Threebond 1217H Three BondChemwatch Hazard Alert Code: 3 Chemwatch: 97-08273 Version No: 3.1 Safety Data Sheet according to WHS Regulations (Hazardous Chemicals) Amendment 2020 and ADG requirements Issue Date: 07/28/2021 Print Date: 03/10/2023 L.GHS.AUS.EN SECTION 1 Identification of the substance / mixture and of the company / undertaking Product Identifier Product name Threebond 1217H Chemical Name Not Applicable Synonyms Not Available Chemical formula Not Applicable Other means of identification Not Available Relevant identified uses of the substance or mixture and uses advised against Relevant identified uses Use according to manufacturer's directions. Details of the manufacturer or supplier of the safety data sheet Registered company name Three Bond Address 6184 Schumacher Park Drive West Chester OH 45069 United States Telephone +1 513 779 7300 Fax +1 513 779 7375 Website https://www.threebond.com/ Email This email address is being protected from spambots. You need JavaScript enabled to view it. Emergency telephone number Association / Organisation Three Bond CHEMWATCH EMERGENCY RESPONSE (24/7) Emergency telephone numbers +1 800 424 9300 +61 1800 951 288 Other emergency telephone numbers Not Available +61 3 9573 3188 Once connected and if the message is not in your preferred language then please dial 01 SECTION 2 Hazards identification Classification of the substance or mixture Poisons Schedule Not Applicable Classification [1] Flammable Liquids Category 4, Skin Corrosion/Irritation Category 2, Sensitisation (Skin) Category 1, Serious Eye Damage/Eye Irritation Category 1, Specific Target Organ Toxicity - Single Exposure (Respiratory Tract Irritation) Category 3 Legend: 1. Classified by Chemwatch; 2. Classification drawn from HCIS; 3. Classification drawn from Regulation (EU) No 1272/2008 - Annex VI Label elements Hazard pictogram(s) Signal word Danger Hazard statement(s) H227 Combustible liquid. H315 Causes skin irritation. H317 May cause an allergic skin reaction. H318 Causes serious eye damage. H335 May cause respiratory irritation. Precautionary statement(s) Prevention P210 Keep away from heat, hot surfaces, sparks, open flames and other ignition sources. No smoking. P271 Use only outdoors or in a well-ventilated area. P280 Wear protective gloves, protective clothing, eye protection and face protection. P261 Avoid breathing mist/vapours/spray. P264 Wash all exposed external body areas thoroughly after handling. P272 Contaminated work clothing should not be allowed out of the workplace. Precautionary statement(s) Response P305+P351+P338 IF IN EYES: Rinse cautiously with water for several minutes. Remove contact lenses, if present and easy to do. Continue rinsing. P310 Immediately call a POISON CENTER/doctor/physician/first aider. P370+P378 In case of fire: Use alcohol resistant foam or normal protein foam to extinguish. P302+P352 IF ON SKIN: Wash with plenty of water and soap. P333+P313 If skin irritation or rash occurs: Get medical advice/attention. P362+P364 Take off contaminated clothing and wash it before reuse. P304+P340 IF INHALED: Remove person to fresh air and keep comfortable for breathing. Precautionary statement(s) Storage P405 Store locked up. P403+P233 Store in a well-ventilated place. Keep container tightly closed. Precautionary statement(s) Disposal P501 Dispose of contents/container to authorised hazardous or special waste collection point in accordance with any local regulation. SECTION 3 Composition / information on ingredients Substances See section below for composition of Mixtures Mixtures CAS No %[weight] Name 70131-67-8 40-50 dimethylsiloxane, hydroxy-terminated 471-34-1 40-50 calcium carbonate 68611-44-9 1-5 silica amorphous, fumed 2224-33-1 <5 vinyltris(methylethylketoxime)silane 108-88-3 <1 toluene 76735-64-3 <0.5 3-[methylbis[(1-methylethenyl)oxy]silyl]propoxy] ethoxylated 1333-86-4 <0.1 carbon black 96-29-7 NotSpec methyl ethyl ketoxime Legend: 1. Classified by Chemwatch; 2. Classification drawn from HCIS; 3. Classification drawn from Regulation (EU) No 1272/2008 - Annex VI; 4. Classification drawn from C&L; * EU IOELVs available SECTION 4 First aid measures Description of first aid measures Eye Contact If this product comes in contact with the eyes: ? Immediately hold eyelids apart and flush the eye continuously with running water. ? 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. Skin Contact If skin contact occurs: ? Immediately remove all contaminated clothing, including footwear. ? Flush skin and hair with running water (and soap if available). ? Seek medical attention in event of irritation. Inhalation ? 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 if necessary. ? Transport to hospital, or doctor, without delay. Ingestion ? Immediately give a glass of water. ? First aid is not generally required. If in doubt, contact a Poisons Information Centre or a doctor. Indication of any immediate medical attention and special treatment needed Treat symptomatically. SECTION 5 Firefighting measures Extinguishing media ? Foam. ? Dry chemical powder. ? BCF (where regulations permit). ? Carbon dioxide. ? Water spray or fog - Large fires only. Special hazards arising from the substrate or mixture Fire Incompatibility ? Avoid contamination with oxidising agents i.e. nitrates, oxidising acids, chlorine bleaches, pool chlorine etc. as ignition may result Advice for firefighters Fire Fighting ? When silica dust is dispersed in air, firefighters should wear inhalation protection as hazardous substances from the fire may be adsorbed on the silica particles. ? When heated to extreme temperatures, (>1700 deg.C) amorphous silica can fuse. ? Alert Fire Brigade and tell them location and nature of hazard. ? Wear breathing apparatus plus protective gloves. ? Prevent, by any means available, spillage from entering drains or water courses. ? Use water delivered as a fine spray to control fire and cool adjacent 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. Fire/Explosion Hazard ? High temperature decomposition products include silicon dioxide, small amounts of formaldehyde, formic acid, acetic acid and traces of silicon polymers. ? These gases may ignite and, depending on circumstances, may cause the resin/polymer to ignite. ? An outer skin of silica may also form. Extinguishing of fire, beneath the skin, may be difficult. ? When silica dust is dispersed in air, firefighters should wear inhalation protection as hazardous substances from the fire may be adsorbed on the silica particles. ? When heated to extreme temperatures, (>1700 deg.C) amorphous silica can fuse. ? 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 monoxide (CO) carbon dioxide (CO2) nitrogen oxides (NOx) silicon dioxide (SiO2) metal oxides other pyrolysis products typical of burning organic material. May emit poisonous fumes. May emit corrosive fumes. Heating calcium carbonate at high temperatures( 825 C.) causes decomposition, releases carbon dioxide gas and leaves a residue of alkaline lime HAZCHEM Not Applicable SECTION 6 Accidental release measures Personal precautions, protective equipment and emergency procedures See section 8 Environmental precautions See section 12 Methods and material for containment and cleaning up Minor Spills Environmental hazard - contain spillage. Slippery when spilt. ? Clean up all spills immediately. ? Avoid contact with skin and eyes. ? Wear impervious gloves and safety goggles. ? Trowel up/scrape up. ? Place spilled material in clean, dry, sealed container. ? Flush spill area with water. Major Spills Environmental hazard - contain spillage. Slippery when spilt. Minor hazard. ? Clear area of personnel. ? Alert Fire Brigade and tell them location and nature of hazard. ? Control personal contact with the substance, by using protective equipment as required. ? Prevent spillage from entering drains or water ways. ? Contain spill with sand, earth or vermiculite. ? Collect recoverable product into labelled containers for recycling. ? Absorb remaining product with sand, earth or vermiculite and place in appropriate containers for disposal. ? Wash area and prevent runoff into drains or waterways. ? 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 Safe handling ? Avoid all personal contact, including inhalation. ? Wear protective clothing when risk of exposure occurs. ? Use in a well-ventilated area. ? Prevent concentration in hollows and sumps. ? DO NOT enter confined spaces until atmosphere has been checked. ? DO NOT allow material to contact humans, exposed food or food utensils. ? 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 SDS. ? Atmosphere should be regularly checked against established exposure standards to ensure safe working conditions are maintained. Other information ? Store in original containers. ? Keep containers securely sealed. ? No smoking, naked lights or ignition sources. ? 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 SDS. Conditions for safe storage, including any incompatibilities Suitable container ? Metal can or drum ? Packaging as recommended by manufacturer. ? Check all containers are clearly labelled and free from leaks. Storage incompatibility Traces of benzene, a carcinogen, may form when silicones are heated in air above 230 degrees C. Concentrated acids and bases cause degradation of polymer. Boiling water may soften and weaken material. Calcium carbonate: ? is incompatible with acids, ammonium salts, fluorine, germanium, lead diacetate, magnesium, mercurous chloride, silicon, silver nitrate, titanium. Contact with acid generates carbon dioxide gas, which may pressurise and then rupture closed containers The substance may be or contains a "metalloid" The following elements are considered to be metalloids; boron,silicon, germanium, arsenic, antimony, tellurium and (possibly) polonium The electronegativities and ionisation energies of the metalloids are between those of the metals and nonmetals, so the metalloids exhibit characteristics of both classes. The reactivity of the metalloids depends on the element with which they are reacting. For example, boron acts as a nonmetal when reacting with sodium yet as a metal when reacting with fluorine. Unlike most metals, most metalloids are amphoteric- that is they can act as both an acid and a base. For instance, arsenic forms not only salts such as arsenic halides, by the reaction with certain strong acid, but it also forms arsenites by reactions with strong bases. Most metalloids have a multiplicity of oxidation states or valences. For instance, tellurium has the oxidation states +2, -2, +4, and +6. Metalloids react like non-metals when they react with metals and act like metals when they react with non-metals. Silicas: ? react with hydrofluoric acid to produce silicon tetrafluoride gas ? react with xenon hexafluoride to produce explosive xenon trioxide ? reacts exothermically with oxygen difluoride, and explosively with chlorine trifluoride (these halogenated materials are not commonplace industrial materials) and other fluorine-containing compounds ? may react with fluorine, chlorates ? are incompatible with strong oxidisers, manganese trioxide, chlorine trioxide, strong alkalis, metal oxides, concentrated orthophosphoric acid, vinyl acetate ? may react vigorously when heated with alkali carbonates. ? Avoid strong acids, bases. ? Avoid reaction with oxidising agents SECTION 8 Exposure controls / personal protection Control parameters Occupational Exposure Limits (OEL) INGREDIENT DATA Source Ingredient Material name TWA STEL Peak Notes Australia Exposure Standards calcium carbonate Calcium carbonate 10 mg/m3 Not Available Not Available (a) This value is for inhalable dust containing no asbestos and < 1% crystalline silica. Australia Exposure Standards toluene Toluene 50 ppm / 191 mg/m3 574 mg/m3 / 150 ppm Not Available Not Available Australia Exposure Standards carbon black Carbon black 3 mg/m3 Not Available Not Available Not Available Emergency Limits Ingredient TEEL-1 TEEL-2 TEEL-3 dimethylsiloxane, hydroxy-terminated 190 mg/m3 2,100 mg/m3 13,000 mg/m3 calcium carbonate 45 mg/m3 210 mg/m3 1,300 mg/m3 silica amorphous, fumed 18 mg/m3 100 mg/m3 630 mg/m3 toluene Not Available Not Available Not Available carbon black 9 mg/m3 99 mg/m3 590 mg/m3 methyl ethyl ketoxime 30 ppm 56 ppm 250 ppm Ingredient Original IDLH Revised IDLH dimethylsiloxane, hydroxy-terminated Not Available Not Available calcium carbonate Not Available Not Available silica amorphous, fumed Not Available Not Available vinyltris(methylethylketoxime)silane Not Available Not Available toluene 500 ppm Not Available Ingredient TEEL-1 TEEL-2 TEEL-3 3-[methylbis[(1- methylethenyl)oxy]silyl]propoxy] ethoxylated Not Available Not Available carbon black 1,750 mg/m3 Not Available methyl ethyl ketoxime Not Available Not Available Occupational Exposure Banding Ingredient Occupational Exposure Band Rating Occupational Exposure Band Limit vinyltris(methylethylketoxime)silane D > 0.1 to ? 1 ppm methyl ethyl ketoxime D > 0.1 to ? 1 ppm Notes: Occupational exposure banding is a process of assigning chemicals into specific categories or bands based on a chemical's potency and the adverse health outcomes associated with exposure. The output of this process is an occupational exposure band (OEB), which corresponds to a range of exposure concentrations that are expected to protect worker health. MATERIAL DATA Exposure controls Appropriate engineering controls Engineering controls are used to remove a hazard or place a barrier between the worker and the hazard. Well-designed engineering controls can be highly effective 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 match the particular process and chemical or contaminant in use. Employers may need to use multiple types of controls to prevent employee overexposure. Local exhaust ventilation usually required. If risk of overexposure exists, wear approved respirator. Correct fit is essential to obtain adequate protection. Supplied-air type respirator may be required in special circumstances. Correct fit is essential to ensure adequate protection. An approved self contained breathing apparatus (SCBA) may be required in some situations. Provide adequate ventilation in warehouse or closed storage area. Air contaminants generated in the workplace possess varying "escape" velocities which, in turn, determine the "capture velocities" of fresh circulating air required to effectively remove the contaminant. Type of Contaminant: Air Speed: solvent, vapours, degreasing etc., evaporating from tank (in still air). 0.25-0.5 m/s (50-100 f/min.) aerosols, fumes from 0.5-1 m/s (100-200 f/min.) pouring operations, intermittent container filling, low speed conveyer transfers, welding, spray drift, plating 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 zone of rapid air motion) 1-2.5 m/s (200-500 f/min.) grinding, abrasive blasting, tumbling, high speed wheel generated dusts (released at high initial velocity into zone of very high rapid air motion). 2.5-10 m/s (500-2000 f/min.) 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 square of distance from the extraction point (in simple cases). Therefore the air speed at the extraction point should be adjusted, accordingly, after reference to distance 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 of solvents generated in a tank 2 meters distant from the extraction point. Other mechanical considerations, producing performance deficits within the extraction apparatus, make it essential that theoretical air velocities are multiplied by factors of 10 or more when extraction systems are installed or used. Individual protection measures, such as personal protective equipment Eye and face protection ? Safety glasses with side shields. ? Chemical goggles. ? Contact lenses may pose a special hazard; soft contact lenses may absorb and concentrate irritants. A written policy document, describing the wearing of lenses 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 chemicals in use and an account of injury experience. Medical and first- aid personnel should be trained in their removal and suitable equipment should be readily available. In the event of chemical exposure, begin eye irrigation immediately and remove contact lens as soon as practicable. Lens should be removed at the first signs of eye redness or irritation - lens should be removed in a clean environment only after workers have washed hands thoroughly. [CDC NIOSH Current Intelligence Bulletin 59], [AS/NZS 1336 or national equivalent] Skin protection See Hand protection below Hands/feet protection ? Wear chemical protective gloves, e.g. PVC. ? Wear safety footwear or safety gumboots, e.g. Rubber NOTE: ? The material may produce skin sensitisation in predisposed individuals. Care must be taken, when removing gloves and other protective equipment, to avoid all possible skin contact. ? Contaminated leather items, such as shoes, belts and watch-bands should be removed and destroyed. Body protection See Other protection below Other protection ? Overalls. ? P.V.C apron. ? Barrier cream. ? Skin cleansing cream. ? Eye wash unit. Recommended material(s) GLOVE SELECTION INDEX Glove selection is based on a modified presentation of the: "Forsberg Clothing Performance Index". The effect(s) of the following substance(s) are taken into account in the computer-generated selection: Threebond 1217H Material CPI PE/EVAL/PE A PVA A VITON A VITON/CHLOROBUTYL A TEFLON B BUTYL C CPE C NEOPRENE C NEOPRENE/NATURAL C NITRILE C NITRILE+PVC C PVC C SARANEX-23 C SARANEX-23 2-PLY C VITON/NEOPRENE C * CPI - Chemwatch Performance Index A: Best Selection B: 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 be unsuitable following long-term or frequent use. A qualified practitioner should be consulted. Respiratory protection Type A-P Filter of sufficient capacity. (AS/NZS 1716 & 1715, EN 143:2000 & 149:2001, ANSI Z88 or national equivalent) Where the concentration of gas/particulates in the breathing zone, approaches or exceeds the "Exposure Standard" (or ES), respiratory protection is required. Degree of protection varies with both face-piece and Class of filter; the nature of protection varies with Type of filter. Required Minimum Protection Factor Half-Face Respirator Full-Face Respirator Powered Air Respirator up to 10 x ES A-AUS P2 - A-PAPR-AUS / Class 1 P2 up to 50 x ES - A-AUS / Class 1 P2 - up to 100 x ES - A-2 P2 A-PAPR-2 P2 ^ ^ - Full-face A(All classes) = Organic vapours, B AUS or B1 = Acid gasses, B2 = Acid gas or hydrogen 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) ? Cartridge respirators should never be used for emergency ingress or in areas of unknown vapour concentrations or oxygen content. ? The wearer must be warned to leave the contaminated area immediately on detecting any odours through the respirator. The odour may indicate that the mask is not functioning properly, that the vapour concentration is too high, or that the mask is not properly fitted. Because of these limitations, only restricted use of cartridge respirators is considered appropriate. ? Cartridge performance is affected by humidity. Cartridges should be changed after 2 hr of continuous use unless it is determined that the humidity is less than 75%, in which case, cartridges can be used for 4 hr. Used cartridges should be discarded daily, regardless of the length of time used SECTION 9 Physical and chemical properties Information on basic physical and chemical properties Appearance Gray paste; does not mix with water. Physical state Non Slump Paste Relative density (Water = 1) Not Available Odour Not Available Partition coefficient n- octanol / water Not Available Odour threshold Not Available Auto-ignition temperature (?C) Not Available pH (as supplied) Not Applicable Decomposition temperature (?C) Not Available Melting point / freezing point (?C) Not Available Viscosity (cSt) 275 Initial boiling point and boiling range (?C) Not Available Molecular weight (g/mol) Not Applicable Flash point (?C) 73 Taste Not Available Evaporation rate <1 Explosive properties Not Available Flammability Combustible. Oxidising properties Not Available Upper Explosive Limit (%) Not Available Surface Tension (dyn/cm or mN/m) Not Available Lower Explosive Limit (%) Not Available Volatile Component (%vol) Not Available Vapour pressure (kPa) Not Available Gas group Not Available Solubility in water Immiscible pH as a solution (1%) Not Applicable Vapour density (Air = 1) >1 VOC g/L <2.5 SECTION 10 Stability and reactivity Reactivity See section 7 Chemical stability ? Silicone fluids are stable under normal storage conditions. ? Hazardous polymerisation will not occur. ? At temperatures > 150 C, silicones can slowly react with the oxygen in air. ? When heated > 300 C, silicones can slowly depolymerise to volatile siloxanes whether or not air is present. Product is considered stable and hazardous polymerisation will not occur. Possibility of hazardous reactions See section 7 Conditions to avoid See section 7 Incompatible materials See section 7 Hazardous decomposition products See section 5 SECTION 11 Toxicological information Information on toxicological effects Inhaled Evidence shows, or practical experience predicts, that the material produces irritation of the respiratory system, in a substantial number of individuals, following inhalation. In contrast to most organs, the lung is able to respond to a chemical insult by first removing or neutralising the irritant and then repairing the damage. The repair process, which initially evolved to protect mammalian lungs from foreign matter and antigens, may however, produce further lung damage resulting in the impairment of gas exchange, the primary function of the lungs. Respiratory tract irritation often results in an inflammatory response involving the recruitment and activation of many cell types, mainly derived from the vascular system. Inhalation of vapours may cause drowsiness and dizziness. This may be accompanied by narcosis, reduced alertness, loss of reflexes, lack of coordination and vertigo. The principal toxic effects of methyl ethyl ketoxime MEKO in animal studies, regardless of the route of administration, include haemolytic anaemia, increased respiration; and reversible reduction in spontaneous activity, motor coordination and muscle tone. At high vapour concentration the product has a reversible narcotic action Extremely high concentrations may lead to coma and respiratory failure. Not normally a hazard due to non-volatile nature of product Ingestion The material has NOT been classified by EC Directives or other classification systems as "harmful by ingestion". This is because of the lack of corroborating animal or human evidence. The material may still be damaging to the health of the individual, following ingestion, especially where pre-existing organ (e.g liver, kidney) damage is evident. Present definitions of harmful or toxic substances are generally based on doses producing mortality rather than those producing morbidity (disease, ill-health). Gastrointestinal tract discomfort may produce nausea and vomiting. In an occupational setting however, ingestion of insignificant quantities is not thought to be cause for concern. Skin Contact The material produces moderate skin irritation; evidence exists, or practical experience predicts, that the material either ? produces moderate inflammation of the skin in a substantial number of individuals following direct contact, and/or ? produces significant, but moderate, inflammation when applied to the healthy intact skin of animals (for up to four hours), such inflammation being present twenty-four hours or more after the end of the exposure period. Skin irritation may also be present after prolonged or repeated exposure; this may result in a form of contact dermatitis (nonallergic). The dermatitis is often characterised by skin redness (erythema) and swelling (oedema) which may progress to blistering (vesiculation), scaling and thickening of the epidermis. At the microscopic level there may be intercellular oedema of the spongy layer of the skin (spongiosis) and intracellular oedema of the epidermis. Skin contact is not thought to have harmful health effects (as classified under EC Directives); the material may still produce health damage following entry through wounds, lesions or abrasions. Application of 0.5 gm methyl ethyl ketoxime (MEKO) to the backs of rabbits for 24 hours under an occlusive dressing produced mild irritation (Draize score 1.5 out of 8). MEKO was a strong sensitiser in the maximisation test (8 out of 10 guinea pigs were sensitised. Open cuts, abraded or irritated skin should not be exposed to this material Entry into the blood-stream through, for example, cuts, abrasions, puncture wounds or lesions, may produce systemic injury with harmful effects. Examine the skin prior to the use of the material and ensure that any external damage is suitably protected. Low molecular weight silicone fluids may exhibit solvent action and may produce skin irritation. Excessive use or prolonged contact may lead to defatting, drying and irritation of sensitive skin Eye When applied to the eye(s) of animals, the material produces severe ocular lesions which are present twenty-four hours or more after instillation. 0.1 ml of methyl ethyl ketoxime (MEKO) was corrosive to the rabbit eye. When the eyes of human subjects where exposed to silicone fluids, there was evidence of transitory conjunctival irritation within a few hours; this resolved within 24 hours. When applied to the eyes of rabbits, silicone fluids produced transitory irritation which lasted no longer than 48 hours. Injection into the various structures of the eye of animals produced corneal scarring, degenerative changes in the retina, foreign body reaction and cataracts. Chronic Long-term exposure to respiratory irritants may result in disease of the airways involving difficult breathing and related systemic problems. Practical experience shows that skin contact with the material is capable either of inducing a sensitisation reaction in a substantial number of individuals, and/or of producing a positive response in experimental animals. Substances that can cause occupational asthma (also known as asthmagens and respiratory sensitisers) can induce a state of specific airway hyper-responsiveness via an immunological, irritant or other mechanism. Once the airways have become hyper-responsive, further exposure to the substance, sometimes even to tiny quantities, may cause respiratory symptoms. These symptoms can range in severity from a runny nose to asthma. Not all workers who are exposed to a sensitiser will become hyper-responsive and it is impossible to identify in advance who are likely to become hyper-responsive. Substances than can cuase occupational asthma should be distinguished from substances which may trigger the symptoms of asthma in people with pre-existing air-way hyper-responsiveness. The latter substances are not classified as asthmagens or respiratory sensitisers Wherever it is reasonably practicable, exposure to substances that can cuase occupational asthma should be prevented. Where this is not possible the primary aim is to apply adequate standards of control to prevent workers from becoming hyper-responsive. Activities giving rise to short-term peak concentrations should receive particular attention when risk management is being considered. Health surveillance is appropriate for all employees exposed or liable to be exposed to a substance which may cause occupational asthma and there should be appropriate consultation with an occupational health professional over the degree of risk and level of surveillance. Exposure to the material may cause concerns for human fertility, generally on the basis that results in animal studies provide sufficient evidence to cause a strong suspicion of impaired fertility in the absence of toxic effects, or evidence of impaired fertility occurring at around the same dose levels as other toxic effects, but which are not a secondary non-specific consequence of other toxic effects. Exposure to the material may cause concerns for humans owing to possible developmental toxic effects, generally on the basis that results in appropriate animal studies provide strong suspicion of developmental toxicity in the absence of signs of marked maternal toxicity, or at around the same dose levels as other toxic effects but which are not a secondary non-specific consequence of other toxic effects. Limited evidence suggests that repeated or long-term occupational exposure may produce cumulative health effects involving organs or biochemical systems. The synthetic, amorphous silicas are believed to represent a very greatly reduced silicosis hazard compared to crystalline silicas and are considered to be nuisance dusts. When heated to high temperature and a long time, amorphous silica can produce crystalline silica on cooling. Inhalation of dusts containing crystalline silicas may lead to silicosis, a disabling pulmonary fibrosis that may take years to develop. Discrepancies between various studies showing that fibrosis associated with chronic exposure to amorphous silica and those that do not may be explained by assuming that diatomaceous earth (a non-synthetic silica commonly used in industry) is either weakly fibrogenic or nonfibrogenic and that fibrosis is due to contamination by crystalline silica content Pure calcium carbonate does not produce pneumoconiosis probably being eliminated from the lungs slowly by solution. As mined, unsterilised particulates can carry bacteria into the air passages and lungs, producing infection and bronchitis. Methyl ethyl ketoxime (MEKO) administered to rats by gavage at 25, 75 and 225 mg/kg/day, 7 days/week for 13 weeks, produced dose-related decreases in red blood cell counts and haemoglobin and haematocrit values accompanied by a mild to marked reticulocytosis (increased number of young red blood cells). Other effects included a dose-related pattern of spleen, liver and kidney weights. The spleen and liver showed evidence of compensatory red blood cell production suggesting that, in the rat, MEKO induces haemolytic anaemia with complementary erythropoiesis. A no-observed-effect-level was not established but effects at 25 mg/kg were described as minimal. When MEKO was administered to rats at dose levels of 0.5, and 1.0 ml/kg/day, daily for 4 weeks, transient central nervous system depression immediately followed. At 4 weeks dose-related decreases were seen in red blood cell count and haemoglobin. Dose- related increases were evident in spleen weight (from 1.7 to 3.2 fold). It was concluded that 0.1 ml/kg produced only minimal effects. When rats were exposed by inhalation to MEKO vapour for 6 hours/day, 5 days/week for 4 weeks, mild increases in blood mean corpuscular volume, mean corpuscular haemoglobin, reticulocyte count and red blood cell count were seen at 533 and 714 ppm. Spleen weights were increased and haemosiderosis (deposits of iron) in the spleen were seen at 714 ppm. Haemosiderosis probably resulted from red blood cell haemolysis. Exposures at 60 and 283 ppm produced no observed effects. An increased incidence of liver tumours was observed microscopically in male mice exposed to 375 ppm for 18 months. Both male and female mice exposed at 375 ppm showed enlarged livers but tumours did not occur in females. High blood concentrations of calcium ion may give rise to vasodilation and depress cardiac function leading to hypotension and syncope. Calcium ions enhance the effects of digitalis on the heart and may precipitate digitalis intoxication. Calcium salts also reduce the absorption of tetracyclines In neonates calcification of soft-tissue has been observed following therapeutic administration. Some studies show that large quantities of calcium intake can cause hypercalcemia, which can in turn lead to renal failure Renal failure can occur within hours or days or, alternatively, settles gradually, evolving over several years until it reaches terminal stages. Similarly, acute renal failure can also develop into chronic forms of the disease. Hypercalcaemia conditions can be associated with normal or reduced calcium serum levels, as the body tends to maintain a balanced metabolism of the mineral, known as the compensation phase. When there is a slight increase in the concentration of ions in the blood, calcium excretion markedly increases, while intestinal absorption decreases After kidney damage has set in, a loss of calcium may occur, thereby decreasing the serum concentration. Serum protein levels may decrease as a result of proteinuria in cases of renal complications. Proteinuria is an indicator of kidney disease and represents an independent risk factor for the progression of such a condition. Increased serum creatinine levels may represent an important parameter, given that kidney diseases are associated with increased serum creatinine levels. When renal pathology occurs, a progressive loss of glomerular filtration begins, resulting in increased plasma creatinine concentrations. During the course of kidney failure, discrete, but constant, increments in plasma creatinine levels occur. Renal disease with albuminuria may also be the cause of hypoalbuminemia in patients with liver disease. In cases of established liver damage, increased calcium urinary excretion may occur. Therefore, a similar increase may cause the decline in serum calcium levels in the current study. Repeated exposure to synthetic amorphous silicas may produce skin dryness and cracking. Available data confirm the absence of significant toxicity by oral and dermal routes of exposure. Numerous repeated-dose, subchronic and chronic inhalation toxicity studies have been conducted in a number of species, at airborne concentrations ranging from 0.5 mg/m3 to 150 mg/m3. Lowest-observed adverse effect levels (LOAELs) were typically in the range of 1 to 50 mg/m3. When available, the no-observed adverse effect levels (NOAELs) were between 0.5 and 10 mg/m3. Differences in values may be due to particle size, and therefore the number of particles administered per unit dose. Generally, as particle size diminishes so does the NOAEL/ LOAEL. Exposure produced transient increases in lung inflammation, markers of cell injury and lung collagen content. There was no evidence of interstitial pulmonary fibrosis. On the basis, primarily, of animal experiments, concern has been expressed that the material may produce carcinogenic or mutagenic effects; in respect of the available information, however, there presently exists inadequate data for making a satisfactory assessment. Threebond 1217H TOXICITY IRRITATION Not Available Not Available dimethylsiloxane, hydroxy- terminated TOXICITY IRRITATION Dermal (rabbit) LD50: >2000 mg/kg[2] Not Available Oral (Rat) LD50: >5000 mg/kg[2] calcium carbonate TOXICITY IRRITATION dermal (rat) LD50: >2000 mg/kg[1] Eye (rabbit): 0.75 mg/24h - SEVERE Inhalation(Rat) LC50: >3 mg/l4h[1] Eye: no adverse effect observed (not irritating)[1] Oral (Rat) LD50: >2000 mg/kg[1] Skin (rabbit): 500 mg/24h-moderate Skin: no adverse effect observed (not irritating)[1] silica amorphous, fumed TOXICITY IRRITATION Inhalation(Rat) LC50: 0.45 mg/L4h[2] Not Available Oral (Rat) LD50: >5000 mg/kg[2] vinyltris(methylethylketoxime)silane TOXICITY IRRITATION dermal (rat) LD50: >2009 mg/kg[1] Eye: adverse effect observed (irritating)[1] Oral (Rat) LD50: >2000 mg/kg[1] Skin: no adverse effect observed (not irritating)[1] toluene TOXICITY IRRITATION Dermal (rabbit) LD50: 12124 mg/kg[2] Eye (rabbit): 2mg/24h - SEVERE Inhalation(Rat) LC50: >13350 ppm4h[2] Eye (rabbit):0.87 mg - mild Oral (Rat) LD50: 636 mg/kg[2] Eye (rabbit):100 mg/30sec - mild Eye: adverse effect observed (irritating)[1] Skin (rabbit):20 mg/24h-moderate Skin (rabbit):500 mg - moderate Skin: adverse effect observed (irritating)[1] Skin: no adverse effect observed (not irritating)[1] 3-[methylbis[(1- methylethenyl)oxy]silyl]propoxy] ethoxylated TOXICITY IRRITATION Not Available Not Available carbon black TOXICITY IRRITATION Dermal (rabbit) LD50: >2000 mg/kg[1] Eye: no adverse effect observed (not irritating)[1] Oral (Rat) LD50: >2000 mg/kg[1] Skin: no adverse effect observed (not irritating)[1] methyl ethyl ketoxime TOXICITY IRRITATION Dermal (rabbit) LD50: >184<1840 mg/kg[1] Eye (rabbit): 0.1 ml - SEVERE Inhalation(Rat) LC50: >4.83 mg/l4h[1] Oral (Rat) LD50: >900 mg/kg[1] Legend: 1. Value obtained from Europe ECHA Registered Substances - Acute toxicity 2. Value obtained from manufacturer's SDS. Unless otherwise specified data extracted from RTECS - Register of Toxic Effect of chemical Substances DIMETHYLSILOXANE, HYDROXY- TERMINATED * [Mobay Chemical Corp] **[GE] For siloxanes: Effects which based on the reviewed literature do not seem to be problematic are acute toxicity, irritant effects, sensitization and genotoxicity. Some studies indicate that some of the siloxanes may have endocrine disrupting properties, and reproductive effects have caused concern about the possible effects of the siloxanes on humans and the environment. Only few siloxanes are described in the literature with regard to health effects, and it is therefore not possible to make broad conclusions and comparisons of the toxicity related to short-chained linear and cyclic siloxanes based on the present evaluation. Data are primarily found on the cyclic siloxanes D4 (octamethylcyclotetrasiloxane) and D5 (decamethylcyclopentasiloxane) and the short-linear HMDS (hexamethyldisiloxane). These three siloxanes have a relatively low order of acute toxicity by oral, dermal and inhalatory routes and do not require classification for this effect. They are not found to be irritating to skin or eyes and are also not found sensitizing by skin contact. Data on respiratory sensitization have not been identified. Subacute and subchronic toxicity studies show that the liver is the main target organ for D4 which also induces liver cell enzymes. This enzyme induction contributes to the elimination of the substance from the tissues. Primary target organ for D5 exposure by inhalation is the lung. D5 has an enzyme induction profile similar to that of D4. Subacute and subchronic inhalation of HMDS affect in particular the lungs and kidneys in rats. None of the investigated siloxanes show any signs of genotoxic effects in vitro or in vivo. Preliminary results indicate that D5 has a potential carcinogenic effect. D4 is considered to impair fertility in rats by inhalation and is classified as a substance toxic to reproduction in category 3 with the risk phrase R62 ('Possible risk of impaired fertility'). The results of a study to screen for oestrogen activity indicate that D4 has very weak oestrogenic and antioestrogenic activity and is a partial agonist (enhances the effect of the estrogen). It is not uncommon for compounds that are weakly oestrogenic to also have antioestrogenic properties. Comparison of the oestrogenic potency of D4 relative to ethinyloestradiol (steroid hormone) indicates that D4 is 585,000 times less potent than ethinyloestradiol in the rat stain Sprague- Dawley and 3.7 million times less potent than ethinyloestradiol in the Fisher-344 rat strain. Because of the lack of effects on other endpoints designated to assess oestrogenicity, the oestrogenicity as mode of action for the D4 reproductive effects has been questioned. An indirect mode of action causing a delay of the LH (luteinising hormone) surge necessary for optimal timing of ovulation has been suggested as the mechanism. Based on the reviewed information, the critical effects of the siloxanes are impaired fertility (D4) and potential carcinogenic effects (uterine tumours in females). Furthermore there seem to be some effects on various organs following repeated exposures, the liver (D4), kidney (HMDS) and lung (D5 and HMDS) being the target organs. A possible oestrogenic effect contributing to the reproductive toxicity of D4 is debated. There seems however to be some indication that this toxicity may be caused by another mechanism than oestrogen activity. Studies are available for linear siloxanes from an analogue group comprising di- to hexa- siloxanes, as well as key physicochemical properties, The results of the acute toxicity studies for this analogue group are in agreement: there is no evidence from any of the available studies that the substances in this group have any potential for acute toxicity (in terms of either lethality or adverse clinical effects) by any route up to and exceeding the maximum dose levels tested according to current OECD guidelines. It is therefore valid to read- across the lack of acute toxicity between the members of the group where there are data gaps The metabolism of silanes and siloxanes is influenced by the chemistry of silicon, and it is fundamentally different from that of carbon compounds. These differences are due to the fact that silicon is more electropositive than carbon; Si-Si bonds are less stable than C-C bonds and Si-O bonds form very readily, the latter due to their high bond energy. Functional groups such as -OH, -CO2H, and -CH2OH are commonly seen in organic drug metabolites. If such functionalities are formed from siloxane metabolism, they will undergo rearrangement with migration of the Si atom from carbon to oxygen. Consequently, alpha hydroxysilanes may isomerise to silanols and this provides a mechanism by which very polar metabolites may be formed from highly hydrophobic alkylsiloxanes in relatively few metabolic steps CALCIUM CARBONATE No evidence of carcinogenic properties. No evidence of mutagenic or teratogenic effects. Asthma-like symptoms may continue for months or even years after exposure to the material ends. This may be due to a non-allergic condition known as reactive airways dysfunction syndrome (RADS) which can occur after exposure to high levels of highly irritating compound. Main criteria for diagnosing RADS include the absence of previous airways disease in a non-atopic individual, with sudden onset of persistent asthma-like symptoms within minutes to hours of a documented exposure to the irritant. Other criteria for diagnosis of RADS include a reversible airflow pattern on lung function tests, moderate to severe bronchial hyperreactivity on methacholine challenge testing, and the lack of minimal lymphocytic inflammation, without eosinophilia. 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. On the other hand, industrial bronchitis is a disorder that occurs as a result of exposure due to high concentrations of irritating substance (often particles) and is completely reversible after exposure ceases. The disorder is characterized by difficulty breathing, cough and mucus production. The material may produce severe irritation to the eye causing pronounced inflammation. Repeated or prolonged exposure to irritants may produce conjunctivitis. SILICA AMORPHOUS, FUMED For silica amorphous: Derived No Adverse Effects Level (NOAEL) in the range of 1000 mg/kg/d. In humans, synthetic amorphous silica (SAS) is essentially non-toxic by mouth, skin or eyes, and by inhalation. Epidemiology studies show little evidence of adverse health effects due to SAS. Repeated exposure (without personal protection) may cause mechanical irritation of the eye and drying/cracking of the skin. When experimental animals inhale synthetic amorphous silica (SAS) dust, it dissolves in the lung fluid and is rapidly eliminated. If swallowed, the vast majority of SAS is excreted in the faeces and there is little accumulation in the body. Following absorption across the gut, SAS is eliminated via urine without modification in animals and humans. SAS is not expected to be broken down (metabolised) in mammals. After ingestion, there is limited accumulation of SAS in body tissues and rapid elimination occurs. Intestinal absorption has not been calculated, but appears to be insignificant in animals and humans. SASs injected subcutaneously are subjected to rapid dissolution and removal. There is no indication of metabolism of SAS in animals or humans based on chemical structure and available data. In contrast to crystalline silica, SAS is soluble in physiological media and the soluble chemical species that are formed are eliminated via the urinary tract without modification. Both the mammalian and environmental toxicology of SASs are significantly influenced by the physical and chemical properties, particularly those of solubility and particle size. SAS has no acute intrinsic toxicity by inhalation. Adverse effects, including suffocation, that have been reported were caused by the presence of high numbers of respirable particles generated to meet the required test atmosphere. These results are not representative of exposure to commercial SASs and should not be used for human risk assessment. Though repeated exposure of the skin may cause dryness and cracking, SAS is not a skin or eye irritant, and it is not a sensitiser. Repeated-dose and chronic toxicity studies confirm the absence of toxicity when SAS is swallowed or upon skin contact. Long-term inhalation of SAS caused some adverse effects in animals (increases in lung inflammation, cell injury and lung collagen content), all of which subsided after exposure. Numerous repeated-dose, subchronic and chronic inhalation toxicity studies have been conducted with SAS in a number of species, at airborne concentrations ranging from 0.5 mg/m3 to 150 mg/m3. Lowest-observed adverse effect levels (LOAELs) were typically in the range of 1 to 50 mg/m3. When available, the no- observed adverse effect levels (NOAELs) were between 0.5 and 10 mg/m3. The difference in values may be explained by different particle size, and therefore the number of particles administered per unit dose. In general, as particle size decreases so does the NOAEL/LOAEL. Neither inhalation nor oral administration caused neoplasms (tumours). SAS is not mutagenic in vitro. No genotoxicity was detected in in vivo assays. SAS does not impair development of the foetus. Fertility was not specifically studied, but the reproductive organs in long-term studies were not affected. For Synthetic Amorphous Silica (SAS) Repeated dose toxicity Oral (rat), 2 weeks to 6 months, no significant treatment-related adverse effects at doses of up to 8% silica in the diet. Inhalation (rat), 13 weeks, Lowest Observed Effect Level (LOEL) =1.3 mg/m3 based on mild reversible effects in the lungs. Inhalation (rat), 90 days, LOEL = 1 mg/m3 based on reversible effects in the lungs and effects in the nasal cavity. For silane treated synthetic amorphous silica: Repeated dose toxicity: oral (rat), 28-d, diet, no significant treatment-related adverse effects at the doses tested. There is no evidence of cancer or other long-term respiratory health effects (for example, silicosis) in workers employed in the manufacture of SAS. Respiratory symptoms in SAS workers have been shown to correlate with smoking but not with SAS exposure, while serial pulmonary function values and chest radiographs are not adversely affected by long-term exposure to SAS. For silane, dichlorodimethyl-, reaction products with silica Acute oral toxicity is very low for treated silica. Acute inhalation toxicity was only tested for inhalable particles and is not relevant for the material used industrially. Changes in respiratory organs (inflammatory processes) after repeated exposure were reversible in animals that survived the exposure and were observed above the valid TLV values, only. If TLV values are maintained no health hazards are expected. Repeated dose toxicity is sufficiently investigated. Treated silica is not mutagenic. The NOAEL for repro/developmental toxicity is 500 mg/kg bw. Acute toxicity: In a limit test giving 10% in the diet (5000 mg/kg bw) to rats the acute oral LD50 was determined to be higher than 5000 mg/kg bw. In another study administering single doses of 2500 and 5000 mg/kg bw to rats the LD50 was also concluded to be higher than 5000 mg/kg bw. In an acute oral toxicity study giving still higher single doses in olive oil the LD50 appeared to be above 7900 mg/kg bw. No signs of toxicity were observed in any of these studies. All inhalation testing has been conducted with a substance that differs significantly from the commercial product based on particle size. In these animal tests the experimental design caused the particle size to be reduced resulting in nearly 100% of the particle fraction being below 10 um and capable of entering the deep lung (alveolar particle fraction). The alveolar fraction is responsible for the toxicological effects (suffocation; overloading of the lung due to poor dust clearance mechanisms) which were observed with LC50 values of > 477, 450, 520-1120, and >2280 mg/m3 and corresponding mass median aerodynamic diameters (MMAD) of 2.9 um, 1.24 um, 0.8 ? 0.9 um and 0.15 um, respectively. In comparison to the particle size used in these acute inhalation animal tests, only minor amounts (less than 1 %) of the commercially available commercial substance have been measured as respirable (alveolar fraction < 10 um MMAD) using test method EN/DIN 481 (ref.35). Using the same method > 99% of the particle fraction is in excess of 90 um and can only reach the upper airways (nasal passages and throat) or cannot be inhaled at all. Therefore the tests do not represent the toxicological behavior of the commercial product and are not considered relevant for inclusion in the hazard definition/hazard assessment of the commercial substance. Genetic toxicity: The test substance was not mutagenic in the Bacterial Reverse Mutation Assay (Ames test) with Salmonella typhimurium TA98, TA100, TA1535, TA1537 and TA1538 strains and with E. coli WP2 uvrA strain. Also an in vitro chromosomal aberration study in CHO cells gave negative results. Repeat dose toxicity: A 24-month oral feeding study administering a 100 mg/kg dose to 20 male and 20 female rats resulted in a NOAEL of 100 mg/kg. No clinical signs or treatment-related changes (e.g. bodyweight) were observed. There were no carcinogenic effects.A 6-month oral feeding study showed no treatment-related effects at the given dose of 500 mg/kg bw to rats (40/sex) resulting in a NOAEL of 500 mg/kg bw; a slight progressive ? but reversible -transformation of the adrenal cortex in females was attributed to chronic stress. Another oral feeding study (5-8 weeks) exposed rats (5/sex/treatment) to a dose of 500, 1000 or 2000 mg/kg bw initially and increasing these doses gradually to 4000, 8000 and 16000 mg/kg bw, respectively. Decrease in body weight and food consumption combined with apathy and decreased grooming activity and decreased cytoplasmic glycogen in hepatocytes may indicate a starving condition of these animals. At the highest dose group four animals died. The NOAEL was determined to be 500 mg/kg bw (LOAEL = 1000 mg/kg bw). In a limited reported study where a dose of 500 or 1000 mg/kg bw was administered by gavage to 30 rats no treatment-related effects could be found, resulting in a NOAEL of 1000 mg/kg bw. A 13-week inhalation study exposing 70 animals/sex to 35 mg/m3 resulted in granuloma-like lesions of the lungs, accumulations of alveolar macrophages, alveolar spaces filled with granular material, debris and polymorphonuclear leucocytes, alveolar bronchiolisation, interstitial fibrosis and enlarged mediastinal lymph nodes. In a 2-week study administering 0, 31, 87 or 420 mg/m3 to a total number of 40 rats/sex 4 males and 2 females died at the top dose level. The rats at the top dose level showed severe respiratory distress and apathy. A dose-related decrease in body weight was observed at 87 mg/m3 and higher. The lungs showed similar effects as those observed in the 13-week inhalation study. A 3-day study and an 8-12-month study both with a concentration of 50 mg/m3 to rats yielded similar results to the above studies in the lungs and the size of the particles was determined to be smaller than 7 ?m. Changes in respiratory organs (inflammatory processes) observed in inhalative repeated dose toxicity testing were reversible in animals that survived the exposure. There was no indication of silicosis. Concentrations of the substances with toxicological effects in inhalative toxicity testing were above the valid TLV values (10mg/m3 USA). If TLV values are maintained no health hazards are expected. Reproductive and developmental toxicity: Two studies are included on repro/developmental toxicity. A 6- month, 1-generation study in rats combining fertility and prenatal toxicity testing administered 500 mg/kg bw in the food to 10 females and 2 males. No treatment-related effects were observed in the parents or in the offspring. Therefore the NOAEL for parents and offspring was 500 mg/kg. No effects on the female/male gonads were observed. In a 2-generation reproduction study 20 male and 20 female rats were given 100 mg/kg bw via oral feed for 24 months (see also repeated dose). No abnormalities were observed in the offspring resulting in a NOAEL of 100 mg/kg bw. VINYLTRIS(METHYLETHYLKETOXIME)SILANE alpha,beta-Unsaturated oximes represent two previously unknown classes of prohaptens.Three putative metabolites were proposed as sensitising agents. These included two diastereometric alpha,beta-epoxy oximes and a nitro analogue. When tested in the LLNA,alpha,beta-epoxy oximes. Allergic Contact Dermatitis??Formation, Structural Requirements,and Reactivity of Skin Sensitizers. Ann-Therese Karlberg et al: Chem. Res. Toxicol. 2008, 21, pp 53?69 https://ftp.cdc.gov/pub/Documents/OEL/06.%20Dotson/References/Karlberg_2008.pdf TOLUENE For toluene: Acute Toxicity Humans exposed to intermediate to high levels of toluene for short periods of time experience adverse central nervous system effects ranging from headaches to intoxication, convulsions, narcosis, and death. Similar effects are observed in short-term animal studies. Humans - Toluene ingestion or inhalation can result in severe central nervous system depression, and in large doses, can act as a narcotic. The ingestion of about 60 mL resulted in fatal nervous system depression within 30 minutes in one reported case. Constriction and necrosis of myocardial fibers, markedly swollen liver, congestion and haemorrhage of the lungs and acute tubular necrosis were found on autopsy. Central nervous system effects (headaches, dizziness, intoxication) and eye irritation occurred following inhalation exposure to 100 ppm toluene 6 hours/day for 4 days. Exposure to 600 ppm for 8 hours resulted in the same and more serious symptoms including euphoria, dilated pupils, convulsions, and nausea . Exposure to 10,000-30,000 ppm has been reported to cause narcosis and death Toluene can also strip the skin of lipids causing dermatitis Animals - The initial effects are instability and incoordination, lachrymation and sniffles (respiratory exposure), followed by narcosis. Animals die of respiratory failure from severe nervous system depression. Cloudy swelling of the kidneys was reported in rats following inhalation exposure to 1600 ppm, 18-20 hours/day for 3 days Subchronic/Chronic Effects: Repeat doses of toluene cause adverse central nervous system effects and can damage the upper respiratory system, the liver, and the kidney. Adverse effects occur as a result from both oral and the inhalation exposures. A reported lowest-observed-effect level in humans for adverse neurobehavioral effects is 88 ppm. Humans - Chronic occupational exposure and incidences of toluene abuse have resulted in hepatomegaly and liver function changes. It has also resulted in nephrotoxicity and, in one case, was a cardiac sensitiser and fatal cardiotoxin. Neural and cerebellar dystrophy were reported in several cases of habitual "glue sniffing." An epidemiological study in France on workers chronically exposed to toluene fumes reported leukopenia and neutropenia. Exposure levels were not given in the secondary reference; however, the average urinary excretion of hippuric acid, a metabolite of toluene, was given as 4 g/L compared to a normal level of 0.6 g/L Animals - The major target organs for the subchronic/chronic toxicity of toluene are the nervous system, liver, and kidney. Depressed immune response has been reported in male mice given doses of 105 mg/kg/day for 28 days. Toluene in corn oil administered to F344 male and female rats by gavage 5 days/week for 13 weeks, induced prostration, hypoactivity, ataxia, piloerection, lachrymation, excess salivation, and body tremors at doses 2500 mg/kg. Liver, kidney, and heart weights were also increased at this dose and histopathologic lesions were seen in the liver, kidneys, brain and urinary bladder. The no- observed-adverse effect level (NOAEL) for the study was 312 mg/kg (223 mg/kg/day) and the lowest- observed-adverse effect level (LOAEL) for the study was 625 mg/kg (446 mg/kg/day) . Developmental/Reproductive Toxicity Exposures to high levels of toluene can result in adverse effects in the developing human foetus. Several studies have indicated that high levels of toluene can also adversely effect the developing offspring in laboratory animals. Humans - Variable growth, microcephaly, CNS dysfunction, attentional deficits, minor craniofacial and limb abnormalities, and developmental delay were seen in three children exposed to toluene in utero as a result of maternal solvent abuse before and during pregnancy Animals - Sternebral alterations, extra ribs, and missing tails were reported following treatment of rats with 1500 mg/m3 toluene 24 hours/day during days 9-14 of gestation. Two of the dams died during the exposure. Another group of rats received 1000 mg/m3 8 hours/day during days 1-21 of gestation. No maternal deaths or toxicity occurred, however, minor skeletal retardation was present in the exposed fetuses. CFLP Mice were exposed to 500 or 1500 mg/m3 toluene continuously during days 6-13 of pregnancy. All dams died at the high dose during the first 24 hours of exposure, however none died at 500 mg/m3. Decreased foetal weight was reported, but there were no differences in the incidences of skeletal malformations or anomalies between the treated and control offspring. Absorption - Studies in humans and animals have demonstrated that toluene is readily absorbed via the lungs and the gastrointestinal tract. Absorption through the skin is estimated at about 1% of that absorbed by the lungs when exposed to toluene vapor. Dermal absorption is expected to be higher upon exposure to the liquid; however, exposure is limited by the rapid evaporation of toluene . Distribution - In studies with mice exposed to radiolabeled toluene by inhalation, high levels of radioactivity were present in body fat, bone marrow, spinal nerves, spinal cord, and brain white matter. Lower levels of radioactivity were present in blood, kidney, and liver. Accumulation of toluene has generally been found in adipose tissue, other tissues with high fat content, and in highly vascularised tissues . Metabolism - The metabolites of inhaled or ingested toluene include benzyl alcohol resulting from the hydroxylation of the methyl group. Further oxidation results in the formation of benzaldehyde and benzoic acid. The latter is conjugated with glycine to yield hippuric acid or reacted with glucuronic acid to form benzoyl glucuronide. o-cresol and p-cresol formed by ring hydroxylation are considered minor metabolites Excretion - Toluene is primarily (60-70%) excreted through the urine as hippuric acid. The excretion of benzoyl glucuronide accounts for 10-20%, and excretion of unchanged toluene through the lungs also accounts for 10-20%. Excretion of hippuric acid is usually complete within 24 hours after exposure. 3-[METHYLBIS[(1- METHYLETHENYL)OXY]SILYL]PROPOXY] ETHOXYLATED Polyethers, for example, ethoxylated surfactants and polyethylene glycols, are highly susceptible towards air oxidation as the ether oxygens will stabilize intermediary radicals involved. Investigations of a chemically well-defined alcohol (pentaethylene glycol mono-n-dodecyl ether) ethoxylate, showed that polyethers form complex mixtures of oxidation products when exposed to air. Sensitization studies in guinea pigs revealed that the pure nonoxidized surfactant itself is nonsensitizing but that many of the investigated oxidation products are sensitizers. Two hydroperoxides were identified in the oxidation mixture, but only one (16-hydroperoxy- 3,6,9,12,15-pentaoxaheptacosan-1-ol ) was stable enough to be isolated. It was found to be a strong sensitizer in LLNA (local lymph node assay for detection of sensitization capacity). The formation of other hydroperoxides was indicated by the detection of their corresponding aldehydes in the oxidation mixture . On the basis of the lower irritancy, nonionic surfactants are often preferred to ionic surfactants in topical products. However, their susceptibility towards autoxidation also increases the irritation. Because of their irritating effect, it is difficult to diagnose ACD to these compounds by patch testing. Allergic Contact Dermatitis??Formation, Structural Requirements,and Reactivity of Skin Sensitizers. Ann-Therese Karlberg et al; Chem. Res. Toxicol.2008,21,53-69 Polyethylene glycols (PEGs) have a wide variety of PEG-derived mixtures due to their readily linkable terminal primary hydroxyl groups in combination with many possible compounds and complexes such as ethers, fatty acids, castor oils, amines, propylene glycols, among other derivatives. PEGs and their derivatives are broadly utilized in cosmetic products as surfactants, emulsifiers, cleansing agents, humectants, and skin conditioners. PEGs and PEG derivatives were generally regulated as safe for use in cosmetics, with the conditions that impurities and by-products, such as ethylene oxides and 1,4-dioxane, which are known carcinogenic materials, should be removed before they are mixed in cosmetic formulations. Most PEGs are commonly available commercially as mixtures of different oligomer sizes in broadly- or narrowly-defined molecular weight (MW) ranges. For instance, PEG-10,000 typically designates a mixture of PEG molecules (n = 195 to 265) having an average MW of 10,000. PEG is also known as polyethylene oxide (PEO) or polyoxyethylene (POE), with the three names being chemical synonyms. However, PEGs mainly refer to oligomers and polymers with molecular masses below 20,000 g/mol, while PEOs are polymers with molecular masses above 20,000 g/mol, and POEs are polymers of any molecular mass. Relatively small molecular weight PEGs are produced by the chemical reaction between ethylene oxide and water or ethylene glycol (or other ethylene glycol oligomers), as catalyzed by acidic or basic catalysts. To produce PEO or high-molecular weight PEGs, synthesis is performed by suspension polymerization. It is necessary to hold the growing polymer chain in solution during the course of the poly- condensation process. The reaction is catalyzed by magnesium-, aluminum-, or calcium- organoelement compounds. To prevent coagulation of polymer chains in the solution, chelating additives such as dimethylglyoxime are used Safety Evaluation of Polyethyene Glycol (PEG) Compounds for Cosmetic Use: Toxicol Res 2015; 31:105-136 The Korean Society of Toxicology https://doi.org/10.5487/TR.2015.31.2.105 CARBON BLACK Inhalation (rat) TCLo: 50 mg/m3/6h/90D-I Nil reported WARNING: This substance has been classified by the IARC as Group 2B: Possibly Carcinogenic to Humans. METHYL ETHYL KETOXIME Mammalian lymphocyte mutagen *Huls Canada ** Merck For methyl ethyl ketoxime (MEKO) Carcinogenicity: Increased incidences of liver tumours were observed in rat and mouse lifetime studies and there was also an increased incidence of mammary gland tumours in female rats, however, this was only seen at mid- and/or high concentrations of MEKO. Consideration of the available information regarding genotoxicity indicate that MEKO is not likely to be genotoxic. Accordingly, although the mode of induction of tumours is not fully elucidated, the tumours observed are not considered to have resulted from direct interaction with genetic material. The European Commission (2000) considered that a possible mechanism for the increased incidences of liver tumours in male rats and mice was the metabolism of MEKO to a carcinogenic agent, mediated by sulfotransferase. The sex and organ specificity of tumour formation correlated with the typically higher activity of this enzyme in male rodents. Genotoxicity: The in vitro and in vivo genotoxicity results for MEKO were mostly negative, including an in vivo study that utilized inhalation exposure and was found to be negative for DNA adducts in rat liver cells. Therefore, based on the available data, MEKO appears to lack mutagenic potential. Repeat dose toxicity: Non-neoplastic effects were also observed in the nasal cavity of rats and/or mice in inhalation studies of short-term through to chronic exposure. Also, repeated dose studies based on oral exposure showed effects in the spleen, liver and kidney of rats as well as haematological effects in both rats and rabbits. Reproductive toxicity: In a one-generation oral rat study, the LOAEL for reproductive toxicity was 100 mg/kg-bw per day, the highest dose, based on a statistically significant decrease in female delivery index (%) , whereas no treatment-related effects on reproductive parameters were observed in a two-generation study in which rats were dosed by gavage at 0-200 mg/kg-bw per day In both the one-generation and two- generation rat studies, a parental LOAEL of 10 mg/kg-bw per day, the lowest dose tested, was established, based on histopathological effects in the spleen and liver (and in the kidney in the one-generation study). Developmental toxicity: Teratogenicity was not observed in pregnant rats and rabbits dosed orally with MEKO during gestation. The lowest oral LOAEL for developmental toxicity was 40 mg/kg-bw per day, the highest dose, based on abortions in 3 of 10 adult females in pregnant rabbits dosed by gavage during gestation . The lowest oral LOAEL for maternal toxicity was 10 mg/kg-bw per day, based on signs of anemia (increased reticulocytes and methaemoglobin) in rabbits dosed at 0-80 mg/kg-bw per day in a range-finding developmental study CALCIUM CARBONATE & VINYLTRIS(METHYLETHYLKETOXIME)SILANE & TOLUENE The material may cause skin irritation after prolonged or repeated exposure and may produce a contact dermatitis (nonallergic). This form of dermatitis is often characterised by skin redness (erythema) and swelling the epidermis. Histologically there may be intercellular oedema of the spongy layer (spongiosis) and intracellular oedema of the epidermis. VINYLTRIS(METHYLETHYLKETOXIME)SILANE & METHYL ETHYL KETOXIME 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 eczema involves 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. VINYLTRIS(METHYLETHYLKETOXIME)SILANE & 3-[METHYLBIS[(1- METHYLETHENYL)OXY]SILYL]PROPOXY] ETHOXYLATED & CARBON BLACK No significant acute toxicological data identified in literature search. Acute Toxicity Carcinogenicity Skin Irritation/Corrosion Reproductivity Serious Eye Damage/Irritation STOT - Single Exposure Respiratory or Skin sensitisation STOT - Repeated Exposure Mutagenicity Aspiration Hazard Legend: ? Data either not available or does not fill the criteria for classification ? Data available to make classification SECTION 12 Ecological information Toxicity Threebond 1217H Endpoint Test Duration (hr) Species Not Available Not Available Not Available dimethylsiloxane, hydroxy- terminated Endpoint Test Duration (hr) Species Not Available Not Available Not Available calcium carbonate Endpoint Test Duration (hr) Species Value NOEC(ECx) 1h Fish 4-320mg/l LC50 96h Fish >165200mg/L EC50 72h Algae or other aquatic plants >14mg/l silica amorphous, fumed Endpoint Test Duration (hr) Species Value NOEC(ECx) 24h Crustacea >=10000mg/l vinyltris(methylethylketoxime)silane Endpoint Test Duration (hr) Species NOEC(ECx) 72h Algae or other aquatic plants EC50 72h Algae or other aquatic plants LC50 96h Fish EC50 48h Crustacea toluene Endpoint Test Duration (hr) Species Value LC50 96h Fish 5-35mg/l EC50 72h Algae or other aquatic plants 12.5mg/l EC50 48h Crustacea 3.78mg/L NOEC(ECx) 168h Crustacea 0.74mg/L EC50 96h Algae or other aquatic plants >376.71mg/L 3-[methylbis[(1- methylethenyl)oxy]silyl]propoxy] ethoxylated Endpoint Test Duration (hr) Species Not Available Not Available Not Available carbon black Endpoint Test Duration (hr) Species LC50 96h Fish EC50 72h Algae or other aquatic plants EC50 48h Crustacea NOEC(ECx) 24h Crustacea methyl ethyl ketoxime Endpoint Test Duration (hr) Species BCF 1008h Fish NOEC(ECx) 72h Algae or other aquatic plants EC50 72h Algae or other aquatic plants EC50 48h Crustacea LC50 96h Fish Legend: Extracted from 1. IUCLID Toxicity Data 2. Europe ECHA Registered Substances - Ecotoxicological Information - Aquatic Toxicity 4. US EPA, Ecotox database - Aquatic Toxicity Data 5. ECETOC Aquatic Hazard Assessment Data 6. NITE (Japan) - Bioconcentration Data 7. METI (Japan) - Bioconcentration Data 8. Vendor Data Toxic to bees. For siloxanes: Environmental fate: It is well accepted that polydimethylsiloxane (PDMS) fluids become permanent residents of sediment but should not exert adverse environmental effects. PDMS in intimate contact with many soils undergo siloxane bond redistribution and hydrolysis Therefore, it is highly likely that substituted polymethylsiloxanes will undergo similar reactions, and this reactivity may prevent suitable adsorption data being obtained. Silicone fluids are very surface active because the flexible siloxane linkages permit alignment of the hydrophobic methyl substituents towards the non-polar phase, and of the polysiloxane backbone towards the polar phase. The polar medium is generally water, and a polar media to which polydimethylsiloxanes become attached may be textiles, sewage sludge, hair, algae, sediment etc. In aqueous environments, polydimethylsiloxanes are adsorbed onto sedimenting particles. Also, in the presence of nitrate ions, which exist at various concentrations in the environment, short chain siloxanes are photodegraded to the level of silicate within days The stability of the siloxanes, desirable from a technical point of view, makes the siloxanes very persistent, and once released to the environment the siloxanes remain for many years. The main source of releases of siloxanes to the air is volatile siloxanes used in cosmetics, wax, polishes, and to a minor extent in several other applications. the volatile siloxanes may account for a significant part of the siloxanes used for cosmetics. Non-volatile silicone fluids used in cosmetics, wax, polishes, cleaning products and for textile applications (softeners) will to a large extent end up in wastewater and be directed to wastewater treatment plants. The cyclic siloxanes and small-chain linear siloxanes are bioconcentrated (bioconcentration factors for long-chained siloxanes have not been assessed). The estimated bioconcentration factors (BCF) of the small siloxanes range from 340 for HMDS to 40,000 for a phenylated trisiloxane (phenyl trimethicone). The small phenylated siloxanes seem to have very high BCF, and model estimates indicate that these substances are the most toxic for aquatic organisms. PBT profiler screening In order to make a first comparison between the substances as to persistence, bioaccumulation and toxicity, the substances were screened using the PBT profiler developed by U.S. EPA (U.S. EPA 2003). The profiler uses a procedure to predict persistence, bioaccumulation, and toxicity of organic chemicals on the basis of the chemical structure and physical parameters of the substances combined with experimental parameters for substance with a similar structure, using a QSAR approach. The results for six members of the siloxane family predict the highest bioconcentration factors for the two phenyl siloxanes, one order of magnitudes higher than the values for the cyclic siloxanes and two orders of magnitudes higher than the values for the small linear methyl siloxanes. The predicted toxicity is as well significantly higher (lowest ChV values) for the phenyl siloxanes. The predicted half-life is nearly the same for all substances. Using U.S. EPA's criteria, the screening indicates that all substances are of high concern as to environmental toxicity, and that the phenyl siloxanes are considered very bioaccumulative. Ecotoxicity: The environmental fate and effects of volatile methylsiloxanes (mainly cyclosiloxanes) and polydimethylsiloxane (PDMS) have been reported: For octamethylcyclosiloxane: Fish acute LC50 (14 day):: rainbow trout 10 ug/l; sheepshead minnow >6.3 ug/l Daphnia magna acute EC50 (48 h): >15 ug/l; NOEC 15 ug/l Mysid shrimp acute LC50 (96 h): >9.1 ug/l; NOEC 9.1 ug/l For PDMS Daphnia magna NOEC 572 mg/kg Physical effects such as surface entrapment have been observed when testing aquatic invertebrates in clean laboratory water, but similar effects are not expected in natural environments where a large variety of other surfaces provide opportunities for deposition Calcium provides an important link between tectonics, climate and the carbon cycle. In the simplest terms, uplift of mountains exposes Ca-bearing rocks to chemical weathering and releases Ca2+ into surface water. This Ca2+ eventually is transported to the ocean where it reacts with dissolved CO2 to form limestone. Some of this limestone settles to the sea floor where it is incorporated into new rocks. Dissolved CO2, along with carbonate and bicarbonate ions, are referred to as dissolved inorganic carbon (DIC). Microbial methylation plays important roles in the biogeochemical cycling of the metalloids and possibly in their detoxification. Many microorganisms (bacteria, fungi, and yeasts) and animals are now known to biomethylate arsenic, forming both volatile (e.g., methylarsines) and nonvolatile (e.g., methylarsonic acid and dimethylarsinic acid) compounds. Antimony and bismuth, also undergo biomethylation to some extent. Trimethylstibine formation by microorganisms is now well established, but this process apparently does not occur in animals. Formation of trimethylbismuth by microorganisms has been reported in a few cases. For Amorphous Silica: Amorphous silica is chemically and biologically inert. It is not biodegradable. Aquatic Fate: Due to its insolubility in water there is a separation at every filtration and sedimentation process. On a global scale, the level of man-made synthetic amorphous silicas (SAS) represents up to 2.4% of the dissolved silica naturally present in the aquatic environment and untreated SAS have a relatively low water solubility and an extremely low vapour pressure. Biodegradability in sewage treatment plants or in surface water is not applicable to inorganic substances like SAS. Terrestrial Fate: Crystalline and/or amorphous silicas are common on the earth in soils and sediments, and in living organisms (e.g. diatoms), but only the dissolved form is bioavailable. On the basis of these properties it is expected that SAS released into the environment will be distributed mainly into soil/sediment. Surface treated silica will be wetted then adsorbed onto soils and sediments. Atmospheric Fate: SAS is not expected to be distributed into the air if released. Ecotoxicity: SAS is not toxic to environmental organisms (apart from physical desiccation in insects). SAS presents a low risk for adverse effects to the environment. For Silica: Environmental Fate: Most documentation on the fate of silica in the environment concerns dissolved silica, in the aquatic environment, regardless of origin, (man-made or natural), or structure, (crystalline or amorphous). Terrestrial Fate: Silicon makes up 25.7% of the Earth's crust, by weight, and is the second most abundant element, being exceeded only by oxygen. Silicon is not found free in nature, but occurs chiefly as the oxide and as silicates. Once released into the environment, no distinction can be made between the initial forms of silica. Aquatic Fate: At normal environmental pH, dissolved silica exists exclusively as monosilicic acid. At pH 9.4, amorphous silica is highly soluble in water. Crystalline silica, in the form of quartz, has low solubility in water. Silicic acid plays an important role in the biological/geological/chemical cycle of silicon, especially in the ocean. Marine organisms such as diatoms, silicoflagellates and radiolarians use silicic acid in their skeletal structures and their skeletal remains leave silica in sea sediment Ecotoxicity: Silicon is important to plant and animal life and is practically non-toxic to fish including zebrafish, and Daphnia magna water fleas. DO NOT discharge into sewer or waterways. Persistence and degradability Ingredient Persistence: Water/Soil Persistence: Air toluene LOW (Half-life = 28 days) LOW (Half-life = 4.33 days) methyl ethyl ketoxime LOW LOW Bioaccumulative potential Ingredient Bioaccumulation toluene LOW (BCF = 90) methyl ethyl ketoxime LOW (BCF = 5.8) Mobility in soil Ingredient Mobility toluene LOW (KOC = 268) methyl ethyl ketoxime LOW (KOC = 130.8) SECTION 13 Disposal considerations Waste treatment methods Product / Packaging disposal ? Containers may still present a chemical hazard/ danger when empty. ? Return to supplier for reuse/ recycling if possible. Otherwise: ? 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, then puncture containers, to prevent re-use, and bury at an authorised landfill. ? Where possible retain label warnings and SDS and observe all notices pertaining to the product. ? 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 or consult manufacturer for recycling options. ? Consult State Land Waste Authority for disposal. ? Bury or incinerate residue at an approved site. ? Recycle containers if possible, or dispose of in an authorised landfill. SECTION 14 Transport information Labels Required Marine Pollutant NO HAZCHEM Not Applicable Land transport (ADG): NOT REGULATED FOR TRANSPORT OF DANGEROUS GOODS Air transport (ICAO-IATA / DGR): NOT REGULATED FOR TRANSPORT OF DANGEROUS GOODS Sea transport (IMDG-Code / GGVSee): NOT REGULATED FOR TRANSPORT OF DANGEROUS GOODS Transport in bulk according to Annex II of MARPOL and the IBC code Not Applicable Transport in bulk in accordance with MARPOL Annex V and the IMSBC Code Product name Group dimethylsiloxane, hydroxy- terminated Not Available calcium carbonate Not Available silica amorphous, fumed Not Available vinyltris(methylethylketoxime)silane Not Available toluene Not Available 3-[methylbis[(1- methylethenyl)oxy]silyl]propoxy] ethoxylated Not Available carbon black Not Available methyl ethyl ketoxime Not Available Transport in bulk in accordance with the IGC Code Product name Ship Type dimethylsiloxane, hydroxy- terminated Not Available calcium carbonate Not Available silica amorphous, fumed Not Available vinyltris(methylethylketoxime)silane Not Available toluene Not Available 3-[methylbis[(1- methylethenyl)oxy]silyl]propoxy] ethoxylated Not Available carbon black Not Available methyl ethyl ketoxime Not Available SECTION 15 Regulatory information Safety, health and environmental regulations / legislation specific for the substance or mixture dimethylsiloxane, hydroxy-terminated is found on the following regulatory lists ? Australia Standard for the Uniform Scheduling of Medicines and Poisons (SUSMP) - Schedule 10 / Appendix C ? Australia Standard for the Uniform Scheduling of Medicines and Poisons (SUSMP) - Schedule 4 ? Australian Inventory of Industrial Chemicals (AIIC) calcium carbonate is found on the following regulatory lists ? Australian Inventory of Industrial Chemicals (AIIC) ? International WHO List of Proposed Occupational Exposure Limit (OEL) Values for Manufactured Nanomaterials (MNMS) silica amorphous, fumed is found on the following regulatory lists ? Australian Inventory of Industrial Chemicals (AIIC) ? International WHO List of Proposed Occupational Exposure Limit (OEL) Values for Manufactured Nanomaterials (MNMS) vinyltris(methylethylketoxime)silane is found on the following regulatory lists ? Australian Inventory of Industrial Chemicals (AIIC) toluene is found on the following regulatory lists ? Australia Hazardous Chemical Information System (HCIS) - Hazardous Chemicals ? Australia Standard for the Uniform Scheduling of Medicines and Poisons (SUSMP) - Schedule 5 ? Australia Standard for the Uniform Scheduling of Medicines and Poisons (SUSMP) - Schedule 6 ? Australian Inventory of Industrial Chemicals (AIIC) ? Chemical Footprint Project - Chemicals of High Concern List ? International Agency for Research on Cancer (IARC) - Agents Classified by the IARC Monographs - Not Classified as Carcinogenic 3-[methylbis[(1-methylethenyl)oxy]silyl]propoxy] ethoxylated is found on the following regulatory lists ? Australian Inventory of Industrial Chemicals (AIIC) carbon black is found on the following regulatory lists ? Australia Hazardous Chemical Information System (HCIS) - Hazardous Chemicals ? Australian Inventory of Industrial Chemicals (AIIC) ? Chemical Footprint Project - Chemicals of High Concern List ? International Agency for Research on Cancer (IARC) - Agents Classified by the IARC Monographs ? International Agency for Research on Cancer (IARC) - Agents Classified by the IARC Monographs - Group 2B: Possibly carcinogenic to humans ? International WHO List of Proposed Occupational Exposure Limit (OEL) Values for Manufactured Nanomaterials (MNMS) methyl ethyl ketoxime is found on the following regulatory lists ? Australia Hazardous Chemical Information System (HCIS) - Hazardous Chemicals ? Australia Standard for the Uniform Scheduling of Medicines and Poisons (SUSMP) - Schedule 6 ? Australian Inventory of Industrial Chemicals (AIIC) ? Chemical Footprint Project - Chemicals of High Concern List National Inventory Status National Inventory Status Australia - AIIC / Australia Non-Industrial Use Yes Canada - DSL No (3-[methylbis[(1-methylethenyl)oxy]silyl]propoxy] ethoxylated) Canada - NDSL No (dimethylsiloxane, hydroxy-terminated; silica amorphous, fumed; vinyltris(methylethylketoxime)silane; toluene; carbon black; methyl ethyl ketoxime) China - IECSC Yes Europe - EINEC / ELINCS / NLP No (dimethylsiloxane, hydroxy-terminated; 3-[methylbis[(1-methylethenyl)oxy]silyl]propoxy] ethoxylated) Japan - ENCS No (3-[methylbis[(1-methylethenyl)oxy]silyl]propoxy] ethoxylated) Korea - KECI Yes New Zealand - NZIoC Yes Philippines - PICCS No (3-[methylbis[(1-methylethenyl)oxy]silyl]propoxy] ethoxylated) USA - TSCA Yes Taiwan - TCSI Yes Mexico - INSQ No (vinyltris(methylethylketoxime)silane; 3-[methylbis[(1-methylethenyl)oxy]silyl]propoxy] ethoxylated) Vietnam - NCI No (3-[methylbis[(1-methylethenyl)oxy]silyl]propoxy] ethoxylated) Russia - FBEPH No (3-[methylbis[(1-methylethenyl)oxy]silyl]propoxy] ethoxylated) National Inventory Status Legend: Yes = All CAS declared ingredients are on the inventory No = One or more of the CAS listed ingredients are not on the inventory. These ingredients may be exempt or will require registration. SECTION 16 Other information Revision Date 07/28/2021 Initial Date 06/30/2020 SDS Version Summary Version Date of Update Sections Updated 2.1 11/22/2020 Physical and chemical properties - Appearance, Ecological Information - Environmental, Composition / information on ingredients - Ingredients, Identification of the substance / mixture and of the company / undertaking - Supplier Information, Identification of the substance / mixture and of the company / undertaking - Use, Name 3.1 07/27/2021 Toxicological information - Acute Health (eye), Toxicological information - Acute Health (inhaled), Toxicological information - Acute Health (skin), Toxicological information - Acute Health (swallowed), Physical and chemical properties - Appearance, Toxicological information - Chronic Health, Hazards identification - Classification, Disposal considerations - Disposal, Exposure controls / personal protection - Engineering Control, Ecological Information - Environmental, Firefighting measures - Fire Fighter (fire/explosion hazard), Firefighting measures - Fire Fighter (fire fighting), First Aid measures - First Aid (skin), First Aid measures - First Aid (swallowed), Handling and storage - Handling Procedure, Composition / information on ingredients - Ingredients, Stability and reactivity - Instability Condition, Exposure controls / personal protection - Personal Protection (other), Exposure controls / personal protection - Personal Protection (hands/feet), Accidental release measures - Spills (major), Accidental release measures - Spills (minor), Handling and storage - Storage (storage requirement), Handling and storage - Storage (suitable container), Identification of the substance / mixture and of the company / undertaking - Supplier Information, Identification of the substance / mixture and of the company / undertaking - Synonyms, Transport information - Transport, Transport Information, Identification of the substance / mixture and of the company / undertaking - Use, Name Other information 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. The 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 other settings. Risks may be determined by reference to Exposures Scenarios. Scale of use, frequency of use and current or available engineering controls must be considered. Definitions and abbreviations PC?TWA: Permissible Concentration-Time Weighted Average PC?STEL: Permissible Concentration-Short Term Exposure Limit IARC: International Agency for Research on Cancer ACGIH: American Conference of Governmental Industrial Hygienists STEL: Short Term Exposure Limit TEEL: Temporary Emergency Exposure Limit? IDLH: Immediately Dangerous to Life or Health Concentrations ES: Exposure Standard OSF: Odour Safety Factor NOAEL :No Observed Adverse Effect Level LOAEL: Lowest Observed Adverse Effect Level TLV: Threshold Limit Value LOD: Limit Of Detection OTV: Odour Threshold Value BCF: BioConcentration Factors BEI: Biological Exposure Index AIIC: Australian Inventory of Industrial Chemicals DSL: Domestic Substances List NDSL: Non-Domestic Substances List IECSC: Inventory of Existing Chemical Substance in China EINECS: European INventory of Existing Commercial chemical Substances ELINCS: European List of Notified Chemical Substances NLP: No-Longer Polymers ENCS: Existing and New Chemical Substances Inventory KECI: Korea Existing Chemicals Inventory NZIoC: New Zealand Inventory of Chemicals PICCS: Philippine Inventory of Chemicals and Chemical Substances TSCA: Toxic Substances Control Act TCSI: Taiwan Chemical Substance Inventory INSQ: Inventario Nacional de Sustancias Qu?micas NCI: National Chemical Inventory FBEPH: Russian Register of Potentially Hazardous Chemical and Biological Substances This document is copyright. 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 written permission from CHEMWATCH. TEL (+61 3) 9572 4700.