult fishes. Alkylphenols are not readily biodegradable. The full breakdown pathway for APES has not yet been determined. Biodegradation of APEs produces less biodegradable products: alkylphenol mono- and di-ethoxylates, alkylphenoxy acetic/alkylphenoxypolyethoxy acetic acids, and alkylphenols. These metabolitesfrequently persist through sewage treatment and in rivers. Alkylphenols will accumulate in low oxygen conditions. Metabolites of APES accumulate in organisms and are more toxic than theoriginal compound. Estrogen mimicking effects have been seen in rainbow trout, mice, and chicken embryos. The insecticide chlordecone, (Kepone), shows similar behavior to alkylphenols,accumulating in liver and fat tissue, and eliciting estrogen mimicking activity. Green algae are the most sensitive species.
For benzene-1,3-dimethanamine (m-xylene-alpha,alpha'- diamine)
Environmental fate:
The chemical has a log Pow value of 0.18 at 2 a vapour pressure 5 C, of 0.04 hPa at 25 C, and a water solubility of > 100 000 mg/L. Fugacity model Mackay level III calculations suggest that the
majority of the chemical would distribute to soil if released to soil and/or air compartment(s), and water if released to aquatic compartment.
The chemical is not readily biodegradable (49% after 28 d) or inherently biodegradable (BOD = 22%, TOC = 6% and analysis in HPLC = 21%) and it does not hydrolyse (half-life >1 y at 25 C).
However, the chemical does not bioaccumulate (BCF < 2.7 at 0.2 mg/L). The chemical will react with carbon dioxide to form the carbamate acid, and will undergo indirect photo-oxidation with
hydroxy radicals (T1/2= 5.39 h), and will therefore not persist in the atmosphere.
Ecotoxicity:
Fish LC50 (96 h): Medaka 87.6 mg/l; golden orfe 75 mg/l; rainbow trout >100 mg/l
Daphnia magna EC50 (48 h): 15.2 - 16 mg/l
Daphnia magna EC50 (21 d): 6.77 mg/l (reproduction inhibition); NOEC 4.7 mg/l (reproduction inhibition)
Daphnia magna LC50 (21 d): 8.4 mg/l (parental toxicity)
Algae EbC50: Scenedesmus subspicatus 12 g/l; NOEC 6.25 mg/l; EbC50 Selenastrum capricornutum 20.3 mg/l; NOEC (0-72 h) 10.5 mg/l
Terrestrial Fate: Bisphenol A has low to moderate mobility to soil and can be biodegraded in the presence of oxygen following acclimation.
Aquatic Fate: When released in water, bisphenol A can undergo biodegradation and may be adsorb to suspended solids and sediments.
Atmospheric Fate: Bisphenol A in air will exist in the particulate phase and may be removed from the atmosphere through dry deposition or photolysis.
Ecotoxicity: Toxicity tests show that bisphenol A is moderately toxic to aquatic organisms.
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Ramset Chemset Injection Reo 502
Fish LC50 (96 h): 42 mg/l
For Phenols:
Ecotoxicity - Phenols with log Pow >7.4 are expected to exhibit low toxicity to aquatic organisms however; the toxicity of phenols with a lower log Pow is variable. Dinitrophenols are more toxic than
predicted from QSAR estimates. Hazard information for these groups is not generally available.
For ethyleneamines:
Adsorption of the ethyleneamines correlates closely with both the cation exchange capacity (CEC) and organic content of the soil. Soils with increased CEC and organic content exhibited higher
affinities for these amines. This dependence of adsorption on CEC and organic content is most likely due to the strong electrostatic interaction between the positively charged amine and the
negatively charged soil surface.
Prevent, by any means available, spillage from entering drains or water courses.
DO NOT discharge into sewer or waterways.
Persistence and degradability
HIGH (Half-life = 360 days) LOW (Half-life = 0.31 days) LOW (Half-life = 10 days) LOW (Half-life = 0.95 days) LOW (LogKOW = -1.5677) Mobility in soil
LOW (KOC = 914.6) LOW (KOC = 75190) LOW (KOC = 171.7) LOW (KOC = 56010) LOW (KOC = 626.1) SECTION 13 DISPOSAL CONSIDERATIONS
Waste treatment methods
Containers may still present a chemical hazard/ danger when empty. Return to supplier for reuse/ recycling if possible. If container can not be cleaned sufficiently well to ensure that residuals do not remain or if the container cannot be used to store the same product, thenpuncture containers, to prevent re-use, and bury at an authorised landfill. Where possible retain label warnings and MSDS and observe all notices pertaining to the product. Legislation addressing waste disposal requirements may differ by country, state and/ or territory. Each user must refer to laws operating in their area. In someareas, certain wastes must be tracked.
A Hierarchy of Controls seems to be common - the user should investigate: Reduction Reuse Recycling Disposal (if all else fails) Product / Packaging
This material may be recycled if unused, or if it has not been contaminated so as to make it unsuitable for its intended use. If it has been contaminated, it may be possible to reclaim the product by filtration, distillation or some other means. Shelf life considerations should also be applied in making decisions of this type.
Note that properties of a material may change in use, and recycling or reuse may not always be appropriate.
DO NOT allow wash water from cleaning or process equipment to enter drains.
It may be necessary to collect all wash water for treatment before disposal.
In all cases disposal to sewer may be subject to local laws and regulations and these should be considered first.
Where in doubt contact the responsible authority. Recycle wherever possible. Consult manufacturer for recycling options or consult local or regional waste management authority for disposal if no suitable treatment or disposal facilitycan be identified. Treat and neutralise at an approved treatment plant. Treatment should involve: Neutralisation with suitable dilute acid followed by: burial in a land-fill specifically licenced to accept chemical and / or pharmaceutical wastes or Incineration in a licenced apparatus (after admixture with suitable combustible material). Decontaminate empty containers. Observe all label safeguards until containers are cleaned and destroyed. SECTION 14 TRANSPORT INFORMATION
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Land transport (ADG)
UN number
UN proper shipping name
CORROSIVE LIQUID, BASIC, ORGANIC, N.O.S. (contains benzene-1,3-dimethanamine,N-aminoethylpiperazine and nonylphenol) Transport hazard class(es)
Special provisions Special precautions for user
Air transport (ICAO-IATA / DGR)
UN number
UN proper shipping name
Corrosive liquid, basic, organic, n.o.s. * (contains benzene-1,3-dimethanamine,N-aminoethylpiperazine and nonylphenol) Transport hazard class(es)
ICAO / IATA Subrisk Special provisions Cargo Only Packing Instructions Cargo Only Maximum Qty / Pack Special precautions for user
Passenger and Cargo Packing Instructions Passenger and Cargo Maximum Qty / Pack Passenger and Cargo Limited Quantity Packing Instructions Passenger and Cargo Limited Maximum Qty / Pack Sea transport (IMDG-Code / GGVSee)
UN number
UN proper shipping name
CORROSIVE LIQUID, BASIC, ORGANIC, N.O.S. (contains benzene-1,3-dimethanamine,N-aminoethylpiperazine and nonylphenol) Transport hazard class(es)
Special precautions for user
Special provisions Limited Quantities Transport in bulk according to Annex II of MARPOL 73 / 78 and the IBC code
IMO MARPOL 73/78 (AnnexII) - List of Noxious Liquid Substances Carried in Bulk IMO MARPOL 73/78 (AnnexII) - List of Noxious Liquid Substances Carried in Bulk Page 17 of 18
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IMO MARPOL 73/78 (AnnexII) - List of Noxious Liquid Substances Carried in Bulk SECTION 15 REGULATORY INFORMATION
Safety, health and environmental regulations / legislation specific for the substance or mixture
BISPHENOL A/ DIGLYCIDYL ETHER POLYMER, HIGH MOLECULAR WEIGHT(25068-38-6) IS FOUND ON THE FOLLOWING REGULATORY LISTS
Australia Hazardous Substances Information System - Consolidated Lists Australia Inventory of Chemical Substances (AICS) BENZENE-1,3-DIMETHANAMINE(1477-55-0) IS FOUND ON THE FOLLOWING REGULATORY LISTS
Australia Exposure Standards Australia Hazardous Substances Information System - Consolidated Lists Australia Inventory of Chemical Substances (AICS) BISPHENOL A(80-05-7) IS FOUND ON THE FOLLOWING REGULATORY LISTS
Australia Hazardous Substances Information System - Consolidated Lists Australia Inventory of Chemical Substances (AICS) N-AMINOETHYLPIPERAZINE(140-31-8) IS FOUND ON THE FOLLOWING REGULATORY LISTS
Australia Hazardous Substances Information System - Consolidated Lists Australia Inventory of Chemical Substances (AICS) NONYLPHENOL(84852-15-3) IS FOUND ON THE FOLLOWING REGULATORY LISTS
Australia Hazardous Substances Information System - Consolidated Lists Australia Inventory of Chemical Substances (AICS) N,N-DIMETHYLBENZYLAMINE(103-83-3) IS FOUND ON THE FOLLOWING REGULATORY LISTS
Australia Hazardous Substances Information System - Consolidated Lists Australia Inventory of Chemical Substances (AICS) PHENOL(108-95-2) IS FOUND ON THE FOLLOWING REGULATORY LISTS
Australia Exposure Standards Australia Hazardous Substances Information System - Consolidated Lists Australia Inventory of Chemical Substances (AICS) International Agency for Research on Cancer (IARC) - Agents Classified by the IARC Monographs N (phenol; bisphenol A/ diglycidyl ether polymer, high molecular weight; N-aminoethylpiperazine; nonylphenol; bisphenol A; benzene-1,3-dimethanamine; Europe - EINEC / ELINCS / New Zealand - NZIoC Philippines - PICCS Y = All ingredients are on the inventory N = Not determined or one or more ingredients are not on the inventory and are not exempt from listing(see specific ingredients in brackets) SECTION 16 OTHER INFORMATION
Ingredients with multiple cas numbers
137885-53-1, 27360-89-0, 28106-82-3, 37808-08-5, 80-05-7 136-83-4, 139-84-4, 25154-52-3, 84852-15-3 Classification of the preparation and its individual components has drawn on official and authoritative sources as well as independent review by the Chemwatch Classification committee using available literature references.
A list of reference resources used to assist the committee may be found at: www.chemwatch.net The (M)SDS is a Hazard Communication tool and should be used to assist in the Risk Assessment. Many factors determine whether the reported Hazards are Risks in the workplace or othersettings. Risks may be determined by reference to Exposures Scenarios. Scale of use, frequency of use and current or available engineering controls must be considered.
This document is copyright.
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Apart from any fair dealing for the purposes of private study, research, review or criticism, as permitted under the Copyright Act, no part may be reproduced by any process without writtenpermission from CHEMWATCH.
TEL (+61 3) 9572 4700.
end of SDS

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europeanpolio.eu

Chapter 18Post-polio syndromeE. Farbu,1 N. E. Gilhus,2 M. P. Barnes,3 K. Borg,4 M. de Visser,6 R. Howard,7 F. Nollet,6 J. Opara,8 E. Stalberg91Stavanger University Hospital, Norway; 2University of Bergen, and Haukeland University Hospital, Bergen, Norway; 3Hunters Moor Hospital, Newcastle upon Tyne, UK; 4Karolinska Intitutet/Karolinska Hospital, Stochkholm, Sweden; 6University of Amsterdam, 1100 DD Amsterdam, The Netherlands; 7St Thomas' Hospital, London, UK; 8Repty Rehab Centre. ul. Sniadeckio 1, PL 42-604 Tarnowskie Góry, Poland; 9University Hospital, S-75185 Uppsala, Sweden

blog.uchceu.es

Documento descargado de http://http://zl.elsevier.es el 05/11/2013. Copia para uso personal, se prohíbe la transmisión de este documento por cualquier medio o formato. DOCUMENTO DE CONSENSO Consenso de expertos sobre la detección y el manejo clínico de la Lluís Masana, Fernando Civeira, Juan Pedro-Botet , Isabel de Castro, Miguel Pocoví, Núria Plana, Rocío Mateo-Gallego, Estíbaliz Jarauta y Àngels Pedragosa