Safety Data Sheet

Safety8329TFS Slow Cure,Data Thermally Sheet Conductive Adhesive, Flowable (Part A) 8329TFSMG Chemicals8329TFS Slow UK LimitedSlow Cure, Cure, Thermally Thermally Conductive Conductive Adhesive, Adhesive, Flowable Flowable (Part (Part A) A)Chemwatch Hazard Alert Code: 2 VersionMG Chemicals MGNo: 4.7 Chemicals UK Limited UK Limited ChemwatchChemwatch HazardIssue Hazard Date:Alert 29/07/2016 Code: Alert Code:2 2 Safety Data Sheet (Conforms to Regulation (EC) No 2015/830) Print Date: 29/07/2016 Version VersionNo: 4.7 No: 4.7 Issue Date:Issue 29/07/2016 Date: 29/07/2016 L.REACH.GBR.EN Safety DataSafety Sheet Data (Conforms Sheet (Conforms to Regulation to Regulation (EC) No (EC) 2015/830) No 2015/830) Print Date:Print 29/07/2016 Date: 29/07/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part A) L.REACH.GBR.ENL.REACH.GBR.EN SECTION 1 IDENTIFICATION OF THE SUBSTANCE / MIXTURE AND OF THE COMPANY / UNDERTAKING MG Chemicals UK Limited Chemwatch Hazard Alert Code: 2 SECTIONSECTION 1 IDENTIFICATION 1 IDENTIFICATION OF THE OF SUBSTANCE THE SUBSTANCE / MIXTURE / MIXTURE AND OFAND THE OF COMPANY THE COMPANY / UNDERTAKING / UNDERTAKING Version No: Issue Date: 1.1. Product Identifier4.7 29/07/2016 Safety Data Sheet (Conforms to Regulation (EC) No 2015/830) Print Date: 29/07/2016 1.1. Product1.1. Product IdentifierProduct Identifier name Slow Cure, Thermally Conductive Adhesive, Flowable (Part A) L.REACH.GBR.EN ProductSynonymsProduct name nameMC002977 Slow Cure, Slow Thermally Cure, Thermally Conductive Conductive Adhesive, Adhesive, Flowable Flowable (Part A) (Part A) ProperSECTION shippingSynonyms name 1Synonyms IDENTIFICATIONENVIRONMENTALLYMC002977 OF THE HAZARDOUS SUBSTANCE SUBSTANCE, / MIXTURE LIQUID, N.O.S. AND (contains OF THE zinc COMPANY oxide and bisphenol / UNDERTAKING a/ diglycidyl ether resin, liquid) ProperOther Propershipping means shipping name of nameENVIRONMENTALLYENVIRONMENTALLY HAZARDOUS HAZARDOUS SUBSTANCE, SUBSTANCE, LIQUID, LIQUID, N.O.S. (contains N.O.S. (contains zinc oxide zinc and oxide bisphenol and bisphenol a/ diglycidyl a/ diglycidyl ether resin, ether liquid) resin, liquid) Not Available 1.1.identification Product Identifier Other meansOther ofmeans of Not AvailableNot Available identificationidentificationProduct name Slow Cure, Thermally Conductive Adhesive, Flowable (Part A) 1.2. Relevant identified usesSynonyms of the substance or mixture and uses advised against 1.2. RelevantRelevant1.2. Relevant identified identifiedProper identified uses shippingusesThermally of uses name the ofsubstance conductive theENVIRONMENTALLY substance adhesive or mixture for or bonding mixture HAZARDOUS and and uses thermaland advised usesSUBSTANCE, management advised against LIQUID, against N.O.S. (contains zinc oxide and bisphenol a/ diglycidyl ether resin, liquid) RelevantUsesRelevant advised identified identifiedagainst usesOther uses meansThermallyNot Applicable ofThermally conductive conductive adhesive adhesive for bonding for bondingand thermal and managementthermal management Not Available identification Uses advisedUses advised against againstNot ApplicableNot Applicable 1.3. Details of the supplier of the safety data sheet 1.2. Relevant identified uses of the substance or mixture and uses advised against 1.3.Registered Details1.3. Details of company the ofsupplier namethe supplier of the ofsafety the safety data sheet data sheet Relevant identified uses Thermally conductive adhesive for bonding and thermal management RegisteredRegistered company Addresscompany name namePremier Farnell plc Uses advised against Not Applicable TelephoneAddressAddress150 Armley Road, Leeds, LS12 2QQ TelephoneFaxTelephone+44 (0) 870 129 8608 1.3. Details of the supplier of the safety data sheet WebsiteFax FaxNot- Available www.mgchemicals.com Registered company name WebsiteEmailWebsiteNot- AvailableNot Available www.mgchemicals.comwww.mgchemicals.com Address Email Email 1.4. Emergency telephone numberTelephone Fax 1.4.Association Emergency1.4. Emergency / Organisation telephone telephone numberPremier number Farnell plc Website Not Available www.mgchemicals.com AssociationEmergencyAssociation / Organisation telephone / Organisation +44 1865 407333 numbers Email EmergencyEmergency telephone telephone Other emergency telephonenumbersnumbers NA numbers Other emergencyOther1.4. emergency Emergency telephone telephone telephone number numbersnumbers Association / Organisation Emergency telephone SECTION 2 HAZARDS IDENTIFICATIONnumbers SECTIONSECTION 2 HAZARDSOther 2 emergencyHAZARDS IDENTIFICATION telephone IDENTIFICATION 2.1. Classification of the substancenumbers or mixture 2.1. Classification2.1. Classification of the ofsubstance the substance or mixture or mixture Considered a hazardous mixture according to Reg. (EC) No 1272/2008 and their amendments. Classified as Dangerous Goods for transport purposes. ConsideredClassificationConsidered a hazardous according a hazardous mixture to accordingmixture according to Reg. (EC)to Reg. No (EC) 1272/2008 No 1272/2008 and their and amendments. their amendments. Classified Classified as Dangerous as Dangerous Goods for Goods transport for transport purposes. purposes. regulationSECTION (EC) 2 No HAZARDS IDENTIFICATION ClassificationClassification according according to Skin to Corrosion/Irritation Category 2, Eye Irritation Category 2, Skin Sensitizer Category 1, Chronic Aquatic Hazard Category 1 [1] regulation1272/2008regulation [CLP](EC) No (EC) SkinNo Corrosion/IrritationSkin Corrosion/Irritation Category Category 2, Eye Irritation 2, Eye IrritationCategory Category 2, Skin Sensitizer2, Skin Sensitizer Category Category 1, Chronic 1, ChronicAquatic AquaticHazard CategoryHazard Category 1 1 2.1. Classification[1] of the substance or mixture 1272/20081272/2008 [CLP] [CLP]1. [1] Classified by Chemwatch; 2. Classification drawn from EC Directive 67/548/EEC - Annex I ; 3. Classification drawn from EC Directive 1272/2008 - Annex Legend: VI 1. Classified1. Classified by Chemwatch; by Chemwatch; 2. Classification 2. Classification drawn from drawn EC from Directive EC Directive 67/548/EEC 67/548/EEC - Annex -I Annex; 3. Classification I ; 3. Classification drawn from drawn EC from Directive EC Directive 1272/2008 1272/2008 - Annex - Annex ConsideredLegend: a hazardousLegend: mixture according to Reg. (EC) No 1272/2008 and their amendments. Classified as Dangerous Goods for transport purposes. VI VI Classification according to 2.2. Label elements regulation (EC) No Skin Corrosion/Irritation Category 2, Eye Irritation Category 2, Skin Sensitizer Category 1, Chronic Aquatic Hazard Category 1 2.2. Label2.2. Labelelements elements1272/2008 [CLP] [1] 1. Classified by Chemwatch; 2. Classification drawn from EC Directive 67/548/EEC - Annex I ; 3. Classification drawn from EC Directive 1272/2008 - Annex Legend: CLP label elements VI CLP labelCLP elements label elements 2.2. Label elements SIGNAL WORD WARNING SIGNALSIGNAL WORD WORDWARNINGWARNING Hazard statement(s)CLP label elements

HazardHazard statement(s) statement(s)H315 Causes skin irritation. H319H315 H315Causes Causesseriousskin irritation. eyeskin irritation.irritation. SIGNAL WORD WARNING H317H319 H319CausesMay cause Causesserious an allergic eyeserious irritation. skin eye reaction. irritation. H410H317 H317VeryMay causetoxicMay to an aquaticcause allergic an life skinallergic with reaction. long skin lasting reaction. effects. Hazard statement(s) H410 H410Very toxicVery to aquatictoxic to lifeaquatic with longlife with lasting long effects. lasting effects. H315 Causes skin irritation. Continued... H319 Causes serious eye irritation. www.element14.com Continued...Continued... www.farnell.com H317 May cause an allergic skin reaction. www.newark.com H410 Very toxic to aquatic life with long lasting effects.

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Supplementary statement(s) Not Applicable

Precautionary statement(s) Prevention

P280 Wear protective gloves/protective clothing/eye protection/face protection. P261 Avoid breathing mist/vapours/spray. P273 Avoid release to the environment. P272 Contaminated work clothing should not be allowed out of the workplace.

Precautionary statement(s) Response

P302+P352 IF ON SKIN: Wash with plenty of water and soap. P305+P351+P338 IF IN EYES: Rinse cautiously with water for several minutes. Remove contact lenses, if present and easy to do. Continue rinsing. P333+P313 If skin irritation or rash occurs: Get medical advice/attention. P337+P313 If eye irritation persists: Get medical advice/attention. P362+P364 Take off contaminated clothing and wash it before reuse. P391 Collect spillage.

Precautionary statement(s) Storage Not Applicable

Precautionary statement(s) Disposal

P501 Dispose of contents/container in accordance with local regulations.

2.3. Other hazards Inhalation and/or ingestion may produce health damage*.

Cumulative effects may result following exposure*.

May produce discomfort of the respiratory system*.

Limited evidence of a carcinogenic effect*.

Possible respiratory sensitizer*.

REACh - Art.57-59: The mixture does not contain Substances of Very High Concern (SVHC) at the SDS print date.

SECTION 3 COMPOSITION / INFORMATION ON INGREDIENTS

3.1.Substances See 'Composition on ingredients' in Section 3.2

3.2.Mixtures

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Supplementary statement(s) Not Applicable

Precautionary statement(s) Prevention

Precautionary statement(s) Response

Precautionary statement(s) Storage Not Applicable

Precautionary statement(s) Disposal

P501 Dispose of contents/container in accordance with local regulations.

2.3. Other hazards Inhalation and/or ingestion may produce health damage*.

Cumulative effects may result following exposure*.

May produce discomfort of the respiratory system*.

Limited evidence of a carcinogenic effect*.

Possible respiratory sensitizer*.

REACh - Art.57-59: The mixture does not contain Substances of Very High Concern (SVHC) at the SDS print date.

SECTION 3 COMPOSITION / INFORMATION ON INGREDIENTS

3.1.Substances See 'Composition on ingredients' in Section 3.2

3.2.Mixtures

1.CAS No 2.EC No %[weight] Name Classification according to regulation (EC) No 1272/2008 [CLP] 3.Index No 4.REACH No 1.1344-28-1. 2.215-691-6 3.Not Available 40 aluminium oxide Not Applicable 4.01-2119817795-27-XXXX, 01-2119529248-35-XXXX 1.28064-14-4 2.Not Available bisphenol F glycidyl ether/ Skin Corrosion/Irritation Category 2, Eye Irritation Category 2, Skin Sensitizer Category 1, Chronic 26 3.Not Available formaldehyde copolymer Aquatic Hazard Category 2; H315, H319, H317, H411, EUH019 [1] Safety4.Not Available Data Sheet 1.1314-13-2 2.215-222-5 25 zinc oxide Acute Aquatic Hazard Category 1, Chronic Aquatic Hazard Category 1; H410 [3] 3.030-013-00-7 4.01-2119463881-32-XXXX 1.68609-97-2 2.271-846-8 4 (C12-14)alkylglycidyl ether Skin Corrosion/Irritation Category 2, Skin Sensitizer Category 1; H315, H317 [3] 3.603-103-00-4 4.01-2119485289-22-XXXX 1.25068-38-6 2.500-033-5 bisphenol A/ diglycidyl ether resin, Eye Irritation Category 2, Skin Corrosion/Irritation Category 2, Skin Sensitizer Category 1, Chronic 2 3.603-074-00-8 liquid Aquatic Hazard Category 2; H319, H315, H317, H411 [3] 4.01-2119456619-26-XXXX Version No: 4.7 Page 3 of 20 Issue Date: 29/07/2016 Version1.1333-86-4 No: 4.7 Page 3 of 20 Issue Date: 29/07/2016 Print Date: 29/07/2016 2.215-609-9 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part A) Print Date: 29/07/2016 3.Not Available 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part A) 0.7 carbon black Carcinogenicity Category 2; H351 [1] 4.01-2119384822-32-XXXX, 01-2119489801-30-XXXX, 01-2119475601-40-XXXX 01-2119475601-40-XXXX Legend: 1. Classified by Chemwatch; 2. Classification drawn from EC Directive 67/548/EEC - Annex I ; 3. Classification drawn from EC Directive 1272/2008 - Annex 1. Classified by Chemwatch; 2. Classification drawn from EC Directive 67/548/EEC - Annex I ; 3. Classification drawn from EC Directive 1272/2008 Continued...- Annex Legend: VI 4. Classification drawn from C&L VI 4. Classification drawn from C&L

SECTION 4 FIRST AID MEASURES SECTION 4 FIRST AID MEASURES

4.1. Description of first aid measures 4.1. Description of first aid measures If skin contact occurs: If skin contact occurs: Immediately remove all contaminated clothing, including footwear. Immediately remove all contaminated clothing, including footwear. Flush skin and hair with running water (and soap if available). Flush skin and hair with running water (and soap if available). Seek medical attention in event of irritation. Seek medical attention in event of irritation. If this product comes in contact with the eyes: If this product comes in contact with the eyes: Wash out immediately with fresh running water. Wash out immediately with fresh running water. General 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. 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. General Seek medical attention without delay; if pain persists or recurs seek medical attention. Seek medical attention without delay; if pain persists or recurs seek medical attention. Removal of contact lenses after an eye injury should only be undertaken by skilled personnel. Removal of contact lenses after an eye injury should only be undertaken by skilled personnel. If fumes, aerosols or combustion products are inhaled remove from contaminated area. If fumes, aerosols or combustion products are inhaled remove from contaminated area. Other measures are usually unnecessary. Other measures are usually unnecessary. Immediately give a glass of water. Immediately give a glass of water. First aid is not generally required. If in doubt, contact a Poisons Information Centre or a doctor. First aid is not generally required. If in doubt, contact a Poisons Information Centre or a doctor. If this product comes in contact with the eyes: If this product comes in contact with the eyes: Wash out immediately with fresh running water. Wash out immediately with fresh running water. Eye Contact Ensure complete irrigation of the eye by keeping eyelids apart and away from eye and moving the eyelids by occasionally lifting the upper and lower lids. 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. Eye Contact Seek medical attention without delay; if pain persists or recurs seek medical attention. Seek medical attention without delay; if pain persists or recurs seek medical attention. Removal of contact lenses after an eye injury should only be undertaken by skilled personnel. Removal of contact lenses after an eye injury should only be undertaken by skilled personnel. If skin contact occurs: If skin contact occurs: Immediately remove all contaminated clothing, including footwear. Skin Contact Immediately remove all contaminated clothing, including footwear. Skin Contact Flush skin and hair with running water (and soap if available). Flush skin and hair with running water (and soap if available). Seek medical attention in event of irritation. Seek medical attention in event of irritation. If fumes, aerosols or combustion products are inhaled remove from contaminated area. Inhalation If fumes, aerosols or combustion products are inhaled remove from contaminated area. Inhalation Other measures are usually unnecessary. Other measures are usually unnecessary. Immediately give a glass of water. Ingestion Immediately give a glass of water. Ingestion First aid is not generally required. If in doubt, contact a Poisons Information Centre or a doctor. First aid is not generally required. If in doubt, contact a Poisons Information Centre or a doctor.

4.2 Most important symptoms and effects, both acute and delayed 4.2 Most important symptoms and effects, both acute and delayed See Section 11 See Section 11

4.3. Indication of any immediate medical attention and special treatment needed 4.3. Indication of any immediate medical attention and special treatment needed Treat symptomatically. Treat symptomatically. Manifestation of aluminium toxicity include hypercalcaemia, anaemia, Vitamin D refractory osteodystrophy and a progressive encephalopathy (mixed dysarthria-apraxia of speech, asterixis, Manifestation of aluminium toxicity include hypercalcaemia, anaemia, Vitamin D refractory osteodystrophy and a progressive encephalopathy (mixed dysarthria-apraxia of speech, asterixis, tremulousness, myoclonus, dementia, focal seizures). Bone pain, pathological fractures and proximal myopathy can occur. tremulousness, myoclonus, dementia, focal seizures). Bone pain, pathological fractures and proximal myopathy can occur. Symptoms usually develop insidiously over months to years (in chronic renal failure patients) unless dietary aluminium loads are excessive. Symptoms usually develop insidiously over months to years (in chronic renal failure patients) unless dietary aluminium loads are excessive. Serum aluminium levels above 60 ug/ml indicate increased absorption. Potential toxicity occurs above 100 ug/ml and clinical symptoms are present when levels exceed 200 ug/ml. Serum aluminium levels above 60 ug/ml indicate increased absorption. Potential toxicity occurs above 100 ug/ml and clinical symptoms are present when levels exceed 200 ug/ml. Deferoxamine has been used to treat dialysis encephalopathy and osteomalacia. CaNa2EDTA is less effective in chelating aluminium. Deferoxamine has been used to treat dialysis encephalopathy and osteomalacia. CaNa2EDTA is less effective in chelating aluminium. [Ellenhorn and Barceloux: Medical Toxicology] [Ellenhorn and Barceloux: Medical Toxicology] Copper, magnesium, aluminium, antimony, iron, manganese, nickel, zinc (and their compounds) in welding, brazing, galvanising or smelting operations all give rise to thermally produced Copper, magnesium, aluminium, antimony, iron, manganese, nickel, zinc (and their compounds) in welding, brazing, galvanising or smelting operations all give rise to thermally produced particulates of smaller dimension than may be produced if the metals are divided mechanically. Where insufficient ventilation or respiratory protection is available these particulates may produce particulates of smaller dimension than may be produced if the metals are divided mechanically. Where insufficient ventilation or respiratory protection is available these particulates may produce 'metal fume fever' in workers from an acute or long term exposure. 'metal fume fever' in workers from an acute or long term exposure. Onset occurs in 4-6 hours generally on the evening following exposure. Tolerance develops in workers but may be lost over the weekend. (Monday Morning Fever) Onset occurs in 4-6 hours generally on the evening following exposure. Tolerance develops in workers but may be lost over the weekend. (Monday Morning Fever) Pulmonary function tests may indicate reduced lung volumes, small airway obstruction and decreased carbon monoxide diffusing capacity but these abnormalities resolve after several months. Pulmonary function tests may indicate reduced lung volumes, small airway obstruction and decreased carbon monoxide diffusing capacity but these abnormalities resolve after several months. Although mildly elevated urinary levels of heavy metal may occur they do not correlate with clinical effects. Although mildly elevated urinary levels of heavy metal may occur they do not correlate with clinical effects. The general approach to treatment is recognition of the disease, supportive care and prevention of exposure. The general approach to treatment is recognition of the disease, supportive care and prevention of exposure. Seriously symptomatic patients should receive chest x-rays, have arterial blood gases determined and be observed for the development of tracheobronchitis and pulmonary edema. Seriously symptomatic patients should receive chest x-rays, have arterial blood gases determined and be observed for the development of tracheobronchitis and pulmonary edema. [Ellenhorn and Barceloux: Medical Toxicology] [Ellenhorn and Barceloux: Medical Toxicology]

SECTION 5 FIREFIGHTING MEASURES www.element14.comSECTION 5 FIREFIGHTING MEASURES www.farnell.com 5.1. Extinguishing media www.newark.com5.1. Extinguishing media Foam. Foam. Dry chemical powder. Dry chemical powder. BCF (where regulations permit). BCF (where regulations permit). Page <3> 28/10/18 V1.0 Carbon dioxide. Carbon dioxide. Water spray or fog - Large fires only. Water spray or fog - Large fires only.

5.2. Special hazards arising from the substrate or mixture 5.2. 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 Fire Incompatibility Avoid contamination with oxidising agents i.e. nitrates, oxidising acids, chlorine bleaches, pool chlorine etc. as ignition may result

5.3. Advice for firefighters 5.3. Advice for firefighters Alert Fire Brigade and tell them location and nature of hazard. Alert Fire Brigade and tell them location and nature of hazard. Wear full body protective clothing with breathing apparatus. Wear full body protective clothing with breathing apparatus. Prevent, by any means available, spillage from entering drains or water course. Prevent, by any means available, spillage from entering drains or water course. Use water delivered as a fine spray to control fire and cool adjacent area. Fire Fighting Use water delivered as a fine spray to control fire and cool adjacent area. Fire Fighting Avoid spraying water onto liquid pools. Avoid spraying water onto liquid pools. DO NOT approach containers suspected to be hot. approach containers suspected to be hot. CoolDO NOT fire exposed containers with water spray from a protected location. Cool fire exposed containers with water spray from a protected location.

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01-2119475601-40-XXXX

Legend: 1. Classified by Chemwatch; 2. Classification drawn from EC Directive 67/548/EEC - Annex I ; 3. Classification drawn from EC Directive 1272/2008 - Annex VI 4. Classification drawn from C&L

SECTION 4 FIRST AID MEASURES

4.1. Description of first aid measures

4.2 Most important symptoms and effects, both acute and delayed See Section 11

4.3. Indication of any immediate medical attention and special treatment needed Treat symptomatically. Manifestation of aluminium toxicity include hypercalcaemia, anaemia, Vitamin D refractory osteodystrophy and a progressive encephalopathy (mixed dysarthria-apraxia of speech, asterixis, tremulousness, myoclonus, dementia, focal seizures). Bone pain, pathological fractures and proximal myopathy can occur. Symptoms usually develop insidiously over months to years (in chronic renal failure patients) unless dietary aluminium loads are excessive. Serum aluminium levels above 60 ug/ml indicate increased absorption. Potential toxicity occurs above 100 ug/ml and clinical symptoms are present when levels exceed 200 ug/ml. Deferoxamine has been used to treat dialysis encephalopathy and osteomalacia. CaNa2EDTA is less effective in chelating aluminium. [Ellenhorn and Barceloux: Medical Toxicology]

Copper, magnesium, aluminium, antimony, iron, manganese, nickel, zinc (and their compounds) in welding, brazing, galvanising or smelting operations all give rise to thermally produced particulates of smaller dimension than may be produced if the metals are divided mechanically. Where insufficient ventilation or respiratory protection is available these particulates may produce 'metal fume fever' in workers from an acute or long term exposure. Onset occurs in 4-6 hours generally on the evening following exposure. Tolerance develops in workers but may be lost over the weekend. (Monday Morning Fever) Pulmonary function tests may indicate reduced lung volumes, small airway obstruction and decreased carbon monoxide diffusing capacity but these abnormalities resolve after several months. Although mildly elevated urinary levels of heavy metal may occur they do not correlate with clinical effects. SafetyThe general approach to treatmentData is recognition of theSheet disease, supportive care and prevention of exposure. Seriously symptomatic patients should receive chest x-rays, have arterial blood gases determined and be observed for the development of tracheobronchitis and pulmonary edema.

[Ellenhorn and Barceloux: Medical Toxicology]

Version No: 4.7 Page 4 of 20 Issue Date: 29/07/2016 SECTION 5 FIREFIGHTING MEASURES Print Date: 29/07/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part A) 5.1. Extinguishing media Foam. Dry chemical powder. If safe to do so, remove containers from path of fire. BCF (where regulations permit). Carbon dioxide. Combustible. Water spray or fog - Large fires only.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). 5.2. SpecialFire/Explosion hazards Hazard arising fromMay the emit substrate acrid smoke. or mixture Fire Incompatibility AvoidMists containingcontamination combustible with oxidising materials agents may i.e. be nitrates, explosive. oxidising acids, chlorine bleaches, pool chlorine etc. as ignition may result Combustion products include:, carbon dioxide (CO2), aldehydes, other pyrolysis products typical of burning organic material When aluminium oxide dust is dispersed in air, firefighters should wear protection against inhalation of dust particles, which can also contain hazardous substances from the fire absorbed on 5.3. Advice for firefighters the alumina particles.

Alert Fire Brigade and tell them location and nature of hazard. SECTION 6 ACCIDENTAL RELEASEWear full MEASURESbody protective clothing with breathing apparatus. Version No: 4.7 Page 4 of 20 Issue Date: 29/07/2016 Prevent, by any means available, spillage from entering drains or water course. Use water delivered as a fine spray to control fire and cool adjacent area. Print Date: 29/07/2016 6.1. Personal precautions,Fire Fighting protective8329TFS equipment Slow Cure, and Thermallyemergency Conductiveprocedures Adhesive, Flowable (Part A) Avoid spraying water onto liquid pools. See section 8 DO NOT approach containers suspected to be hot. Cool fire exposed containers with water spray from a protected location. 6.2. Environmental precautionsIf safe to do so, remove containers from path of fire. See section 12 Combustible. Continued... Slight fire hazard when exposed to heat or flame. 6.3. Methods and material for containmentHeating may cause and expansion cleaning or decomposition up leading to violent rupture of containers. On combustion, may emit toxic fumes of carbon monoxide (CO). Fire/Explosion Hazard EnvironmentalMay emit acrid hazard smoke. - contain spillage. CleanMists containing up all spills combustible immediately. materials may be explosive. CombustionAvoid breathing products vapours include: and, carbon contact dioxide with skin(CO2) and, aldehydes eyes. , other pyrolysis products typical of burning organic material When aluminium oxide dust is Minor Spills dispersedControl in personalair, firefighters contact should with the wear substance, protection by against using protective inhalation equipment. of dust particles, which can also contain hazardous substances from the fire absorbed on the aluminaContain particles. and absorb spill with sand, earth, inert material or vermiculite. Wipe up. Place in a suitable, labelled container for waste disposal. SECTION 6 ACCIDENTAL RELEASE MEASURES Environmental hazard - contain spillage. Chemical Class: phenols and cresols 6.1. Personal precautions, protective For release ontoequipment land: recommended and emergency sorbents listed procedures in order of priority. See section 8 SORBENT RANK APPLICATION COLLECTION LIMITATIONS TYPE 6.2. Environmental precautions See section 12 LAND SPILL - SMALL

6.3. Methods and material forcross-linked containment polymer and - particulate cleaning up 1 shovel shovel R, W, SS cross-linked polymer - pillow 1 throw pitchfork R, DGC, RT Environmental hazard - contain spillage. woodClean fiber up - pillowall spills immediately. 1 throw pitchfork R, P, DGC, RT Avoid breathing vapours and contact with skin and eyes. foamed glass - pillow 2 shovel shovel R, W, P, DGC Minor Spills Control personal contact with the substance, by using protective equipment. sorbentContain clay and - particulate absorb spill with sand, earth, inert material or vermiculite. 2 shovel shovel R, I, P Wipe up. wood fibre - particulate 3 shovel shovel R, W, P, DGC Place in a suitable, labelled container for waste disposal.

Environmental LAND SPILL - hazard MEDIUM - contain spillage. Chemical Class: phenols and cresols Forcross-linked release onto polymer land: -recommended particulate sorbents listed in order of priority. 1 blower skiploader R,W, SS cross-linked polymer - pillow 2 throw skiploader R, DGC, RT SORBENT RANK APPLICATION COLLECTION LIMITATIONS sorbentTYPE clay - particulate 3 blower skiploader R, I, P polypropylene - particulate 3 blower skiploader R, SS, DGC LAND SPILL - SMALL Major Spills wood fiber - particulate 4 blower skiploader R, W, P, DGC cross-linked polymer - particulate 1 shovel shovel R, W, SS expanded moneral - particulate 4 blower skiploader R, I, W, P, DGC cross-linked polymer - pillow 1 throw pitchfork R, DGC, RT Legend wood fiber - pillow 1 throw pitchfork R, P, DGC, RT DGC: Not effective where ground cover is dense R;foamed Not reusable glass - pillow 2 shovel shovel R, W, P, DGC I: Not incinerable sorbent clay - particulate 2 shovel shovel R, I, P P: Effectiveness reduced when rainy RT:Notwood fibreeffective - particulate where terrain is rugged 3 shovel shovel R, W, P, DGC SS: Not for use within environmentally sensitive sites W: LAND Effectiveness SPILL - MEDIUM reduced when windy Reference: Sorbents for Liquid Hazardous Substance Cleanup and Control; R.Wcross-linked Melvold etpolymer al: Pollution - particulate Technology Review No. 150: Noyes Data Corporation1 blower 1988 skiploader R,W, SS Moderate hazard. cross-linked polymer - pillow 2 throw skiploader R, DGC, RT www.element14.com Clear area of personnel and move upwind. www.farnell.com sorbentAlert clayFire Brigade- particulate and tell them location and nature of hazard. 3 blower skiploader R, I, P Wear breathing apparatus plus protective gloves. polypropylene - particulate 3 blower skiploader R, SS, DGC www.newark.com Prevent, by any means available, spillage from entering drains or water course. Major Spills woodNo fiber smoking, - particulate naked lights or ignition sources. 4 blower skiploader R, W, P, DGC Increase ventilation. expanded moneral - particulate 4 blower skiploader R, I, W, P, DGC Stop leak if safe to do so. Page <4> 28/10/18 V1.0 Contain spill with sand, earth or vermiculite. Legend Collect recoverable product into labelled containers for recycling. DGC: Not effective where ground cover is dense Absorb remaining product with sand, earth or vermiculite. R; Not reusable Collect solid residues and seal in labelled drums for disposal. I: Not incinerable Wash area and prevent runoff into drains. P: Effectiveness reduced when rainy If contamination of drains or waterways occurs, advise emergency services. RT:Not effective where terrain is rugged SS: Not for use within environmentally sensitive sites 6.4. Reference to other sectionsW: Effectiveness reduced when windy Reference: Sorbents for Liquid Hazardous Substance Cleanup and Control; R.W Melvold et al: Pollution Technology Review No. 150: Noyes Data Corporation 1988 Continued... Moderate hazard. Clear area of personnel and move upwind. 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 course. No smoking, naked lights or ignition sources. Increase ventilation. Stop leak if safe to do so. Contain spill with sand, earth or vermiculite. Collect recoverable product into labelled containers for recycling. Absorb remaining product with sand, earth or vermiculite. Collect solid residues and seal in labelled drums for disposal. Wash area and prevent runoff into drains. If contamination of drains or waterways occurs, advise emergency services.

6.4. Reference to other sections

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If safe to do so, remove containers from path of fire. 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). Fire/Explosion Hazard May emit acrid smoke. Mists containing combustible materials may be explosive. Combustion products include:, carbon dioxide (CO2), aldehydes, other pyrolysis products typical of burning organic material When aluminium oxide dust is dispersed in air, firefighters should wear protection against inhalation of dust particles, which can also contain hazardous substances from the fire absorbed on the alumina particles.

SECTION 6 ACCIDENTAL RELEASE MEASURES

6.1. Personal precautions, protective equipment and emergency procedures See section 8

6.2. Environmental precautions See section 12

6.3. Methods and material for containment and cleaning up

SORBENT RANK APPLICATION COLLECTION LIMITATIONS TYPE

LAND SPILL - SMALL

cross-linked polymer - particulate 1 shovel shovel R, W, SS cross-linked polymer - pillow 1 throw pitchfork R, DGC, RT Safety Datawood fiber - pillow Sheet 1 throw pitchfork R, P, DGC, RT foamed glass - pillow 2 shovel shovel R, W, P, DGC sorbent clay - particulate 2 shovel shovel R, I, P wood fibre - particulate 3 shovel shovel R, W, P, DGC

LAND SPILL - MEDIUM

cross-linked polymer - particulate 1 blower skiploader R,W, SS cross-linked polymer - pillow 2 throw skiploader R, DGC, RT sorbent clay - particulate 3 blower skiploader R, I, P polypropylene - particulate 3 blower skiploader R, SS, DGC

Major Spills wood fiber - particulate 4 blower skiploader R, W, P, DGC expanded moneral - particulate 4 blower skiploader R, I, W, P, DGC

Legend DGC: Not effective where ground cover is dense R; Not reusable I: Not incinerable P: Effectiveness reduced when rainy RT:Not effective where terrain is rugged SS: Not for use within environmentally sensitive sites W: Effectiveness reduced when windy Reference: Sorbents for Liquid Hazardous Substance Cleanup and Control; R.W Melvold et al: Pollution Technology Review No. 150: Noyes Data Corporation 1988 Moderate hazard. Clear area of personnel and move upwind. 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 course. No smoking, naked lights or ignition sources. Increase ventilation. Stop leak if safe to do so. Contain spill with sand, earth or vermiculite. Collect recoverable product into labelled containers for recycling. Absorb remaining product with sand, earth or vermiculite. Version No: 4.7 Collect solid residues and seal in labelled drumsPage for 5 disposal. of 20 Issue Date: 29/07/2016 Wash area and prevent runoff into drains. Print Date: 29/07/2016 8329TFSIf contamination Slow of drains Cure, or waterways Thermally occurs, Conductive advise emergency Adhesive, services. Flowable (Part A)

6.4. Reference to other sections Personal Protective Equipment advice is contained in Section 8 of the SDS. Continued...

SECTION 7 HANDLING AND STORAGE

7.1. Precautions for 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. Avoid smoking, naked lights or ignition sources. Avoid contact with incompatible materials. When handling, DO NOT eat, drink or smoke. Safe handling 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. 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. DO NOT allow clothing wet with material to stay in contact with skin Fire and explosion See section 5 protection Store in original containers. Keep containers securely sealed. Store in a cool, dry, well-ventilated area. Other information 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.

7.2. Conditions for safe storage, including any incompatibilities

Metal can or drum Suitable container Packaging as recommended by manufacturer. Check all containers are clearly labelled and free from leaks. www.element14.com For aluminas (aluminium oxide): Incompatible with hot chlorinated rubber. www.farnell.com In the presence of chlorine trifluoride may react violently and ignite. www.newark.com May initiate explosive polymerisation of olefin oxides including ethylene oxide. Produces exothermic reaction above 200 C with halocarbons and an exothermic reaction at ambient temperatures with halocarbons in the presence of other metals. Produces exothermic reaction with oxygen difluoride.Page <5> 28/10/18 V1.0 May form explosive mixture with oxygen difluoride. Forms explosive mixtures with sodium nitrate. Reacts vigorously with vinyl acetate. Zinc oxide: slowly absorbs carbon dioxide from the air. may react, explosively with magnesium and chlorinated rubber when heated is incompatible with linseed oil (may cause ignition) WARNING: Avoid or control reaction with peroxides. All transition metal peroxides should be considered as potentially explosive. For example transition metal complexes of alkyl hydroperoxides may decompose explosively. The pi-complexes formed between chromium(0), vanadium(0) and other transition metals (haloarene-metal complexes) and mono-or poly-fluorobenzene Storage incompatibility show extreme sensitivity to heat and are explosive. Avoid reaction with borohydrides or cyanoborohydrides Avoid reaction with amines, mercaptans, strong acids and oxidising agents Phenols are incompatible with strong reducing substances such as hydrides, nitrides, alkali metals, and sulfides. Avoid use of aluminium, copper and brass alloys in storage and process equipment. Heat is generated by the acid-base reaction between phenols and bases. Phenols are sulfonated very readily (for example, by concentrated sulfuric acid at room temperature), these reactions generate heat. Phenols are nitrated very rapidly, even by dilute nitric acid. Nitrated phenols often explode when heated. Many of them form metal salts that tend toward detonation by rather mild shock. Avoid strong acids, bases. Glycidyl ethers: may form unstable peroxides on storage in air ,light, sunlight, UV light or other ionising radiation, trace metals - inhibitor should be maintained at adequate levels may polymerise in contact with heat, organic and inorganic free radical producing initiators may polymerise with evolution of heat in contact with oxidisers, strong acids, bases and amines react violently with strong oxidisers, permanganates, peroxides, acyl halides, alkalis, ammonium persulfate, bromine dioxide attack some forms of plastics, coatings, and rubber

7.3. Specific end use(s) See section 1.2

SECTION 8 EXPOSURE CONTROLS / PERSONAL PROTECTION

8.1. Control parameters

DERIVED NO EFFECT LEVEL (DNEL) Not Available

PREDICTED NO EFFECT LEVEL (PNEC)

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Personal Protective Equipment advice is contained in Section 8 of the SDS.

SECTION 7 HANDLING AND STORAGE

7.1. Precautions for 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. Avoid smoking, naked lights or ignition sources. Avoid contact with incompatible materials. When handling, DO NOT eat, drink or smoke. Safe handling 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. 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. DO NOT allow clothing wet with material to stay in contact with skin Fire and explosion See section 5 protection Store in original containers. Keep containers securely sealed. Safety DataStore in a cool, dry,Sheet well-ventilated area. Other information 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.

7.2. Conditions for safe storage, including any incompatibilities

Metal can or drum Suitable container Packaging as recommended by manufacturer. Check all containers are clearly labelled and free from leaks. For aluminas (aluminium oxide): Incompatible with hot chlorinated rubber. In the presence of chlorine trifluoride may react violently and ignite. May initiate explosive polymerisation of olefin oxides including ethylene oxide. Produces exothermic reaction above 200 C with halocarbons and an exothermic reaction at ambient temperatures with halocarbons in the presence of other metals. Produces exothermic reaction with oxygen difluoride. May form explosive mixture with oxygen difluoride. Forms explosive mixtures with sodium nitrate. Reacts vigorously with vinyl acetate. Zinc oxide: slowly absorbs carbon dioxide from the air. may react, explosively with magnesium and chlorinated rubber when heated is incompatible with linseed oil (may cause ignition) WARNING: Avoid or control reaction with peroxides. All transition metal peroxides should be considered as potentially explosive. For example transition metal complexes of alkyl hydroperoxides may decompose explosively. The pi-complexes formed between chromium(0), vanadium(0) and other transition metals (haloarene-metal complexes) and mono-or poly-fluorobenzene Storage incompatibility show extreme sensitivity to heat and are explosive. Avoid reaction with borohydrides or cyanoborohydrides Avoid reaction with amines, mercaptans, strong acids and oxidising agents Phenols are incompatible with strong reducing substances such as hydrides, nitrides, alkali metals, and sulfides. Avoid use of aluminium, copper and brass alloys in storage and process equipment. Heat is generated by the acid-base reaction between phenols and bases. Phenols are sulfonated very readily (for example, by concentrated sulfuric acid at room temperature), these reactions generate heat. Phenols are nitrated very rapidly, even by dilute nitric acid. Nitrated phenols often explode when heated. Many of them form metal salts that tend toward detonation by rather mild shock. Avoid strong acids, bases. Glycidyl ethers: may form unstable peroxides on storage in air ,light, sunlight, UV light or other ionising radiation, trace metals - inhibitor should be maintained at adequate levels may polymerise in contact with heat, organic and inorganic free radical producing initiators may polymerise with evolution of heat in contact with oxidisers, strong acids, bases and amines react violently with strong oxidisers, permanganates, peroxides, acyl halides, alkalis, ammonium persulfate, bromine dioxide attack some forms of plastics, coatings, and rubber

7.3. Specific end use(s) See section 1.2

SECTION 8 EXPOSURE CONTROLS / PERSONAL PROTECTION

8.1. Control parameters Version No: 4.7 Page 6 of 20 Issue Date: 29/07/2016 DERIVED NO EFFECT LEVEL (DNEL) Print Date: 29/07/2016 Not Available 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part A)

PREDICTED NO EFFECT LEVEL (PNEC) Not Available Continued... OCCUPATIONAL EXPOSURE LIMITS (OEL) INGREDIENT DATA Source Ingredient Material name TWA STEL Peak Notes UK Workplace Exposure Limits aluminium Aluminium oxides inhalable dust / Aluminium oxides 10 mg/m3 / 4 Not Not Not (WELs) oxide respirable dust mg/m3 Available Available Available UK Workplace Exposure Limits Not Not carbon black Carbon black 3.5 mg/m3 7 mg/m3 (WELs) Available Available

EMERGENCY LIMITS Ingredient Material name TEEL-1 TEEL-2 TEEL-3 aluminium oxide Aluminum oxide; (Alumina) 1.5 mg/m3 15 mg/m3 25 mg/m3 bisphenol F glycidyl ether/ Phenol, polymer with formaldehyde, oxiranylmethyl ether 12 mg/m3 130 mg/m3 790 mg/m3 formaldehyde copolymer zinc oxide Zinc oxide 10 mg/m3 15 mg/m3 2500 mg/m3 bisphenol A/ diglycidyl ether Epoxy resin (EPON 1001) 90 mg/m3 990 mg/m3 5900 mg/m3 resin, liquid bisphenol A/ diglycidyl ether www.element14.com Epoxy resin (EPON 1007) 90 mg/m3 990 mg/m3 5900 mg/m3 www.farnell.comresin, liquid bisphenol A/ diglycidyl ether Epoxy resin (EPON 820) 41 mg/m3 450 mg/m3 2700 mg/m3 www.newark.comresin, liquid bisphenol A/ diglycidyl ether Epoxy resin ERL-2795 32 mg/m3 350 mg/m3 2100 mg/m3 resin, liquid Page <6> 28/10/18 V1.0 carbon black Carbon black 9 mg/m3 99 mg/m3 590 mg/m3

Ingredient Original IDLH Revised IDLH aluminium oxide Not Available Not Available bisphenol F glycidyl ether/ Not Available Not Available formaldehyde copolymer zinc oxide 2,500 mg/m3 500 mg/m3 (C12-14)alkylglycidyl ether Not Available Not Available bisphenol A/ diglycidyl ether Not Available Not Available resin, liquid carbon black N.E. mg/m3 / N.E. ppm 1,750 mg/m3

MATERIAL DATA for zinc oxide: Zinc oxide intoxication (intoxication zincale) is characterised by general depression, shivering, headache, thirst, colic and diarrhoea. Exposure to the fume may produce metal fume fever characterised by chills, muscular pain, nausea and vomiting. Short-term studies with guinea pigs show pulmonary function changes and morphologic evidence of small airway inflammation. A no-observed-adverse-effect level (NOAEL) in guinea pigs was 2.7 mg/m3 zinc oxide. Based on present data, the current TLV-TWA may be inadequate to protect exposed workers although known physiological differences in the guinea pig make it more susceptible to functional impairment of the airways than humans. For aluminium oxide and pyrophoric grades of aluminium: Twenty seven year experience with aluminium oxide dust (particle size 96% 1,2 um) without adverse effects either systemically or on the lung, and at a calculated concentration equivalent to 2 mg/m3 over an 8-hour shift has lead to the current recommendation of the TLV-TWA. The limit should also apply to aluminium pyro powders whose toxicity is reportedly greater than aluminium dusts and should be protective against lung changes.

8.2. Exposure 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.

General exhaust is adequate under normal operating conditions. Local exhaust ventilation may be required in specific circumstances. If risk of overexposure exists, wear approved respirator. Correct fit is essential to obtain adequate protection. Provide adequate ventilation in warehouse or closed storage areas. Air 8.2.1. Appropriate contaminants generated in the workplace possess varying 'escape' velocities which, in turn, determine the 'capture velocities' of fresh circulating air required engineering controls to effectively remove the contaminant.

Type of Contaminant: Air Speed: 0.25-0.5 m/s (50-100 solvent, vapours, degreasing etc., evaporating from tank (in still air). f/min) aerosols, fumes from pouring operations, intermittent container filling, low speed conveyer transfers, welding, spray drift, plating 0.5-1 m/s (100-200 acid fumes, pickling (released at low velocity into zone of active generation) f/min.) direct spray, spray painting in shallow booths, drum filling, conveyer loading, crusher dusts, gas discharge (active generation into 1-2.5 m/s (200-500 zone of rapid air motion) f/min.)

Continued... Version No: 4.7 Page 6 of 20 Issue Date: 29/07/2016 Print Date: 29/07/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part A)

Not Available

OCCUPATIONAL EXPOSURE LIMITS (OEL) INGREDIENT DATA Source Ingredient Material name TWA STEL Peak Notes UK Workplace Exposure Limits aluminium Aluminium oxides inhalable dust / Aluminium oxides 10 mg/m3 / 4 Not Not Not (WELs) oxide respirable dust mg/m3 Available Available Available UK Workplace Exposure Limits Not Not carbon black Carbon black 3.5 mg/m3 7 mg/m3 (WELs) Available Available

EMERGENCY LIMITS SafetyIngredient DataMaterial name Sheet TEEL-1 TEEL-2 TEEL-3 aluminium oxide Aluminum oxide; (Alumina) 1.5 mg/m3 15 mg/m3 25 mg/m3 bisphenol F glycidyl ether/ Phenol, polymer with formaldehyde, oxiranylmethyl ether 12 mg/m3 130 mg/m3 790 mg/m3 formaldehyde copolymer zinc oxide Zinc oxide 10 mg/m3 15 mg/m3 2500 mg/m3 bisphenol A/ diglycidyl ether Epoxy resin (EPON 1001) 90 mg/m3 990 mg/m3 5900 mg/m3 resin, liquid bisphenol A/ diglycidyl ether Epoxy resin (EPON 1007) 90 mg/m3 990 mg/m3 5900 mg/m3 resin, liquid bisphenol A/ diglycidyl ether Epoxy resin (EPON 820) 41 mg/m3 450 mg/m3 2700 mg/m3 resin, liquid bisphenol A/ diglycidyl ether Epoxy resin ERL-2795 32 mg/m3 350 mg/m3 2100 mg/m3 resin, liquid carbon black Carbon black 9 mg/m3 99 mg/m3 590 mg/m3

8.2. Exposure controls

Type of Contaminant: Air Speed: 0.25-0.5 m/s (50-100 solvent, vapours, degreasing etc., evaporating from tank (in still air). Version No: 4.7 Page 7 of 20 f/min)Issue Date: 29/07/2016 aerosols, fumes from pouring operations, intermittent container filling, low speed conveyer transfers, welding, spray drift, plating 0.5-1Print m/s Date:(100-200 29/07/2016 acid8329TFS fumes, pickling Slow (released Cure, at Thermallylow velocity into Conductivezone of active generation) Adhesive, Flowable (Part A) f/min.) direct spray, spray painting in shallow booths, drum filling, conveyer loading, crusher dusts, gas discharge (active generation into 1-2.5 m/s (200-500 zone of rapid air motion) f/min.) grinding, abrasive blasting, tumbling, high speed wheel generated dusts (released at high initial velocity into zone of very high rapid 2.5-10 m/s (500-2000 air motion). f/min.) Continued... 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 www.element14.com 4: Large hood or large air mass in motion 4: Small hood-local control only

www.farnell.com 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 www.newark.com 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 velocitiesPage are multiplied <7> by factors of 10 or more when extraction systems are installed or used.28/10/18 V1.0

8.2.2. Personal 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 Eye and face protection chemicals in use and an account of injury experience. Medical and first-aid personnel should be trained in their removal and suitable equipment should 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 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. The selection of suitable gloves does not only depend on the material, but also on further marks of quality which vary from manufacturer to manufacturer. Where the chemical is a preparation of several substances, the resistance of the glove material can not be calculated in advance and has therefore to be checked prior to the application. The exact break through time for substances has to be obtained from the manufacturer of the protective gloves and.has to be observed when making a final choice. Suitability and durability of glove type is dependent on usage. Important factors in the selection of gloves include: frequency and duration of contact, chemical resistance of glove material, glove thickness and Hands/feet protection dexterity Select gloves tested to a relevant standard (e.g. Europe EN 374, US F739, AS/NZS 2161.1 or national equivalent). When prolonged or frequently repeated contact may occur, a glove with a protection class of 5 or higher (breakthrough time greater than 240 minutes according to EN 374, AS/NZS 2161.10.1 or national equivalent) is recommended. When only brief contact is expected, a glove with a protection class of 3 or higher (breakthrough time greater than 60 minutes according to EN 374, AS/NZS 2161.10.1 or national equivalent) is recommended. Some glove polymer types are less affected by movement and this should be taken into account when considering gloves for long-term use. Contaminated gloves should be replaced. Gloves must only be worn on clean hands. After using gloves, hands should be washed and dried thoroughly. Application of a non-perfumed moisturiser is recommended. When handling liquid-grade epoxy resins wear chemically protective gloves (e.g nitrile or nitrile-butatoluene rubber), boots and aprons. DO NOT use cotton or leather (which absorb and concentrate the resin), polyvinyl chloride, rubber or polyethylene gloves (which absorb the resin). DO NOT use barrier creams containing emulsified fats and oils as these may absorb the resin; silicone-based barrier creams should be reviewed prior to use.

Body protection See Other protection below Overalls. P.V.C. apron. Other protection Barrier cream. Skin cleansing cream. Eye wash unit.

Thermal hazards Not Available

Respiratory protection 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. Selectionof the Class and Type of respirator will depend upon the level of breathingzone contaminant and the chemical nature of the contaminant. Protection Factors(defined as the ratio of contaminant outside and inside the mask) may also beimportant.

Required minimum protection factor Maximum gas/vapour concentration present in air p.p.m. (by volume) Half-face Respirator Full-Face Respirator up to 10 1000 A-AUS / Class 1 - up to 50 1000 - A-AUS / Class 1 up to 50 5000 Airline * - up to 100 5000 - A-2 up to 100 10000 - A-3

Continued... Version No: 4.7 Page 6 of 20 Issue Date: 29/07/2016 Print Date: 29/07/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part A)

Not Available

EMERGENCY LIMITS Ingredient Material name TEEL-1 TEEL-2 TEEL-3 aluminium oxide Aluminum oxide; (Alumina) 1.5 mg/m3 15 mg/m3 25 mg/m3 bisphenol F glycidyl ether/ Phenol, polymer with formaldehyde, oxiranylmethyl ether 12 mg/m3 130 mg/m3 790 mg/m3 formaldehyde copolymer zinc oxide Zinc oxide 10 mg/m3 15 mg/m3 2500 mg/m3 bisphenol A/ diglycidyl ether Epoxy resin (EPON 1001) 90 mg/m3 990 mg/m3 5900 mg/m3 resin, liquid bisphenol A/ diglycidyl ether Epoxy resin (EPON 1007) 90 mg/m3 990 mg/m3 5900 mg/m3 resin, liquid bisphenol A/ diglycidyl ether Epoxy resin (EPON 820) 41 mg/m3 450 mg/m3 2700 mg/m3 resin, liquid bisphenol A/ diglycidyl ether Epoxy resin ERL-2795 32 mg/m3 350 mg/m3 2100 mg/m3 resin, liquid carbon black Carbon black 9 mg/m3 99 mg/m3 590 mg/m3

For aluminium oxide: The experimental and clinical data indicate that aluminium oxide acts as an 'inert' material when inhaled and seems to have little effect on the lungs nor does it produce significant organic disease or toxic effects when exposures are kept under reasonable control. Version[Documentation No: 4.7 of the Threshold Limit Values], ACGIH, Sixth Edition Page 7 of 20 Issue Date: 29/07/2016 Print Date: 29/07/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part A) Safety8.2. Exposure controls Data Sheet 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. Thegrinding, basic abrasivetypes of engineering blasting, tumbling, controls high are: speed wheel generated dusts (released at high initial velocity into zone of very high rapid 2.5-10 m/s (500-2000 Processair motion). controls which involve changing the way a job activity or process is done to reduce the risk. f/min.) Enclosure and/or isolation of emission source which keeps a selected hazard 'physically' away from the worker and ventilation that strategically 'adds' and Within'removes' each air range in the the work appropriate environment. value Ventilation depends on: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. EmployersLower end may of the need range to use multiple types of controls to prevent employee overexposure. Upper end of the range 1: Room air currents minimal or favourable to capture 1: Disturbing room air currents General exhaust is adequate under normal operating conditions. Local exhaust ventilation may be required in specific circumstances. If risk of overexposure exists,2: Contaminants wear approved of low respirator. toxicity or Correct of nuisance fit is essentialvalue only. to obtain adequate protection. Provide adequate2: Contaminants ventilation in warehouse of high toxicity or closed storage areas. Air 8.2.1. Appropriate contaminants3: Intermittent, generated low production. in the workplace possess varying 'escape' velocities which, in turn, determine3: theHigh 'capture production, velocities' heavy of use fresh circulating air required engineering controls to effectively remove the contaminant. 4: Large hood or large air mass in motion 4: Small hood-local control only Type of Contaminant: Air Speed: 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 0.25-0.5 m/s (50-100 ofsolvent, distance vapours, from the degreasing extraction point etc., (inevaporating simple cases). from tankTherefore (in still the air). 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)f/min) for extraction of solventsaerosols, generated fumes from in a pouringtank 2 meters operations, distant intermittent from the extraction container point. filling, Other low speed mechanical conveyer considerations, transfers, welding, producing spray performance drift, plating deficits 0.5-1within m/s the (100-200extraction apparatus,acid fumes, make pickling it essential (released that at theoretical low velocity air intovelocities zone ofare active multiplied generation) by factors of 10 or more when extraction systems are installed or used.f/min.) direct spray, spray painting in shallow booths, drum filling, conveyer loading, crusher dusts, gas discharge (active generation into 1-2.5 m/s (200-500 zone of rapid air motion) f/min.) 8.2.2. Personal protection

Continued... 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 Eye and face protection chemicals in use and an account of injury experience. Medical and first-aid personnel should be trained in their removal and suitable equipment should 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]

Body protection See Other protection below Overalls. P.V.C. apron. Other protection Barrier cream. Skin cleansing cream. Eye wash unit.

Thermal hazards Not Available

Required minimum protection factor Maximum gas/vapour concentration present in air p.p.m. (by volume) Half-face Respirator Full-Face Respirator www.element14.comup to 10 1000 A-AUS / Class 1 - www.farnell.comup to 50 1000 - A-AUS / Class 1 www.newark.comup to 50 5000 Airline * - up to 100 5000 - A-2 up to 100 10000 Page <8> - A-3 28/10/18 V1.0

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grinding, abrasive blasting, tumbling, high speed wheel generated dusts (released at high initial velocity into zone of very high rapid 2.5-10 m/s (500-2000 air motion). 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.

8.2.2. Personal protection

Body protection See Other protection below Overalls. P.V.C. apron. Other protection Barrier cream. Skin cleansing cream. Eye wash unit.

Thermal hazards Not Available

Respiratory protection SafetyCartridge respirators should never Data be used for emergency Sheetingress 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. Selectionof the Class and Type of respirator will depend upon the level of breathingzone contaminant and the chemical nature of the contaminant. Protection Factors(defined as the ratio of contaminant outside and inside the mask) may also beimportant.

Required minimum protection factor Maximum gas/vapour concentration present in air p.p.m. (by volume) Half-face Respirator Full-Face Respirator up to 10 1000 A-AUS / Class 1 -

Versionup toNo: 50 4.74.7 1000 Page 88 ofof 2020 - A-AUS IssueIssue/ Class Date:Date: 1 29/07/201629/07/2016 Print Date: 29/07/201629/07/2016 up to 50 8329TFS5000 Slow Cure, Thermally Conductive Adhesive, Flowable (PartAirline A) * - up to 100 5000 - A-2 up to 100 10000 - A-3 100+100+ -- Airline** Continued... ** -Continuous-Continuous FlowFlow **** -Continuous-flow-Continuous-flow oror positivepositive pressurepressure demand.demand. A(Allclasses) = Organic vapours, B AUS or B1 = Acid gases, B2 = Acid gas or hydrogencyanide(HCN), B3 = Acid gas or hydrogen cyanide(HCN), E = Sulfur dioxide(SO2),G = Agricultural chemicals,chemicals, KK == Ammonia(NH3),Ammonia(NH3), HgHg == Mercury,Mercury, NONO == OxidesOxides ofnitrogen,ofnitrogen, MBMB == MethylMethyl bromide,bromide, AXAX == LowLow boilingboiling pointpoint organicorganic compounds(below65compounds(below65 degdeg C)C)

8.2.3. Environmental exposure controls See section 12

SECTION 9 PHYSICAL AND CHEMICAL PROPERTIES

9.1. Information on basic physical and chemical properties

Appearance darkdark greygrey

Physical state LiquidLiquid Relative density (Water = 1) 2.22.2 Partition coefficient Odour Not Available Not Available n-octanol / water Auto-ignition temperature Odour threshold Not Available Not Available (°C)(°C) Decomposition pH (as supplied) Not Available Not Available temperaturetemperature Melting point / freezing Not Available Viscosity (cSt) >20.5>20.5 point (°C) InitialInitial boilingboiling pointpoint andand >207>207 Molecular weight (g/mol) Not Available boiling range (°C) Flash point (°C) >149>149 Taste Not Available Evaporation rate Not Available Explosive properties Not Available Flammability Not Applicable Oxidising properties Not Available Surface Tension (dyn/cm or Upper Explosive Limit (%) Not Available Not Available mN/m) Lower Explosive Limit (%) Not Available Volatile Component (%vol) Not Available Vapour pressure (kPa) Not Available Gas group Not Available Solubility in water (g/L) ImmiscibleImmiscible pH as a solution (1%) Not Available Vapour density (Air = 1) Not Available VOC g/L Not Available

9.2. Other information Not Available

SECTION 10 STABILITY AND REACTIVITY

10.1.10.1.Reactivity See section 7.2 Unstable in the presence of incompatible materials. 10.2.10.2. Chemical stability Product is considered stable. Hazardous polymerisation will not occur.

10.3.10.3. PossibilityPossibility ofof See section 7.2 hazardous reactions 10.4.10.4. Conditions to avoid See section 7.2 10.5.10.5. IncompatibleIncompatible materialsmaterials See section 7.2 10.6.10.6. Hazardous See section 5.3 decomposition products

SECTION 11 TOXICOLOGICAL INFORMATION www.element14.com www.farnell.com11.1. Information on toxicological effects

www.newark.com The material is not thought to produce adverse health effects or irritation of the respiratory tract (as classified by EC Directives using animal models). Nevertheless, good hygiene practice requires that exposure be kept to a minimum and that suitable control measures be used in an occupational setting.

InhalationInhalation ofof freshlyfreshly formedformed metalmetal oxideoxide particlesparticles sizedsizedPage belowbelow 1.51.5 <9> micronsmicrons andand generallygenerally betweenbetween 0.020.02 toto 0.050.05 micronsmicrons maymay resultresult inin 'metal'metal fumefume28/10/18 fever'.fever'. V1.0 InhaledInhaled Symptoms may be delayed for up to 12 hours and begin with the sudden onset of thirst, and a sweet, metallic or foul taste in the mouth. Other symptoms include upperupper respiratoryrespiratory tracttract irritationirritation accompaniedaccompanied byby coughingcoughing andand aa drynessdryness ofof thethe mucousmucous membranes,membranes, lassitudelassitude andand aa generalisedgeneralised feelingfeeling ofof malaise.malaise. MildMild toto severesevere headache,headache, nausea,nausea, occasionaloccasional vomiting,vomiting, feverfever oror chills,chills, exaggeratedexaggerated mentalmental activity,activity, profuseprofuse sweating,sweating, diarrhoea,diarrhoea, excessiveexcessive urinationurination andand prostrationprostration may also occur. Tolerance to the fumes develops rapidly, but is quickly lost. All symptoms usually subside within 24-36 hours following removal from exposure. Acute toxic responses to aluminium are confined to the more soluble forms. The material has NOT beenbeen classifiedclassified byby ECEC DirectivesDirectives oror otherother classificationclassification systemssystems asas 'harmful'harmful byby ingestion'.ingestion'. ThisThis isis becausebecause ofof thethe lacklack ofof corroboratingcorroborating animalanimal oror humanhuman evidence.evidence. TheThe materialmaterial maymay stillstill bebe damagingdamaging toto thethe healthhealth ofof thethe individual,individual, followingfollowing ingestion,ingestion, especiallyespecially wherewhere pre-existingpre-existing organorgan (e.g(e.g liver,liver, IngestionIngestion kidney)kidney) damagedamage isis evident.evident. PresentPresent definitionsdefinitions ofof harmfulharmful oror toxictoxic substancessubstances areare generallygenerally basedbased onon dosesdoses producingproducing mortalitymortality ratherrather thanthan thosethose producingproducing morbidity (disease, ill-health). Gastrointestinal tract discomfort may produce nausea and vomiting. In an occupational setting however, ingestion of insignificant quantitiesquantities isis notnot thoughtthought toto bebe causecause forfor concern.concern.

Continued... Version No: 4.7 Page 8 of 20 Issue Date: 29/07/2016 Print Date: 29/07/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part A)

100+ - Airline**

* -Continuous Flow ** -Continuous-flow or positive pressure demand. A(Allclasses) = Organic vapours, B AUS or B1 = Acid gases, B2 = Acid gas or hydrogencyanide(HCN), B3 = Acid gas or hydrogen cyanide(HCN), E = Sulfur dioxide(SO2),G = Agricultural chemicals, K = Ammonia(NH3), Hg = Mercury, NO = Oxides ofnitrogen, MB = Methyl bromide, AX = Low boiling point organic compounds(below65 deg C)

8.2.3. Environmental exposure controls See section 12

SECTION 9 PHYSICAL AND CHEMICAL PROPERTIES

9.1. Information on basic physical and chemical properties

Appearance dark grey

Physical state Liquid Relative density (Water = 1) 2.2 Partition coefficient Odour Not Available Not Available n-octanol / water Auto-ignition temperature Odour threshold Not Available Not Available (°C) Decomposition pH (as supplied) Not Available Not Available temperature Melting point / freezing Not Available Viscosity (cSt) >20.5 point (°C) Initial boiling point and >207 Molecular weight (g/mol) Not Available boiling range (°C) Flash point (°C) >149 Taste Not Available Evaporation rate Not Available Explosive properties Not Available Flammability Not Applicable Oxidising properties Not Available Surface Tension (dyn/cm or Upper Explosive Limit (%) Not Available Not Available mN/m) Lower Explosive Limit (%) Not Available Volatile Component (%vol) Not Available Vapour pressure (kPa) Not Available Gas group Not Available Solubility in water (g/L) Immiscible pH as a solution (1%) Not Available Vapour density (Air = 1) Not Available VOC g/L Not Available

9.2. Other information Not Available

SECTION 10 STABILITY AND REACTIVITY

10.1.Reactivity See section 7.2 Unstable in the presence of incompatible materials. 10.2. Chemical stability Product is considered stable. Hazardous polymerisation will not occur.

10.3. Possibility of See section 7.2 hazardous reactions Safety10.4. Conditions to avoid DataSee section 7.2 Sheet Version10.5. No: Incompatible 4.7 materials See section 7.2 Page 9 of 20 Issue Date: 29/07/2016 Print Date: 29/07/2016 10.6. Hazardous See8329TFS section 5.3 Slow Cure, Thermally Conductive Adhesive, Flowable (Part A) decomposition products

SECTION 11 TOXICOLOGICAL INFORMATION Evidence exists, or practical experience predicts, that the material either produces inflammation of the skin in a substantial number of individuals following 11.1. Information on toxicologicaldirect contact, effects and/or produces significant 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 formThe materialof contact is notdermatitis thought (nonallergic). to produce adverse The dermatitis health effectsis often or characterised irritation of the by respiratoryskin redness tract (erythema) (as classified and swellingby EC Directives (oedema) using which animal may progressmodels). to blisteringNevertheless, (vesiculation), good hygiene scaling practice and thickening requires that of the exposure epidermis. be kept At the to amicroscopic minimum and level that there suitable may controlbe intercellular measures oedema be used of inthe an spongy occupational layer of setting. the skin Skin Contact (spongiosis) and intracellular oedema of the epidermis. Inhalation of freshly formed metal oxide particles sized below 1.5 microns and generally between 0.02 to 0.05 microns may result in 'metal fume fever'. Inhaled The material may accentuate any pre-existing dermatitis condition SymptomsSkin contact may is not be thoughtdelayed tofor have up to harmful 12 hours health and begineffects with (as theclassified sudden under onset EC of thirst,Directives); and a sweet,the material metallic may or foulstill producetaste in the health mouth. damage Other following symptoms entry include upperthrough respiratory wounds, lesionstract irritation or abrasions. accompanied by coughing and a dryness of the mucous membranes, lassitude and a generalised feeling of malaise. Mild to severeContact headache, with aluminas nausea, (aluminium occasional oxides) vomiting, may produce fever or achills, form exaggerated of irritant dermatitis mental accompaniedactivity, profuse by sweating, pruritus. diarrhoea, excessive urination and prostration mayThough also considered occur. Tolerance non-harmful, to the fumes slight irritationdevelops may rapidly, result but from is quickly contact lost. because All symptoms of the abrasive usually subsidenature of within the aluminium 24-36 hours oxide following particles. removal from exposure.

Version No:Version 4.7 No: 4.7 AcuteEvidence toxic exists, responses or practical to aluminium experience are confinedpredicts, tothatPage the the more 9 material of 20solublePage may 9 forms. of cause 20 eye irritation in a substantial number of individuals and/or may Issueproduce Date: significantIssue 29/07/2016 Date: 29/07/2016 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 ocular lesions which are present twenty-four hours or more after instillation into the eye(s) of experimental animals. Print Date: 29/07/2016 Eye animal or human evidence. The material may still be damaging to the health of the individual, following ingestion, especially where pre-existingPrint organ Date: (e.g 29/07/2016 liver, Ingestion Repeated8329TFS or prolonged8329TFS Slow eyeCure, Slowcontact Thermally mayCure, cause Thermally inflammation Conductive characterisedConductive Adhesive, by temporary Adhesive, Flowable redness Flowable (similar (Part to windburn)A) (Part of A) the conjunctiva (conjunctivitis); kidney)temporary damage impairment is evident. of vision Present and/or definitions other transient of harmful eye ordamage/ulceration toxic substances may are generallyoccur. 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 Practicalquantities experience is not thought shows to be that cause skin forcontact concern. 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. Chronic exposure to aluminas (aluminium oxides) of particle size 1.2 microns did not produce significant systemic or respiratory system effects in workers. Evidence exists,Evidence or practical exists, experienceor practical predicts,experience that predicts, the material that the either material produces either inflammation produces inflammation of the skin in of a the substantial skin in a numbersubstantial of individuals number of following individuals following When hydrated aluminas were injected intratracheally, they produced dense and numerous nodules of advanced fibrosis in rats, a reticulin network with direct contact,direct and/or contact, produces and/or significant produces inflammation significant inflammation when applied when to the applied healthy to intactthe healthy skin of intact animals, skin forof animals,up to four for hours, up to suchfour hours,inflammation such inflammation being present being present occasional collagen fibres in mice and guinea pigs, and only a slight reticulin network in rabbits. Shaver's disease, a rapidly progressive and often fatal twenty-four hourstwenty-four or more hours after or the more end after of the the exposure end of the period. exposure Skin period. irritation Skin may irritation also be may present also afterbe present prolonged after or prolonged repeated orexposure; repeated this exposure; may result thisContinued... in may a result in a interstitial fibrosis of the lungs, is associated with a process involving the fusion of bauxite (aluminium oxide) with iron, coke and silica at 2000 deg. C. form of contactform dermatitis of contact (nonallergic). dermatitis (nonallergic). The dermatitis The is dermatitis often characterised is often characterised by skin redness by skin (erythema) redness and(erythema) swelling and (oedema) swelling which (oedema) may progresswhich may to progress to The weight of evidence suggests that catalytically active alumina and the large surface area aluminas can induce lung fibrosis(aluminosis) in experimental blistering (vesiculation),blistering (vesiculation), scaling and scalingthickening and of thickening the epidermis. of the At epidermis. the microscopic At the microscopic level there may level be there intercellular may be intercellularoedema of theoedema spongy of layerthe spongy of the skinlayer of the skin Skin ContactSkin Contactanimals, but only when given by the intra-tracheal route. The pertinence of such experiments in relation to workplace exposure is doubtful especially since it has (spongiosis)(spongiosis) and intracellular and intracellularoedema of theoedema epidermis. of the epidermis. been demonstrated that the most reactive of the aluminas (i.e. the chi and gamma forms), when given by inhalation, are non-fibrogenic in experimental animals. The materialThe may material accentuate may anyaccentuate pre-existing any pre-existingdermatitis condition dermatitis condition However rats exposed by inhalation to refractory aluminium fibre showed mild fibrosis and possibly carcinogenic effects indicating that fibrous aluminas might Skin contactSkin is not contact thought is notto have thought harmful to have health harmful effects health (as classified effects (as under classified EC Directives); under EC Directives);the material the may material still produce may still health produce damage health following damage entry following entry exhibit different toxicology to non-fibrous forms. Aluminium oxide fibres administered by the intrapleural route produce clear evidence of carcinogenicity. through wounds,through lesions wounds, or abrasions. lesions or abrasions. Saffil fibre an artificially produced form alumina fibre used as refractories, consists of over 95% alumina, 3-4 % silica. Animal tests for fibrogenic, Contact withContact aluminas with (aluminium aluminas oxides)(aluminium may oxides) produce may a form produce of irritant a form dermatitis of irritant accompanied dermatitis accompanied by pruritus. by pruritus. carcinogenic potential and oral toxicity have included in-vitro, intraperitoneal injection, intrapleural injection, inhalation, and feeding. The fibre has generally Though consideredThough non-harmful,considered non-harmful, slight irritation slight may irritation result from may contactresult from because contact of thebecause abrasive of the nature abrasive of the nature aluminium of the oxide aluminium particles. oxide particles. been inactive in animal studies. Also studies of Saffil dust clouds show very low respirable fraction. EvidenceThere is general exists,Evidence oragreement practical exists, experienceorthat practical particle predicts,experience size determines that predicts, the materialthat that the thedegreemay material cause of pathogenicity eyemay irritation cause eye (thein a irritation substantialability of in a a micro-organism numbersubstantial of individuals number to produce of and/or individuals infectious may and/orproduce disease) may significant produce of significant elementaryocular lesions aluminium,ocular which lesions are or present itswhich oxides aretwenty-four or present hydroxides twenty-fourhours when or more they hours after occur or instillation more as dusts, after into fumesinstillation the eye(s)or vapours. into of the experimental eye(s)Only those of experimental animals.particles small animals. enough to enter the alveolii (sub 5 Eye Eye um)Repeated are able orRepeated prolongedto produce or eye pathogenicprolonged contact eye mayeffects contact cause in the inflammationmay lungs. cause inflammation characterised characterised by temporary by redness temporary (similar redness to windburn) (similar to of windburn) the conjunctiva of the conjunctiva(conjunctivitis); (conjunctivitis); Occupationaltemporary impairmenttemporary exposure ofimpairment to vision aluminium and/or of visioncompounds other and/or transient may other eye produce transient damage/ulceration asthma,chronic eye damage/ulceration may obstructive occur. may lung occur. disease and pulmonary fibrosis. Long-term overexposuremay produce dyspnoea, cough, pneumothorax, variable sputum production andnodular interstitial fibrosis; death has been reported. Chronic interstitialpneumonia Practical experiencePractical showsexperience that skinshows contact that skin with contact the material with the is capable material either is capable of inducing either aof sensitisation inducing a sensitisation reaction in a reaction substantial in a numbersubstantial of individuals, number of and/orindividuals, and/or with severe cavitations in the right upper lung and small cavities inthe remaining lung tissue, have been observed in gross pathology. Shaver'sDisease may of producingof a producing positive response a positive in responseexperimental in experimental animals. animals. result from occupational exposure to fumes or dusts; this mayproduce respiratory distress and fibrosis with large blebs. Animal studiesproduce no indication Chronic exposureChronic to exposure aluminas to(aluminium aluminas oxides)(aluminium of particle oxides) size of particle 1.2 microns size 1.2 did micronsnot produce did not significant produce systemic significant or systemicrespiratory or systemrespiratory effects system in workers. effects in workers. that aluminium or its compounds are carcinogenic. When hydratedWhen aluminas hydrated were aluminas injected were intratracheally, injected intratracheally, they produced they dense produced and numerous dense and nodules numerous of advanced nodules of fibrosis advanced in rats, fibrosis a reticulin in rats, network a reticulin with network with Because aluminium competes with calcium for absorption, increasedamounts of dietary aluminium may contribute to the reduced skeletalmineralisation occasional collagenoccasional fibres collagen in mice fibres and inguinea mice andpigs, guinea and only pigs, a slight and only reticulin a slight network reticulin in rabbits. network Shaver's in rabbits. disease, Shaver's a rapidly disease, progressive a rapidly progressive and often fatal and often fatal (osteopenia) observed in preterm infants and infants with growthretardation. In very high doses, aluminium can cause neurotoxicity, and isassociated with interstitial fibrosisinterstitial of the fibrosis lungs, of is the associated lungs, is withassociated a process with involving a process the involving fusion of the bauxite fusion (aluminium of bauxite (aluminiumoxide) with iron,oxide) coke with and iron, silica coke at and 2000 silica deg. at C. 2000 deg. C. altered function of the blood-brain barrier. A small percentageof people are allergic to aluminium and experience contact dermatitis,digestive disorders, The weight Theof evidence weight ofsuggests evidence that suggests catalytically that catalyticallyactive alumina active and alumina the large and surface the large area surface aluminas area can aluminas induce lungcan inducefibrosis(aluminosis) lung fibrosis(aluminosis) in experimental in experimental vomiting or other symptoms upon contact or ingestion ofproducts containing aluminium, such as deodorants or antacids. In those withoutallergies, aluminium is animals, butanimals, only when but given only whenby the given intra-tracheal by the intra-tracheal route. The pertinence route. The of pertinence such experiments of such experiments in relation to in workplace relation to exposure workplace is exposuredoubtful especially is doubtful since especially it has since it has not as toxic as heavy metals, but there is evidence ofsome toxicity if it is consumed in excessive amounts. Although the use ofaluminium cookware has not been been demonstratedbeen demonstrated that the most that reactive the most of the reactive aluminas of the (i.e. aluminas the chi and(i.e. gammathe chi and forms), gamma when forms), given whenby inhalation, given by are inhalation, non-fibrogenic are non-fibrogenic in experimental in experimental animals. animals. shown to lead to aluminium toxicity in general,excessive consumption of antacids containing aluminium compounds and excessiveuse of aluminium-containing However ratsHowever exposed rats by exposedinhalation by to inhalation refractory to aluminium refractory fibre aluminium showed fibre mild showed fibrosis mild and fibrosispossibly and carcinogenic possibly carcinogenic effects indicating effects that indicating fibrous aluminasthat fibrous might aluminas might antiperspirants provide more significant exposurelevels. Studies have shown that consumption of acidic foods or liquids withaluminium significantly increases exhibit differentexhibit toxicology different to toxicology non-fibrous to non-fibrousforms. Aluminium forms. oxideAluminium fibres oxideadministered fibres administered by the intrapleural by the routeintrapleural produce route clear produce evidence clear of evidencecarcinogenicity. of carcinogenicity. aluminium absorption, and maltol has beenshown to increase the accumulation of aluminium in nervous and osseus tissue.Furthermore, aluminium increases Saffil fibre anSaffil artificially fibre an produced artificially form produced alumina form fibre alumina used as fibre refractories, used as refractories, consists of overconsists 95% of alumina, over 95% 3-4 alumina, % silica. 3-4 Animal % silica. tests Animal for fibrogenic, tests for fibrogenic, oestrogen-related gene expression in human breastcancer cells cultured in the laboratory These salts' estrogen-like effects haveled to their classification as a carcinogeniccarcinogenic potential and potential oral toxicity and oralhave toxicity included have in-vitro, included intraperitoneal in-vitro, intraperitoneal injection, intrapleural injection, intrapleuralinjection, inhalation, injection, and inhalation, feeding. and The feeding. fibre has The generally fibre has generally metalloestrogen.Some researchers haveexpressed concerns that the aluminium in antiperspirants may increase the riskof breast cancer. been inactivebeen in animal inactive studies. in animal Also studies. studies Also of Saffil studies dust of clouds Saffil dustshow clouds very low show respirable very low fraction. respirable fraction. After absorption, aluminium distributes to all tissues in animalsand humans and accumulates in some, in particular bone. The main carrier of thealuminium ion There is generalThere agreement is general thatagreement particle thatsize particle determines size determinesthat the degree that ofthe pathogenicity degree of pathogenicity (the ability of (the a micro-organism ability of a micro-organism to produce infectiousto produce disease) infectious of disease) of in plasma is the iron binding protein, transferrin. Aluminium canenter the brain and reach the placenta and foetus. Aluminium may persist for avery long time in elementary aluminium,elementary oraluminium, its oxides or or its hydroxides oxides or whenhydroxides they occur when as they dusts, occur fumes as dusts, or vapours. fumes orOnly vapours. those particlesOnly those small particles enough small to enter enough the toalveolii enter (sub the alveolii5 (sub 5 various organs and tissues before it is excreted in theurine. Although retention times for aluminium appear to be longer in humansthan in rodents, there is little um) are ableum) to produceare able pathogenicto produce effectspathogenic in the effects lungs. in the lungs. Chronic information allowing extrapolation fromrodents to the humans. OccupationalOccupational exposure to exposurealuminium to compounds aluminium compoundsmay produce may asthma,chronic produce asthma,chronic obstructive lungobstructive disease lung and disease pulmonary and fibrosis. pulmonary Long-term fibrosis. overexposuremay Long-term overexposuremay At high levels of exposure, some aluminium compounds may produceDNA damage in vitro and in vivo via indirect mechanisms. The database oncarcinogenicity produce dyspnoea,produce cough, dyspnoea, pneumothorax, cough, pneumothorax, variable sputum variable production sputum andnodular production andnodularinterstitial fibrosis; interstitial death fibrosis; has been death reported. has been Chronic reported. interstitialpneumonia Chronic interstitialpneumonia of aluminium compounds is limited. No indication of anycarcinogenic potential was obtained in mice given aluminium potassium sulphateat high levels in the with severe withcavitations severe incavitations the right upper in the lungright andupper small lung cavities and small inthe cavities remaining inthe lung remaining tissue, lunghave tissue, been observedhave been in observedgross pathology. in gross Shaver'sDisease pathology. Shaver'sDisease may may diet. result from occupationalresult from occupational exposure to exposure fumes or todusts; fumes this or mayproduce dusts; this mayproduce respiratory distressrespiratory and distress fibrosis andwith fibrosislarge blebs. with largeAnimal blebs. studiesproduce Animal studiesproduce no indication no indication Aluminium has shown neurotoxicity in patients undergoing dialysisand thereby chronically exposed parenterally to high concentrations ofaluminium. It has been that aluminiumthat or aluminium its compounds or its compounds are carcinogenic. are carcinogenic. suggested that aluminium is implicated in the aetiologyof Alzheimer’s disease and associated with other neurodegenerative diseases inhumans. However, Because aluminiumBecause competes aluminium with competes calcium with for absorption,calcium for increasedamountsabsorption, increasedamounts of dietary aluminium of dietary may aluminium contribute may to contribute the reduced to the skeletalmineralisation reduced skeletalmineralisation these hypotheses remain controversial. Several compoundscontaining aluminium have the potential to produce neurotoxicity (mice, rats)and to affect the male (osteopenia)(osteopenia) observed in observedpreterm infants in preterm and infantsinfants withand growthretardation.infants with growthretardation. In very high Indoses, very highaluminium doses, can aluminium cause neurotoxicity, can cause neurotoxicity, and isassociated and isassociated with with reproductive system (dogs). In addition, after maternalexposure they have shown embryotoxicity (mice) and have affected the developingnervous system in the altered functionaltered of the function blood-brain of the blood-brainbarrier. A small barrier. percentageof A small percentageof people are allergicpeople toare aluminium allergic to and aluminium experience and experiencecontact dermatitis,digestive contact dermatitis,digestive disorders, disorders, offspring (mice, rats). The available studies have anumber of limitations and do not allow any dose-response relationships to beestablished. The combined vomiting or othervomiting symptoms or other upon symptoms contact upon or ingestion contact orofproducts ingestion containingofproducts aluminium, containing suchaluminium, as deodorants such as deodorantsor antacids. orIn antacids.those withoutallergies, In those withoutallergies, aluminium is aluminium is evidence from several studies in mice, rats and dogsthat used dietary administration of aluminium compounds producelowest-observed-adverse-effect levels not as toxic asnot heavy as toxic metals, as heavy but theremetals, is evidencebut there ofsomeis evidence toxicity ofsome if it is toxicity consumed if it is in consumed excessive in amounts. excessive Although amounts. the Although use ofaluminium the use of cookwarealuminium has cookware not been has not been (LOAELs) for effects on neurotoxicity,testes, embryotoxicity, and the developing nervous system of 52, 75, 100, and50 mg aluminium/kg bw/day, respectively. shown to leadshown to aluminium to lead to toxicity aluminium in general,excessive toxicity in general,excessive consumption consumption of antacids containingof antacids aluminium containing compounds aluminium compoundsand excessiveuse and excessiveuse of aluminium-containing of aluminium-containing Similarly, the lowestno-observed-adverse-effect levels (NOAELs) for effects on these endpoints werereported at 30, 27, 100, and for effects on the developing antiperspirantsantiperspirants provide more provide significant more exposurelevels. significant exposurelevels. Studies have Studies shown have that consumptionshown that consumption of acidic foods of acidic or liquids foods withaluminium or liquids withaluminium significantly significantlyincreases increases nervous system,between 10 and 42 mg aluminium/kg bw per day, respectively. aluminium absorption,aluminium andabsorption, maltol has and beenshown maltol has beenshownto increase theto increase accumulation the accumulation of aluminium of in aluminium nervous and in nervous osseus andtissue.Furthermore, osseus tissue.Furthermore, aluminium increases aluminium increases Controversy exists over whether aluminium is the cause ofdegenerative brain disease (Alzheimer's disease or AD). Several epidemiologicalstudies show a oestrogen-relatedoestrogen-related gene expression gene inexpression human breastcancer in human breastcancer cells cultured cells in the cultured laboratory in the These laboratory salts' These estrogen-like salts' estrogen-like effects haveled effects to theirhaveled classification to their classification as a as a possible correlation between the incidence of AD and high levelsof aluminium in drinking water. A study in Toronto, for example, found a 2.6times increased risk metalloestrogen.Somemetalloestrogen.Some researchers researchers haveexpressed haveexpressed concerns that concerns the aluminium that the in aluminium antiperspirants in antiperspirants may increase may the increase riskof breast the riskof cancer. breast cancer. in people residing for at least 10 years in communitieswhere drinking water contained more than 0.15 mg/l aluminium compared withcommunities where the After absorption,After absorption,aluminium distributes aluminium to distributes all tissues to in all animalsand tissues in animalsandhumans and humans accumulates and accumulates in some, in particularin some, inbone. particular The main bone. carrier The main of thealuminium carrier of thealuminium ion ion aluminium level was lower than 0.1 mg/l. A neurochemicalmodel has been suggested linking aluminium exposure to brain disease. Aluminiumconcentrates in in plasma isin the plasma iron binding is the ironprotein, binding transferrin. protein, Aluminiumtransferrin. canenterAluminium the canenter brain and the reach brain the and placenta reach the and placenta foetus. andAluminium foetus. mayAluminium persist mayfor avery persist long for time avery in long time in brain regions, notably the hippocampus, cerebral cortex andamygdala where it preferentially binds to large pyramid-shaped cells - it doesnot bind to a various organsvarious and organstissues andbefore tissues it is excreted before it inis theurine.excreted inAlthough theurine. retention Although times retention for aluminium times for appear aluminium to be appear longer to in be humansthan longer in humansthan in rodents, therein rodents, is little there is little substantial degree to the smaller interneurons. Aluminiumdisplaces magnesium in key metabolic reactions in brain cells and alsointerferes with calcium Chronic Chronicinformation allowinginformation extrapolation allowing extrapolation fromrodents fromrodents to the humans. to the humans. metabolism and inhibits phosphoinositide metabolism.Phosphoinositide normally controls calcium ion levels at criticalconcentrations. At high levelsAt of high exposure, levels of some exposure, aluminium some compounds aluminium compoundsmay produceDNA may produceDNA damage in vitro damage and inin vivovitro viaand indirect in vivo mechanisms. via indirect mechanisms. The database The oncarcinogenicity database oncarcinogenicity Under the microscope the brain of AD sufferers show thickened fibrils(neurofibrillary tangles - NFT) and plaques consisting of amyloid proteindeposited in the of aluminiumof compounds aluminium compounds is limited. No is indicationlimited. No of indication anycarcinogenic of anycarcinogenic potential was potential obtained was in miceobtained given in aluminiummice given potassium aluminium sulphateat potassium high sulphateat levels inhigh the levels in the matrix between brain cells. Tangles result from alteration of'tau' a brain cytoskeletal protein. AD tau is distinguished fromnormal tau because it is diet. diet. hyperphosphorylated. Aluminium hyperphosphorylates tauin vitro. When AD tau is injected into rat brain NFT-like aggregates form butsoon degrade. Aluminium Aluminium hasAluminium shown neurotoxicityhas shown neurotoxicity in patients undergoing in patients undergoingdialysisand therebydialysisand chronically thereby exposed chronically parenterally exposed parenterallyto high concentrations to high concentrations ofaluminium. ofaluminium. It has been It has been stabilises these aggregates rendering them resistant toprotease degradation. Plaque formation is also enhanced by aluminium whichinduces the accumulation suggested thatsuggested aluminium that is aluminium implicated is in implicated the aetiologyof in the Alzheimer’saetiologyof Alzheimer’sdisease and disease associated and withassociated other neurodegenerative with other neurodegenerative diseases inhumans. diseases However, inhumans. However, of amyloid precursor protein in the thread-likeextensions of nerve cells (axons and dendrites). In addition aluminium has beenshown to depress the activity of these hypothesesthese hypothesesremain controversial. remain controversial. Several compoundscontaining Several compoundscontaining aluminium have aluminium the potential have the to producepotential neurotoxicityto produce neurotoxicity (mice, rats)and (mice, to affectrats)and the tomale affect the male most neuro-transmitters similarly depressed inAD (acetylcholine, norepinephrine, glutamate and GABA). www.element14.com reproductivereproductive system (dogs). system In addition, (dogs). afterIn addition, maternalexposure after maternalexposure they have shown they have embryotoxicity shown embryotoxicity (mice) and have (mice) affected and have the affecteddevelopingnervous the developingnervous system in the system in the Aluminium enters the brain in measurable quantities, even whentrace levels are contained in a glass of tap water. Other sources ofbioavailable aluminium offspring (mice,offspring rats). (mice, The available rats). The studies available have studies anumber have of anumberlimitations of and limitations do not allowand do any not dose-response allow any dose-response relationships relationships to beestablished. to beestablished. The combined The combined www.farnell.com include baking powder, antacids and aluminium productsused for general food preparation and storage (over 12 months, aluminium levelsin soft drink packed in evidence fromevidence several from studies several in mice, studies rats in and mice, dogsthat rats and used dogsthat dietary used administration dietary administration of aluminium of compounds aluminium compounds producelowest-observed-adverse-effect producelowest-observed-adverse-effect levels levels aluminium cans rose from 0.05 to 0.9 mg/l). [Walton,J and Bryson-Taylor, D. - Chemistry in Australia, August 1995] www.newark.com (LOAELs) for(LOAELs) effects on for neurotoxicity,testes, effects on neurotoxicity,testes, embryotoxicity, embryotoxicity, and the developing and the nervousdeveloping system nervous of 52, system 75, 100, of 52,and50 75, mg100, aluminium/kg and50 mg aluminium/kg bw/day, respectively. bw/day, respectively. All glycidyl ethers show genotoxic potential due their alkylating properties. Those glycidyl ethers that have been investigated in long term studies exhibit more Similarly, theSimilarly, lowestno-observed-adverse-effect the lowestno-observed-adverse-effect levels (NOAELs) levels for (NOAELs) effects on for these effects endpoints on these werereported endpoints werereported at 30, 27, 100, at 30, and 27, for 100, effects and on for the effects developing on the developing or less marked carcinogenic potential. Alkylating agents may damage the stem cell which acts as the precursor to components of the blood. Loss of the stem nervous system,betweennervous system,between 10 and 42 mg 10 aluminium/kg and 42 mg aluminium/kg bw per day, respectively.bw per day, respectively. cell may result in pancytopenia (a reduction in the number of red and white blood cells and platelets) with a latency period corresponding to the lifetime of the ControversyControversy exists over whetherexists over aluminium whether is aluminium the causePage is ofdegenerative the cause<10> ofdegenerative brain disease brain (Alzheimer's disease (Alzheimer's disease or AD). disease Several or AD). epidemiologicalstudies Several epidemiologicalstudies28/10/18 show a V1.0 show a individual blood cells. Granulocytopenia (a reduction in granular leukocytes) develops within days and thrombocytopenia (a disorder involving platelets), within possible correlationpossible between correlation the between incidence the of incidence AD and high of AD levelsof and high aluminium levelsof in aluminium drinking water. in drinking A study water. in Toronto, A study for in Toronto,example, for found example, a 2.6times found increased a 2.6times risk increased risk 1-2 weeks, whilst loss of erythrocytes (red blood cells) need months to become clinically manifest. Aplastic anaemia develops due to complete destruction of the in people residingin people for atresiding least 10 for years at least in communitieswhere10 years in communitieswhere drinking water drinking contained water more contained than 0.15 more mg/l than aluminium 0.15 mg/l compared aluminium withcommunities compared withcommunities where the where the stem cells. aluminium levelaluminium was lower level than was 0.1 lower mg/l. than A neurochemicalmodel0.1 mg/l. A neurochemicalmodel has been suggested has been linking suggested aluminium linking exposure aluminium to exposure brain disease. to brain Aluminiumconcentrates disease. Aluminiumconcentrates in in Glycidyl ethers have been shown to cause allergic contact dermatitis in humans. Glycidyl ethers generally cause skin sensitization in experimental animals. brain regions,brain notably regions, the hippocampus,notably the hippocampus, cerebral cortex cerebral andamygdala cortex andamygdala where it preferentially where it preferentially binds to large binds pyramid-shaped to large pyramid-shaped cells - it doesnot cells bind- it doesnot to a bind to a substantial degreesubstantial to the degree smaller to interneurons.the smaller interneurons. Aluminiumdisplaces Aluminiumdisplaces magnesium magnesium in key metabolic in key reactions metabolic in reactionsbrain cells in and brain alsointerferes cells and alsointerferes with calcium with calcium Continued... metabolism metabolismand inhibits andphosphoinositide inhibits phosphoinositide metabolism.Phosphoinositide metabolism.Phosphoinositide normally controls normally calcium controls ion calciumlevels at ion criticalconcentrations. levels at criticalconcentrations. Under the microscopeUnder the microscope the brain of theAD brainsufferers of AD show sufferers thickened show fibrils(neurofibrillary thickened fibrils(neurofibrillary tangles - NFT) tangles and plaques- NFT) and consisting plaques of consisting amyloid proteindeposited of amyloid proteindeposited in the in the matrix betweenmatrix brain between cells. Tanglesbrain cells. result Tangles from alterationresult from of'tau' alteration a brain of'tau' cytoskeletal a brain cytoskeletal protein. AD protein.tau is distinguished AD tau is distinguished fromnormal fromnormaltau because tau it is because it is hyperphosphorylated.hyperphosphorylated. Aluminium hyperphosphorylatesAluminium hyperphosphorylates tauin vitro. When tauin vitro.AD tau When is injected AD tau into is injected rat brain into NFT-like rat brain aggregates NFT-like aggregatesform butsoon form degrade. butsoon Aluminium degrade. Aluminium stabilises thesestabilises aggregates these aggregatesrendering them rendering resistant them toprotease resistant degradation.toprotease degradation. Plaque formation Plaque is formationalso enhanced is also by enhanced aluminium by whichinduces aluminium whichinduces the accumulation the accumulation of amyloid precursorof amyloid protein precursor in the protein thread-likeextensions in the thread-likeextensions of nerve cells of (axonsnerve cells and dendrites).(axons and In dendrites). addition aluminium In addition has aluminium beenshown has beenshownto depress the to depressactivity of the activity of most neuro-transmittersmost neuro-transmitters similarly depressed similarly inADdepressed (acetylcholine, inAD (acetylcholine, norepinephrine, norepinephrine, glutamate and glutamate GABA). and GABA). Aluminium entersAluminium the brain enters in measurablethe brain in measurable quantities, even quantities, whentrace even levels whentrace are contained levels are in contained a glass of in tap a glasswater. of Other tap water. sources Other ofbioavailable sources ofbioavailable aluminium aluminium include bakinginclude powder, baking antacids powder, and antacids aluminium and productsused aluminium productsused for general foodfor general preparation food preparationand storage and (over storage 12 months, (over aluminium12 months, levelsin aluminium soft levelsindrink packed soft drink in packed in aluminium cansaluminium rose from cans 0.05 rose to from 0.9 mg/l).0.05 to [Walton,J 0.9 mg/l). and [Walton,J Bryson-Taylor, and Bryson-Taylor, D. - Chemistry D. -in Chemistry Australia, in August Australia, 1995 August] 1995] All glycidyl ethersAll glycidyl show ethers genotoxic show potential genotoxic due potential their alkylating due their properties. alkylating Thoseproperties. glycidyl Those ethers glycidyl that haveethers been that investigatedhave been investigated in long term in studies long term exhibit studies more exhibit more or less markedor less carcinogenic marked carcinogenic potential. Alkylating potential. agents Alkylating may agentsdamage may the damage stem cell the which stem acts cell as which the precursoracts as the to precursor components to components of the blood. of Loss the blood.of the stemLoss of the stem cell may resultcell in may pancytopenia result in pancytopenia (a reduction (a in reductionthe number in theof red number and white of red blood and whitecells andblood platelets) cells and with platelets) a latency with period a latency corresponding period corresponding to the lifetime to ofthe the lifetime of the individual bloodindividual cells. bloodGranulocytopenia cells. Granulocytopenia (a reduction (a in reductiongranular leukocytes)in granular leukocytes)develops within develops days andwithin thrombocytopenia days and thrombocytopenia (a disorder involving(a disorder platelets), involving within platelets), within 1-2 weeks, whilst1-2 weeks, loss of whilst erythrocytes loss of erythrocytes (red blood cells) (red bloodneed monthscells) need to become months clinicallyto become manifest. clinically Aplastic manifest. anaemia Aplastic develops anaemia due develops to complete due todestruction complete ofdestruction the of the stem cells. stem cells. Glycidyl ethersGlycidyl have ethers been shownhave been to cause shown allergic to cause contact allergic dermatitis contact in dermatitis humans. Glycidylin humans. ethers Glycidyl generally ethers cause generally skin sensitizationcause skin sensitization in experimental in experimental animals. animals.

Continued...Continued... Version No: 4.7 Page 9 of 20 Issue Date: 29/07/2016 Print Date: 29/07/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part A)

Evidence exists, or practical experience predicts, that the material either produces inflammation of the skin in a substantial number of individuals following direct contact, and/or produces significant 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 Skin Contact (spongiosis) and intracellular oedema of the epidermis. The material may accentuate any pre-existing dermatitis condition 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. Contact with aluminas (aluminium oxides) may produce a form of irritant dermatitis accompanied by pruritus. Though considered non-harmful, slight irritation may result from contact because of the abrasive nature of the aluminium oxide particles. Evidence exists, or practical experience predicts, that the material may cause eye irritation in a substantial number of individuals and/or may produce significant ocular lesions which are present twenty-four hours or more after instillation into the eye(s) of experimental animals. Eye Repeated or prolonged eye contact may cause inflammation characterised by temporary redness (similar to windburn) of the conjunctiva (conjunctivitis); temporary impairment of vision and/or other transient eye damage/ulceration may occur. 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. Chronic exposure to aluminas (aluminium oxides) of particle size 1.2 microns did not produce significant systemic or respiratory system effects in workers. When hydrated aluminas were injected intratracheally, they produced dense and numerous nodules of advanced fibrosis in rats, a reticulin network with occasional collagen fibres in mice and guinea pigs, and only a slight reticulin network in rabbits. Shaver's disease, a rapidly progressive and often fatal interstitial fibrosis of the lungs, is associated with a process involving the fusion of bauxite (aluminium oxide) with iron, coke and silica at 2000 deg. C. The weight of evidence suggests that catalytically active alumina and the large surface area aluminas can induce lung fibrosis(aluminosis) in experimental animals, but only when given by the intra-tracheal route. The pertinence of such experiments in relation to workplace exposure is doubtful especially since it has been demonstrated that the most reactive of the aluminas (i.e. the chi and gamma forms), when given by inhalation, are non-fibrogenic in experimental animals. However rats exposed by inhalation to refractory aluminium fibre showed mild fibrosis and possibly carcinogenic effects indicating that fibrous aluminas might exhibit different toxicology to non-fibrous forms. Aluminium oxide fibres administered by the intrapleural route produce clear evidence of carcinogenicity. Saffil fibre an artificially produced form alumina fibre used as refractories, consists of over 95% alumina, 3-4 % silica. Animal tests for fibrogenic, carcinogenic potential and oral toxicity have included in-vitro, intraperitoneal injection, intrapleural injection, inhalation, and feeding. The fibre has generally been inactive in animal studies. Also studies of Saffil dust clouds show very low respirable fraction. There is general agreement that particle size determines that the degree of pathogenicity (the ability of a micro-organism to produce infectious disease) of elementary aluminium, or its oxides or hydroxides when they occur as dusts, fumes or vapours. Only those particles small enough to enter the alveolii (sub 5 um) are able to produce pathogenic effects in the lungs. Occupational exposure to aluminium compounds may produce asthma,chronic obstructive lung disease and pulmonary fibrosis. Long-term overexposuremay Version No: 4.7 Page 9 of 20 Issue Date: 29/07/2016 produce dyspnoea, cough, pneumothorax, variable sputum production andnodular interstitial fibrosis; death has been reported. Chronic interstitialpneumonia Print Date: 29/07/2016 with8329TFS severe cavitations Slow in Cure, the right Thermallyupper lung and Conductivesmall cavities inthe Adhesive, remaining lung Flowabletissue, have been (Part observed A) in gross pathology. Shaver'sDisease may result from occupational exposure to fumes or dusts; this mayproduce respiratory distress and fibrosis with large blebs. Animal studiesproduce no indication that aluminium or its compounds are carcinogenic. Because aluminium competes with calcium for absorption, increasedamounts of dietary aluminium may contribute to the reduced skeletalmineralisation (osteopenia) observed in preterm infants and infants with growthretardation. In very high doses, aluminium can cause neurotoxicity, and isassociated with alteredEvidence function exists, of or the practical blood-brain experience barrier. predicts, A small that percentageof the material people either areproduces allergic inflammation to aluminium of and the experienceskin in a substantial contact dermatitis,digestive number of individuals disorders, following vomitingdirect contact, or other and/or symptoms produces upon significant contact orinflammation ingestion ofproducts when applied containing to the healthy aluminium, intact such skin asof deodorantsanimals, for orup antacids. to four hours, In those such withoutallergies, inflammation being aluminium present is nottwenty-four as toxic hoursas heavy or more metals, after but the there end is of evidence the exposure ofsome period. toxicity Skin if it irritationis consumed may alsoin excessive be present amounts. after prolonged Although orthe repeated use ofaluminium exposure; cookware this may hasresult not in been a formshown of tocontact lead to dermatitis aluminium (nonallergic). toxicity in general,excessive The dermatitis is consumption often characterised of antacids by skin containing redness aluminium (erythema) compounds and swelling and (oedema) excessiveuse which of mayaluminium-containing progress to antiperspirantsblistering (vesiculation), provide more scaling significant and thickening exposurelevels. of the epidermis. Studies Athave the shown microscopic that consumption level there may of acidic be intercellular foods or liquids oedema withaluminium of the spongy significantly layer of the increases skin Skin Contact aluminium(spongiosis) absorption, and intracellular and maltol oedema has beenshown of the epidermis. to increase the accumulation of aluminium in nervous and osseus tissue.Furthermore, aluminium increases oestrogen-relatedThe material may accentuategene expression any pre-existing in human breastcancerdermatitis condition cells cultured in the laboratory These salts' estrogen-like effects haveled to their classification as a metalloestrogen.SomeSkin contact is not thought researchers to have harmful haveexpressed health effects concerns (as classifiedthat the aluminium under EC inDirectives); antiperspirants the material may increase may still the produce riskof breast health cancer. damage following entry Afterthrough absorption, wounds, aluminiumlesions or abrasions.distributes to all tissues in animalsand humans and accumulates in some, in particular bone. The main carrier of thealuminium ion Safety DatainContact plasma with is thealuminas iron bindingSheet (aluminium protein, oxides) transferrin. may produce Aluminium a form canenter of irritant the dermatitisbrain and reachaccompanied the placenta by pruritus. and foetus. Aluminium may persist for avery long time in variousThough organs considered and tissuesnon-harmful, before slight it is excreted irritation mayin theurine. result from Although contact retention because times of the for abrasivealuminium nature appear of theto be aluminium longer in oxide humansthan particles. in rodents, there is little Chronic information allowing extrapolation fromrodents to the humans. AtEvidence high levels exists, of exposure, or practical some experience aluminium predicts, compounds that the may material produceDNA may cause damage eye irritation in vitro inand a substantialin vivo via indirect number mechanisms. of individuals The and/or database may produce oncarcinogenicity significant ofocular aluminium lesions compounds which are present is limited. twenty-four No indication hours of or anycarcinogenic more after instillation potential into was the obtainedeye(s) of inexperimental mice given aluminiumanimals. potassium sulphateat high levels in the Eye diet.Repeated or prolonged eye contact may cause inflammation characterised by temporary redness (similar to windburn) of the conjunctiva (conjunctivitis); Aluminiumtemporary impairmenthas shown ofneurotoxicity vision and/or in otherpatients transient undergoing eye damage/ulceration dialysisand thereby may chronically occur. exposed parenterally to high concentrations ofaluminium. It has been Practicalsuggested experience that aluminium shows is thatimplicated skin contact in the withaetiologyof the material Alzheimer’s is capable disease either and of inducingassociated a sensitisationwith other neurodegenerative reaction in a substantial diseases number inhumans. of individuals, However, and/or ofthese producing hypotheses a positive remain response controversial. in experimental Several compoundscontaining animals. aluminium have the potential to produce neurotoxicity (mice, rats)and to affect the male Chronicreproductive exposure system to (dogs).aluminas In addition,(aluminium after oxides) maternalexposure of particle size they 1.2 have microns shown did embryotoxicity not produce significant (mice) and systemic have affected or respiratory the developingnervous system effects systemin workers. in the Whenoffspring hydrated (mice, rats).aluminas The wereavailable injected studies intratracheally, have anumber they ofproduced limitations dense and anddo not numerous allow any nodules dose-response of advanced relationships fibrosis in torats, beestablished. a reticulin network The combined with evidenceoccasional from collagen several fibres studies in mice in mice, and ratsguinea and pigs, dogsthat and onlyused a dietary slight reticulinadministration network of inaluminium rabbits. Shaver's compounds disease, producelowest-observed-adverse-effect a rapidly progressive and often fatal levels interstitial(LOAELs) fibrosis for effects of the on lungs,neurotoxicity,testes, is associated embryotoxicity,with a process andinvolving the developing the fusion nervous of bauxite system (aluminium of 52, 75, oxide) 100, with and50 iron, mg coke aluminium/kg and silica bw/day,at 2000 respectively.deg. C. Similarly,The weight the of lowestno-observed-adverse-effect evidence suggests that catalytically levels active (NOAELs) alumina forand effects the large on these surface endpoints area aluminas werereported can induce at 30, lung 27, 100,fibrosis(aluminosis) and for effects onin experimentalthe developing nervousanimals, system,betweenbut only when given 10 and by 42the mg intra-tracheal aluminium/kg route. bw Theper day, pertinence respectively. of such experiments in relation to workplace exposure is doubtful especially since it has beenControversy demonstrated exists over that whetherthe most aluminiumreactive of isthe the aluminas cause ofdegenerative (i.e. the chi and brain gamma disease forms), (Alzheimer's when given disease by inhalation, or AD). areSeveral non-fibrogenic epidemiologicalstudies in experimental show animals. a possibleHowever correlation rats exposed between by inhalation the incidence to refractory of AD aluminiumand high levelsof fibre showed aluminium mild in fibrosis drinking and water. possibly A study carcinogenic in Toronto, effects for example, indicating found that a fibrous 2.6times aluminas increased might risk exhibitin people different residing toxicology for at least to non-fibrous10 years in communitieswhereforms. Aluminium oxide drinking fibres water administered contained bymore the thanintrapleural 0.15 mg/l route aluminium produce compared clear evidence withcommunities of carcinogenicity. where the aluminiumSaffil fibre anlevel artificially was lower produced than 0.1 form mg/l. alumina A neurochemicalmodel fibre used as refractories, has been consistssuggested of linkingover 95% aluminium alumina, exposure 3-4 % silica. to brain Animal disease. tests Aluminiumconcentrates for fibrogenic, in braincarcinogenic regions, potential notably theand hippocampus, oral toxicity have cerebral included cortex in-vitro, andamygdala intraperitoneal where injection,it preferentially intrapleural binds injection,to large pyramid-shaped inhalation, and feeding.cells - it doesnotThe fibre bind has to generally a beensubstantial inactive degree in animal to the studies. smaller Also interneurons. studies of SaffilAluminiumdisplaces dust clouds show magnesium very low respirable in key metabolic fraction. reactions in brain cells and alsointerferes with calcium metabolismThere is general and inhibitsagreement phosphoinositide that particle size metabolism.Phosphoinositide determines that the degree normally of pathogenicity controls calcium(the ability ion of levels a micro-organism at criticalconcentrations. to produce infectious disease) of elementaryUnder the microscope aluminium, theor its brain oxides of ADor hydroxides sufferers show when thickened they occur fibrils(neurofibrillary as dusts, fumes or tanglesvapours. - NFT)Only thoseand plaques particles consisting small enough of amyloid to enter proteindeposited the alveolii (sub in5 the matrixum) are between able to producebrain cells. pathogenic Tangles result effects from in the alteration lungs. of'tau' a brain cytoskeletal protein. AD tau is distinguished fromnormal tau because it is hyperphosphorylated.Occupational exposure Aluminium to aluminium hyperphosphorylates compounds may produce tauin vitro. asthma,chronic When AD tau obstructive is injected lung into diseaserat brain and NFT-like pulmonary aggregates fibrosis. form Long-term butsoon overexposuremay degrade. Aluminium producestabilises dyspnoea, these aggregates cough, pneumothorax, rendering them variable resistant sputum toprotease production degradation. andnodular Plaque interstitial formation fibrosis; is also death enhanced has been by aluminium reported. Chronic whichinduces interstitialpneumonia the accumulation withof amyloid severe precursor cavitations protein in the in right the thread-likeextensionsupper lung and small ofcavities nerve inthecells remaining(axons and lung dendrites). tissue, haveIn addition been aluminiumobserved in has gross beenshown pathology. to Shaver'sDiseasedepress the activity may of mostresult neuro-transmitters from occupational similarlyexposure depressed to fumes orinAD dusts; (acetylcholine, this mayproduce norepinephrine, respiratory glutamatedistress and and fibrosis GABA). with large blebs. Animal studiesproduce no indication Aluminiumthat aluminium enters or itsthe compounds brain in measurable are carcinogenic. quantities, even whentrace levels are contained in a glass of tap water. Other sources ofbioavailable aluminium Becauseinclude baking aluminium powder, competes antacids with and calcium aluminium for absorption, productsused increasedamounts for general food of preparation dietary aluminium and storage may (overcontribute 12 months, to the reducedaluminium skeletalmineralisation levelsin soft drink packed in aluminium(osteopenia) cans observed rose from in preterm 0.05 to infants0.9 mg/l). and [ Walton,Jinfants with and growthretardation. Bryson-Taylor, D. In - veryChemistry high doses, in Australia, aluminium August can 1995 cause] neurotoxicity, and isassociated with alteredAll glycidyl function ethers of show the blood-brain genotoxic potentialbarrier. A due small their percentageof alkylating properties. people are Those allergic glycidyl to aluminium ethers that and have experience been investigated contact dermatitis,digestive in long term studies disorders, exhibit more or less marked carcinogenic potential. Alkylating agents may damage the stem cell which acts as the precursor to components of the blood. Loss of the stem Version No: 4.7 vomiting or other symptoms upon contact or ingestionPage ofproducts 10 of 20 containing aluminium, such as deodorants or antacids. In those withoutallergies,Issue Date:aluminium 29/07/2016 is notcell asmay toxic result as heavyin pancytopenia metals, but (a there reduction is evidence in the numberofsome toxicityof red and if it iswhite consumed blood cells in excessive and platelets) amounts. with Although a latency the period use correspondingofaluminium cookware to the lifetime has not of beenthe Print Date: 29/07/2016 shownindividual8329TFS to leadblood to Slowcells. aluminium Granulocytopenia Cure, toxicity Thermally in general,excessive (a reduction Conductive in granular consumption leukocytes) Adhesive, of antacids develops containing Flowable within aluminiumdays and (Part thrombocytopenia compounds A) and excessiveuse (a disorder involving of aluminium-containing platelets), within 1-2antiperspirants weeks, whilst provide loss of more erythrocytes significant (red exposurelevels. blood cells) need Studies months have to shownbecome that clinically consumption manifest. of Aplasticacidic foods anaemia or liquids develops withaluminium due to complete significantly destruction increases of the aluminiumstem cells. absorption, and maltol has beenshown to increase the accumulation of aluminium in nervous and osseus tissue.Furthermore, aluminium increases oestrogen-relatedGlycidyl ethers have gene been expression shown to incause human allergic breastcancer contact dermatitis cells cultured in humans. in the laboratory Glycidyl ethers These generally salts' estrogen-like cause skin effectssensitization haveled in experimental to their classification animals. as a Necrosismetalloestrogen.Some of the mucous researchers membranes haveexpressed of the nasal cavities concerns was inducedthat the aluminiumin mice exposed in antiperspirants to allyl glycidyl may ether. increase the riskof breast cancer. AAfter study absorption, of workers aluminium with mixed distributes exposures to wasall tissues inconclusive in animalsand with regard humans to the and effects accumulates of specific in glycidyl some, ethers.in particular Phenyl bone. glycidyl The ether, main carrierbut not ofn-butyl thealuminium glycidylContinued... ion ether,in plasma induced is the morphological iron binding protein, transformation transferrin. in mammalian Aluminium canentercells in vitro the. brainn-Butyl and glycidyl reach etherthe placenta induced and micronuclei foetus. Aluminium in mice in may vivo persistfollowing for intraperitonealavery long time but in notvarious oral organsadministration. and tissues Phenyl before glycidyl it is excretedether did innot theurine. induce micronucleiAlthough retention or chromosomal times for aluminiumaberrations appear in vivo to or be chromosomal longer in humansthan aberrations in inrodents, animal therecells inis little Chronic vitroinformation. Alkyl C12 allowing or C14 extrapolation glycidyl ether fromrodents did not induce to the DNA humans. damage in cultured human cells or mutation in cultured animal cells. Allyl glycidyl ether induced mutationAt high levels in Drosophila of exposure,. The some glycidyl aluminium ethers werecompounds generally may mutagenic produceDNA to bacteria damage in vitro and in vivo via indirect mechanisms. The database oncarcinogenicity Onof aluminium the basis, compoundsprimarily, of isanimal limited. experiments, No indication concern of anycarcinogenic has been expressed potential by was at least obtained one classification in mice given body aluminium that the potassium material may sulphateat produce high carcinogenic levels in the or mutagenicdiet. effects; in respect of the available information, however, there presently exists inadequate data for making a satisfactory assessment. ZincAluminium is necessary has shown for normal neurotoxicity fetal growth in patients and development. undergoing dialysisand Fetal damage thereby may chronicallyresult from exposed zinc deficiency. parenterally Only oneto high report concentrations in the literature ofaluminium. suggested It adversehas been developmentalsuggested that effectsaluminium in humans is implicated due to in exposure the aetiologyof to excessive Alzheimer’s levels ofdisease zinc. Four and womenassociated were with given other zinc neurodegenerative supplements of 0.6 diseases mg zinc/kg/day inhumans. as However,zinc sulfate duringthese hypotheses the third trimester remain ofcontroversial. pregnancy. ThreeSeveral of compoundscontaining the women had premature aluminium deliveries, have and the potentialone delivered to produce a stillborn neurotoxicity infant. However, (mice, rats)and the significance to affect ofthe these male resultsreproductive cannot system be determined (dogs). In because addition, very after few maternalexposure details were given they regarding have shown the studyembryotoxicity protocol, (mice)reproductive and have histories, affected and the the developingnervous nutritional status ofsystem the women. in the Otheroffspring human (mice, studies rats). haveThe available found no studiesdevelopmental have anumber effects ofin thelimitations newborns and of do mothers not allow consuming any dose-response 0.3 mg zinc/kg/day relationships as zinc to beestablished.sulfate or zinc citrateThe combined or 0.06 mg zinc/kg/dayevidence from as severalzinc aspartate studies during in mice, the rats last and two dogsthat trimesters. used There dietary has administration been a suggestion of aluminium that increased compounds serum producelowest-observed-adverse-effect zinc levels in pregnant women may be levels associated(LOAELs) forwith effects an increase on neurotoxicity,testes, in neural tube defects, embryotoxicity, but others and have the failed developing to confirm nervous this systemassociation. of 52, The 75, developmental100, and50 mg toxicityaluminium/kg of zinc bw/day,in experimental respectively. animals hasSimilarly, been evaluatedthe lowestno-observed-adverse-effect in a number of investigations. levels Exposure (NOAELs) to high for levels effects of on zinc these in the endpoints diet prior werereported to and/or during at 30, gestation 27, 100, has and been for effects associated on the with developing increased fetalnervous resorptions, system,between reduced 10 fetal and weights, 42 mg aluminium/kg altered tissue bw concentrations per day, respectively. of fetal iron and copper, and reduced growth in the offspring. AnimalControversy studies exists suggest over that whether exposure aluminium to very is high the causelevels ofofdegenerative dietary zinc is brain associated disease with (Alzheimer's reduced fetal disease weight, or AD).alopecia, Several decreased epidemiologicalstudies hematocrit, and showcopper a deficiencypossible correlation in offspring. between For example, the incidence second of generation AD and high mice levelsof exposed aluminium to zinc carbonatein drinking duringwater. gestationA study in and Toronto, lactation for example,(260 mg/kg/day found a in 2.6times the maternal increased diet), risk andin people then continued residing for on at that least diet 10 for years 8 weeks, in communitieswhere had reduced body drinking weight, water alopecia, contained and signs more of than copper 0.15 deficiency mg/l aluminium (e.g., lowered compared hematocrit withcommunities and occasional where the achromotrichiaaluminium level [losswas lowerof hair than colour]. 0.1 mg/l. Similarly, A neurochemicalmodel mink kits from dams has that been ingested suggested a time-weighted-average linking aluminium exposure dose of 20.8to brain mg disease.zinc/kg/day Aluminiumconcentrates as zinc sulfate also had in alopeciabrain regions, and achromotrichia. notably the hippocampus, It is likely that cerebral the alopecia cortex andamygdalaresulted from zinc-inducedwhere it preferentially copper deficiency, binds to large which pyramid-shaped is known to cause cells alopecia - it doesnot in monkeys. bind to However,a nosubstantial adverse degreeeffects wereto the observed smaller interneurons. in parental mice Aluminiumdisplaces or mink. No effects magnesium on reproduction in key were metabolic reported reactions in rats exposedin brain cells to 50 and mg alsointerfereszinc/kg/day as with zinc calcium carbonate; however,metabolism increased and inhibits stillbirths phosphoinositide were observed metabolism.Phosphoinositide in rats exposed to 250 mg zinc/kg/day. normally controls calcium ion levels at criticalconcentrations. WeldingUnder the or microscopeflame cutting the of brainmetals of with AD suffererszinc or zinc show dust thickened coatings mayfibrils(neurofibrillary result in inhalation tangles of zinc - NFT) oxide and fume; plaques high concentrations consisting of amyloid of zinc proteindepositedoxide fume may result in the inmatrix 'metal between fume fever'; brain also cells. known Tangles as 'brassresult fromchills', alteration an industrial of'tau' disease a brain of cytoskeletal short duration. protein. [I.L.O] AD Symptoms tau is distinguished include malaise, fromnormal fever, weakness,tau because nausea it is and may appearhyperphosphorylated. quickly if operations Aluminium occur hyperphosphorylatesin enclosed or poorly tauinventilated vitro. areas.When AD tau is injected into rat brain NFT-like aggregates form butsoon degrade. Aluminium Genotoxicitystabilises these studies aggregates conducted rendering in a variety them of resistant test systems toprotease have failed degradation. to provide Plaque evidence formation for mutagenicity is also enhanced of zinc. However,by aluminium there whichinduces are indications the of accumulation weak clastogenicof amyloid precursor effects following protein inzinc the exposure. thread-likeextensions of nerve cells (axons and dendrites). In addition aluminium has beenshown to depress the activity of Bisphenolmost neuro-transmitters F, bisphenol A, similarly fluorine-containing depressed inADbisphenol (acetylcholine, A (bisphenol norepinephrine, AF), and other glutamate diphenylalkanes and GABA). were found to be oestrogenic in a bioassay with MCF7 humanAluminium breast enters cancer the cellsbrain in in culturemeasurable Bisphenol quantities, F (4,4'-dihydroxydiphenylmethane) even whentrace levels are contained has been in areported glass of to tap exhibit water. oestrogen Other sources agonistic ofbioavailable properties aluminiumin the uterotrophicinclude baking assay. powder, Bisphenol antacids F (BPF) and aluminium is present productsusedin the environment for general and as food a contaminant preparation of and food. storage Humans (over may, 12 months,therefore, aluminium be exposed levelsin to BP. soft BPF drink has packedbeen in shownaluminium to have cans genotoxic rose from and 0.05 endocrine-disruptor to 0.9 mg/l). [Walton,J properties and Bryson-Taylor, in a human hepatoma D. - Chemistry cell line in (HepG2), Australia, which August is a1995 model] system for studies of xenobiotic toxicity. BPFAll glycidyl was largely ethers metabolised show genotoxic into thepotential corresponding due their sulfatealkylating by theproperties. HepG2 Thosecell line. glycidyl BPF was ethers metabolised that have intobeen both investigated sulfate and in glucuronidelong term studies by human exhibit more hepatocytes,or less marked but carcinogenic with differences potential. between Alkylating individuals. agents The may metabolism damage theof BPF stem in cell both which HepG2 acts cells as theand precursor human hepatocytes to components suggests of the the blood. existence Loss of of the a stem detoxificationcell may result pathway in pancytopenia (a reduction in the number of red and white blood cells and platelets) with a latency period corresponding to the lifetime of the Bisphenolindividual bloodF was cells. orally Granulocytopenia administered at doses (a reduction 0, 20, 100 in granular and 500 leukocytes) mg/kg per day develops for at least within 28 days days, and but thrombocytopenia no clear endocrine-mediated (a disorder involvingchanges platelets),were detected, within and1-2 weeks,it was concluded whilst loss to of have erythrocytes no endocrine-mediated (red blood cells) effects need monthsin young to adult become rats. clinicallyOn the other manifest. hand, Aplastic the main anaemia effect of develops bisphenol due F was to complete concluded destruction to be liver of the toxicitystem cells. based on clinical biochemical parameters and liver weight, but without histopathological changes. The no-observed-effect level for bisphenol F is concludedGlycidyl ethers to be have under been 20 mg/kg shown per to daycause since allergic decreased contact body dermatitis weight in accompanied humans. Glycidyl by decreased ethers generally serum totalcause cholesterol, skin sensitization glucose, in and experimental albumin values animals. were observed in the female rats given 20 mg/kg per day or higher doses of bisphenol F. Bisphenol A exhibits hormone-like properties that raise concern about its suitability in consumer products and food containers. Bisphenol A is thoughtContinued... to be an endocrine disruptor which can mimic oestrogen and may lead to negative health effects. More specifically, bisphenol A closely mimics the structure and function of the hormone oestradiol with the ability to bind to and activate the same oestrogen receptor as the natural hormone.. Early developmental stages appear to be the period of greatest sensitivity to its effects and some studies have linked prenatal exposure to later physical and neurological difficulties. Regulatory bodies www.element14.com have determined safety levels for humans, but those safety levels are being questioned or are under review. A 2009 study on Chinese workers in bisphenol A factories found that workers were four times more likely to report erectile dysfunction, reduced sexual desire www.farnell.com and overall dissatisfaction with their sex life than workers with no heightened bisphenol A exposure. Bisphenol A workers were also seven times more likely to www.newark.com have ejaculation difficulties. They were also more likely to report reduced sexual function within one year of beginning employment at the factory, and the higher the exposure, the more likely they were to have sexual difficulties. Bisphenol A in weak concentrations is sufficient to produce a negative reaction on the human testicle. The researchers found that a concentration equal to 2 ug/ litre of bisphenol A in the culture medium, a concentrationPage equal <11> to the average concentration generally found in the blood, urine and amniotic28/10/18 fluid of the V1.0 population, was sufficient to produce the effects. The researchers believe that exposure of pregnant women to bisphenol A may be one of the causes of congenital masculinisation defects of the hypospadia and cryptorchidism types the frequency of which has doubled overall since the 70's. They also suggested that 'it is also possible that bisphenol A contributes to a reduction in the production of sperm and the increase in the incidence of testicular cancer in adults that have been observed in recent decades' One review has concluded that obesity may be increased as a function of bisphenol A exposure, which '...merits concern among scientists and public health officials' One study demonstrated that adverse neurological effects occur in non-human primates regularly exposed to bisphenol A at levels equal to the United States Environmental Protection Agency's (EPA) maximum safe dose of 50 ug/kg/day This research found a connection between bisphenol A and interference with brain cell connections vital to memory, learning, and mood. A further review concluded that bisphenol-A has been shown to bind to thyroid hormone receptor and perhaps have selective effects on its functions. Carcinogenicity studies have shown increases in leukaemia and testicular interstitial cell tumours in male rats. However, 'these studies have not been considered as convincing evidence of a potential cancer risk because of the doubtful statistical significance of the small differences in incidences from controls'. Another in vitro study has concluded that bisphenol A is able to induce neoplastic transformation in human breast epithelial cells.[whilst a further study concluded that maternal oral exposure to low concentrations of bisphenol A, during lactation, increases mammary carcinogenesis in a rodent model. In vitro studies have suggested that bisphenol A can promote the growth of neuroblastoma cells and potently promotes invasion and metastasis of neuroblastoma cells. Newborn rats exposed to a low-dose of bisphenol A (10 ug/kg) showed increased prostate cancer susceptibility when adults. At least one study has suggested that bisphenol A suppresses DNA methylation which is involved in epigenetic changes. Bisphenol A is the isopropyl adduct of 4,4'-dihydroxydiphenyl oxide (DHDPO). A series of DHDPO analogues have been investigated as potential oestrogen receptor/anti-tumour drug carriers in the development of a class of therapeutic drugs called 'cytostatic hormones'. Oestrogenic activity is induced with 1 to 100 mg/kg body weight in animal models. Bisphenol A sealants are frequently used in dentistry for treatment of dental pits and fissures. Samples of saliva collected from dental patients during a 1-hour period following application contain the monomer. A bisphenol-A sealant has been shown to be oestrogenic in vitro; such sealants may represent an additional source of xenoestrogens in humans and may be the cause of additional concerns in children. Concerns have been raised about the possible developmental effects on the foetus/embryo or neonate resulting from the leaching of bisphenol A from epoxy linings in metal cans which come in contact with food-stuffs. Many drugs, including naproxen, salicylic acid, carbamazepine and mefenamic acid can, in vitro, significantly inhibit bisphenol A glucuronidation (detoxification).

Slow Cure, TOXICITY IRRITATION Thermally Conductive Adhesive, Flowable (Part A) Not Available Not Available

Continued... Version No: 4.7 Page 10 of 20 Issue Date: 29/07/2016 Print Date: 29/07/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part A)

Necrosis of the mucous membranes of the nasal cavities was induced in mice exposed to allyl glycidyl ether. A study of workers with mixed exposures was inconclusive with regard to the effects of specific glycidyl ethers. Phenyl glycidyl ether, but not n-butyl glycidyl Version No: 4.7 ether, induced morphological transformation in mammalianPage 9 of cells 20 in vitro. n-Butyl glycidyl ether induced micronuclei in mice in vivo following Issueintraperitoneal Date: 29/07/2016 but not oral administration. Phenyl glycidyl ether did not induce micronuclei or chromosomal aberrations in vivo or chromosomal aberrations in animalPrint Date: cells in29/07/2016 vitro8329TFS. Alkyl C12 orSlow C14 glycidyl Cure, ether Thermally did not induce Conductive DNA damage in culturedAdhesive, human Flowablecells or mutation (Part in cultured A) animal cells. Allyl glycidyl ether induced mutation in Drosophila. The glycidyl ethers were generally mutagenic to bacteria On the basis, primarily, of animal experiments, concern has been expressed by at least one classification body 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. Zinc is necessary for normal fetal growth and development. Fetal damage may result from zinc deficiency. Only one report in the literature suggested adverse Evidence exists, or practical experience predicts, that the material either produces inflammation of the skin in a substantial number of individuals following developmental effects in humans due to exposure to excessive levels of zinc. Four women were given zinc supplements of 0.6 mg zinc/kg/day as zinc sulfate direct contact, and/or produces significant inflammation when applied to the healthy intact skin of animals, for up to four hours, such inflammation being present during the third trimester of pregnancy. Three of the women had premature deliveries, and one delivered a stillborn infant. However, the significance of these 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 results cannot be determined because very few details were given regarding the study protocol, reproductive histories, and the nutritional status of the women. form of contact dermatitis (nonallergic). The dermatitis is often characterised by skin redness (erythema) and swelling (oedema) which may progress to Other human studies have found no developmental effects in the newborns of mothers consuming 0.3 mg zinc/kg/day as zinc sulfate or zinc citrate or 0.06 mg blistering (vesiculation), scaling and thickening of the epidermis. At the microscopic level there may be intercellular oedema of the spongy layer of the skin Skin Contact zinc/kg/day as zinc aspartate during the last two trimesters. There has been a suggestion that increased serum zinc levels in pregnant women may be (spongiosis) and intracellular oedema of the epidermis. associated with an increase in neural tube defects, but others have failed to confirm this association. The developmental toxicity of zinc in experimental animals The material may accentuate any pre-existing dermatitis condition has been evaluated in a number of investigations. Exposure to high levels of zinc in the diet prior to and/or during gestation has been associated with increased Skin contact is not thought to have harmful health effects (as classified under EC Directives); the material may still produce health damage following entry fetal resorptions, reduced fetal weights, altered tissue concentrations of fetal iron and copper, and reduced growth in the offspring. through wounds, lesions or abrasions. Animal studies suggest that exposure to very high levels of dietary zinc is associated with reduced fetal weight, alopecia, decreased hematocrit, and copper Contact with aluminas (aluminium oxides) may produce a form of irritant dermatitis accompanied by pruritus. deficiency in offspring. For example, second generation mice exposed to zinc carbonate during gestation and lactation (260 mg/kg/day in the maternal diet), Though considered non-harmful, slight irritation may result from contact because of the abrasive nature of the aluminium oxide particles. and then continued on that diet for 8 weeks, had reduced body weight, alopecia, and signs of copper deficiency (e.g., lowered hematocrit and occasional achromotrichiaEvidence exists, [loss or practical of hair colour].experience Similarly, predicts, mink that kits the from material dams maythat ingestedcause eye a time-weighted-averageirritation in a substantial dosenumber of 20.8 of individuals mg zinc/kg/day and/or as may zinc produce sulfate significantalso had alopeciaocular lesions and achromotrichia. which are present It is twenty-fourlikely that the hours alopecia or more resulted after instillationfrom zinc-induced into the eye(s)copper of deficiency, experimental which animals. is known to cause alopecia in monkeys. However, Eye noRepeated adverse or effects prolonged were eyeobserved contact in mayparental cause mice inflammation or mink. No characterised effects on reproduction by temporary were redness reported (similar in rats to exposed windburn) to of50 the mg conjunctiva zinc/kg/day (conjunctivitis); as zinc carbonate; however,temporary increased impairment stillbirths of vision were and/or observed other transient in rats exposed eye damage/ulceration to 250 mg zinc/kg/day. may occur. Welding or flame cutting of metals with zinc or zinc dust coatings may result in inhalation of zinc oxide fume; high concentrations of zinc oxide fume may result 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 in 'metal fume fever'; also known as 'brass chills', an industrial disease of short duration. [I.L.O] Symptoms include malaise, fever, weakness, nausea and may of producing a positive response in experimental animals. appear quickly if operations occur in enclosed or poorly ventilated areas. Chronic exposure to aluminas (aluminium oxides) of particle size 1.2 microns did not produce significant systemic or respiratory system effects in workers. Genotoxicity studies conducted in a variety of test systems have failed to provide evidence for mutagenicity of zinc. However, there are indications of weak When hydrated aluminas were injected intratracheally, they produced dense and numerous nodules of advanced fibrosis in rats, a reticulin network with clastogenic effects following zinc exposure. occasional collagen fibres in mice and guinea pigs, and only a slight reticulin network in rabbits. Shaver's disease, a rapidly progressive and often fatal Bisphenol F, bisphenol A, fluorine-containing bisphenol A (bisphenol AF), and other diphenylalkanes were found to be oestrogenic in a bioassay with MCF7 interstitial fibrosis of the lungs, is associated with a process involving the fusion of bauxite (aluminium oxide) with iron, coke and silica at 2000 deg. C. human breast cancer cells in culture Bisphenol F (4,4'-dihydroxydiphenylmethane) has been reported to exhibit oestrogen agonistic properties in the The weight of evidence suggests that catalytically active alumina and the large surface area aluminas can induce lung fibrosis(aluminosis) in experimental uterotrophic assay. Bisphenol F (BPF) is present in the environment and as a contaminant of food. Humans may, therefore, be exposed to BP. BPF has been animals, but only when given by the intra-tracheal route. The pertinence of such experiments in relation to workplace exposure is doubtful especially since it has shown to have genotoxic and endocrine-disruptor properties in a human hepatoma cell line (HepG2), which is a model system for studies of xenobiotic toxicity. been demonstrated that the most reactive of the aluminas (i.e. the chi and gamma forms), when given by inhalation, are non-fibrogenic in experimental animals. BPF was largely metabolised into the corresponding sulfate by the HepG2 cell line. BPF was metabolised into both sulfate and glucuronide by human However rats exposed by inhalation to refractory aluminium fibre showed mild fibrosis and possibly carcinogenic effects indicating that fibrous aluminas might hepatocytes, but with differences between individuals. The metabolism of BPF in both HepG2 cells and human hepatocytes suggests the existence of a exhibit different toxicology to non-fibrous forms. Aluminium oxide fibres administered by the intrapleural route produce clear evidence of carcinogenicity. detoxification pathway Safety DataSaffil fibre an artificially Sheet produced form alumina fibre used as refractories, consists of over 95% alumina, 3-4 % silica. Animal tests for fibrogenic, Bisphenol F was orally administered at doses 0, 20, 100 and 500 mg/kg per day for at least 28 days, but no clear endocrine-mediated changes were detected, carcinogenic potential and oral toxicity have included in-vitro, intraperitoneal injection, intrapleural injection, inhalation, and feeding. The fibre has generally and it was concluded to have no endocrine-mediated effects in young adult rats. On the other hand, the main effect of bisphenol F was concluded to be liver been inactive in animal studies. Also studies of Saffil dust clouds show very low respirable fraction. toxicity based on clinical biochemical parameters and liver weight, but without histopathological changes. The no-observed-effect level for bisphenol F is There is general agreement that particle size determines that the degree of pathogenicity (the ability of a micro-organism to produce infectious disease) of concluded to be under 20 mg/kg per day since decreased body weight accompanied by decreased serum total cholesterol, glucose, and albumin values were elementary aluminium, or its oxides or hydroxides when they occur as dusts, fumes or vapours. Only those particles small enough to enter the alveolii (sub 5 observed in the female rats given 20 mg/kg per day or higher doses of bisphenol F. um) are able to produce pathogenic effects in the lungs. Bisphenol A exhibits hormone-like properties that raise concern about its suitability in consumer products and food containers. Bisphenol A is thought to be an Occupational exposure to aluminium compounds may produce asthma,chronic obstructive lung disease and pulmonary fibrosis. Long-term overexposuremay endocrine disruptor which can mimic oestrogen and may lead to negative health effects. More specifically, bisphenol A closely mimics the structure and function produce dyspnoea, cough, pneumothorax, variable sputum production andnodular interstitial fibrosis; death has been reported. Chronic interstitialpneumonia of the hormone oestradiol with the ability to bind to and activate the same oestrogen receptor as the natural hormone.. Early developmental stages appear to be with severe cavitations in the right upper lung and small cavities inthe remaining lung tissue, have been observed in gross pathology. Shaver'sDisease may the period of greatest sensitivity to its effects and some studies have linked prenatal exposure to later physical and neurological difficulties. Regulatory bodies result from occupational exposure to fumes or dusts; this mayproduce respiratory distress and fibrosis with large blebs. Animal studiesproduce no indication have determined safety levels for humans, but those safety levels are being questioned or are under review. that aluminium or its compounds are carcinogenic. A 2009 study on Chinese workers in bisphenol A factories found that workers were four times more likely to report erectile dysfunction, reduced sexual desire Because aluminium competes with calcium for absorption, increasedamounts of dietary aluminium may contribute to the reduced skeletalmineralisation and overall dissatisfaction with their sex life than workers with no heightened bisphenol A exposure. Bisphenol A workers were also seven times more likely to (osteopenia) observed in preterm infants and infants with growthretardation. In very high doses, aluminium can cause neurotoxicity, and isassociated with have ejaculation difficulties. They were also more likely to report reduced sexual function within one year of beginning employment at the factory, and the higher altered function of the blood-brain barrier. A small percentageof people are allergic to aluminium and experience contact dermatitis,digestive disorders, the exposure, the more likely they were to have sexual difficulties. vomiting or other symptoms upon contact or ingestion ofproducts containing aluminium, such as deodorants or antacids. In those withoutallergies, aluminium is Bisphenol A in weak concentrations is sufficient to produce a negative reaction on the human testicle. The researchers found that a concentration equal to 2 ug/ not as toxic as heavy metals, but there is evidence ofsome toxicity if it is consumed in excessive amounts. Although the use ofaluminium cookware has not been litre of bisphenol A in the culture medium, a concentration equal to the average concentration generally found in the blood, urine and amniotic fluid of the shown to lead to aluminium toxicity in general,excessive consumption of antacids containing aluminium compounds and excessiveuse of aluminium-containing population, was sufficient to produce the effects. The researchers believe that exposure of pregnant women to bisphenol A may be one of the causes of antiperspirants provide more significant exposurelevels. Studies have shown that consumption of acidic foods or liquids withaluminium significantly increases congenital masculinisation defects of the hypospadia and cryptorchidism types the frequency of which has doubled overall since the 70's. They also suggested aluminium absorption, and maltol has beenshown to increase the accumulation of aluminium in nervous and osseus tissue.Furthermore, aluminium increases that 'it is also possible that bisphenol A contributes to a reduction in the production of sperm and the increase in the incidence of testicular cancer in adults that oestrogen-related gene expression in human breastcancer cells cultured in the laboratory These salts' estrogen-like effects haveled to their classification as a have been observed in recent decades' metalloestrogen.Some researchers haveexpressed concerns that the aluminium in antiperspirants may increase the riskof breast cancer. One review has concluded that obesity may be increased as a function of bisphenol A exposure, which '...merits concern among scientists and public health After absorption, aluminium distributes to all tissues in animalsand humans and accumulates in some, in particular bone. The main carrier of thealuminium ion officials' in plasma is the iron binding protein, transferrin. Aluminium canenter the brain and reach the placenta and foetus. Aluminium may persist for avery long time in One study demonstrated that adverse neurological effects occur in non-human primates regularly exposed to bisphenol A at levels equal to the United States various organs and tissues before it is excreted in theurine. Although retention times for aluminium appear to be longer in humansthan in rodents, there is little Environmental Protection Agency's (EPA) maximum safe dose of 50 ug/kg/day This research found a connection between bisphenol A and interference with Chronic information allowing extrapolation fromrodents to the humans. brain cell connections vital to memory, learning, and mood. At high levels of exposure, some aluminium compounds may produceDNA damage in vitro and in vivo via indirect mechanisms. The database oncarcinogenicity A further review concluded that bisphenol-A has been shown to bind to thyroid hormone receptor and perhaps have selective effects on its functions. of aluminium compounds is limited. No indication of anycarcinogenic potential was obtained in mice given aluminium potassium sulphateat high levels in the Carcinogenicity studies have shown increases in leukaemia and testicular interstitial cell tumours in male rats. However, 'these studies have not been diet. considered as convincing evidence of a potential cancer risk because of the doubtful statistical significance of the small differences in incidences from Aluminium has shown neurotoxicity in patients undergoing dialysisand thereby chronically exposed parenterally to high concentrations ofaluminium. It has been controls'. Another in vitro study has concluded that bisphenol A is able to induce neoplastic transformation in human breast epithelial cells.[whilst a further study suggested that aluminium is implicated in the aetiologyof Alzheimer’s disease and associated with other neurodegenerative diseases inhumans. However, concluded that maternal oral exposure to low concentrations of bisphenol A, during lactation, increases mammary carcinogenesis in a rodent model. In vitro these hypotheses remain controversial. Several compoundscontaining aluminium have the potential to produce neurotoxicity (mice, rats)and to affect the male studies have suggested that bisphenol A can promote the growth of neuroblastoma cells and potently promotes invasion and metastasis of neuroblastoma cells. reproductive system (dogs). In addition, after maternalexposure they have shown embryotoxicity (mice) and have affected the developingnervous system in the Newborn rats exposed to a low-dose of bisphenol A (10 ug/kg) showed increased prostate cancer susceptibility when adults. At least one study has suggested offspring (mice, rats). The available studies have anumber of limitations and do not allow any dose-response relationships to beestablished. The combined that bisphenol A suppresses DNA methylation which is involved in epigenetic changes. evidence from several studies in mice, rats and dogsthat used dietary administration of aluminium compounds producelowest-observed-adverse-effect levels Bisphenol A is the isopropyl adduct of 4,4'-dihydroxydiphenyl oxide (DHDPO). A series of DHDPO analogues have been investigated as potential oestrogen (LOAELs) for effects on neurotoxicity,testes, embryotoxicity, and the developing nervous system of 52, 75, 100, and50 mg aluminium/kg bw/day, respectively. receptor/anti-tumour drug carriers in the development of a class of therapeutic drugs called 'cytostatic hormones'. Oestrogenic activity is induced with 1 to 100 Similarly, the lowestno-observed-adverse-effect levels (NOAELs) for effects on these endpoints werereported at 30, 27, 100, and for effects on the developing mg/kg body weight in animal models. Bisphenol A sealants are frequently used in dentistry for treatment of dental pits and fissures. Samples of saliva collected nervous system,between 10 and 42 mg aluminium/kg bw per day, respectively. from dental patients during a 1-hour period following application contain the monomer. A bisphenol-A sealant has been shown to be oestrogenic in vitro; such Controversy exists over whether aluminium is the cause ofdegenerative brain disease (Alzheimer's disease or AD). Several epidemiologicalstudies show a sealants may represent an additional source of xenoestrogens in humans and may be the cause of additional concerns in children. possible correlation between the incidence of AD and high levelsof aluminium in drinking water. A study in Toronto, for example, found a 2.6times increased risk Concerns have been raised about the possible developmental effects on the foetus/embryo or neonate resulting from the leaching of bisphenol A from epoxy in people residing for at least 10 years in communitieswhere drinking water contained more than 0.15 mg/l aluminium compared withcommunities where the linings in metal cans which come in contact with food-stuffs. aluminium level was lower than 0.1 mg/l. A neurochemicalmodel has been suggested linking aluminium exposure to brain disease. Aluminiumconcentrates in Many drugs, including naproxen, salicylic acid, carbamazepine and mefenamic acid can, in vitro, significantly inhibit bisphenol A glucuronidation brain regions, notably the hippocampus, cerebral cortex andamygdala where it preferentially binds to large pyramid-shaped cells - it doesnot bind to a (detoxification). substantial degree to the smaller interneurons. Aluminiumdisplaces magnesium in key metabolic reactions in brain cells and alsointerferes with calcium metabolism and inhibits phosphoinositide metabolism.Phosphoinositide normally controls calcium ion levels at criticalconcentrations. Version No: 4.7 Under the microscope the brain of AD sufferers showPage thickened 11 of 20 fibrils(neurofibrillary tangles - NFT) and plaques consisting of amyloid proteindepositedIssue Date: 29/07/2016 in the matrix between brain cells. Tangles result from alteration of'tau' a brain cytoskeletal protein. AD tau is distinguished fromnormal tau because it is Slow Cure, Print Date: 29/07/2016 hyperphosphorylated.TOXICITY8329TFS Slow Aluminium Cure, hyperphosphorylatesThermally Conductive tauin vitro. When Adhesive, AD tau isIRRITATION injected Flowable into rat brain (Part NFT-like A) aggregates form butsoon degrade. Aluminium Thermally Conductive stabilises these aggregates rendering them resistant toprotease degradation. Plaque formation is also enhanced by aluminium whichinduces the accumulation Adhesive, Flowable (Part A) Not Available Not Available of amyloid precursor protein in the thread-likeextensions of nerve cells (axons and dendrites). In addition aluminium has beenshown to depress the activity of most neuro-transmitters similarly depressed inAD (acetylcholine, norepinephrine, glutamate and GABA). Aluminium enters the brain in measurable quantities, even whentrace levels are contained in a glass of tap water. Other sources ofbioavailable aluminium includeTOXICITY baking powder, antacids and aluminium productsused for general food preparation and storage (over 12 IRRITATIONmonths, aluminium levelsin soft drink packed in aluminium oxide aluminium cans rose from 0.05 to 0.9 mg/l). [Walton,J and Bryson-Taylor, D. - Chemistry in Australia, August 1995] Oral (rat) LD50: >2000 mg/kg[1] Not Available All glycidyl ethers show genotoxic potential due their alkylating properties. Those glycidyl ethers that have been investigated in long term studies exhibitContinued... more or less marked carcinogenic potential. Alkylating agents may damage the stem cell which acts as the precursor to components of the blood. Loss of the stem cell may result in pancytopenia (a reduction in the number of red and white blood cells and platelets) with a latency period corresponding to the lifetime of the individualTOXICITY blood cells. Granulocytopenia (a reduction in granular leukocytes) develops withinIRRITATION days and thrombocytopenia (a disorder involving platelets), within 1-2 weeks, whilst loss of erythrocytes (red blood cells) need months to become clinically manifest. Aplastic anaemia develops due to complete destruction of the [2] * [Ciba-Geigy] stemdermal cells. (rat) LD50: 4000 mg/kg Glycidyl ethers have been shown[2] to cause allergic contact dermatitis in humans. Glycidyl ethers generally cause skin sensitization in experimental animals. bisphenol F glycidyl ether/ Oral (rat) LD50: 4000 mg/kg Effects transient formaldehyde copolymer Eyes * (-) (-) Slight irritant Continued... May cause allergic response Skin * (-) (-) Slight irritant

TOXICITY IRRITATION

zinc oxide Oral (rat) LD50: >5000 mg/kg[1] Eye (rabbit) : 500 mg/24 h - mild Skin (rabbit) : 500 mg/24 h- mild

TOXICITY IRRITATION

Oral (rat) LD50: 16896 mg/kg[1] Eye (rabbit): mild [Ciba] Skin (guinea pig): sensitiser (C12-14)alkylglycidyl ether Skin (human): Irritant Skin (human): non- sensitiser Skin (rabbit): moderate www.element14.com Skin : Moderate www.farnell.com

www.newark.com TOXICITY IRRITATION bisphenol A/ diglycidyl ether dermal (rat) LD50: >800 mg/kg[1] Eye (rabbit): 100mg - Mild resin, liquid Page <12> 28/10/18 V1.0 Oral (rat) LD50: 13447 mg/kg[1]

TOXICITY IRRITATION [2] carbon black Dermal (rabbit) LD50: >3000 mg/kg Not Available

Oral (rat) LD50: >8000 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

Continued... Version No: 4.7 Page 11 of 20 Issue Date: 29/07/2016 Print Date: 29/07/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part A)

TOXICITY IRRITATION aluminium oxide Oral (rat) LD50: >2000 mg/kg[1] Not Available

TOXICITY IRRITATION

dermal (rat) LD50: 4000 mg/kg[2] * [Ciba-Geigy] [2] bisphenol F glycidyl ether/ Oral (rat) LD50: 4000 mg/kg Effects transient formaldehyde copolymer Eyes * (-) (-) Slight irritant May cause allergic response Skin * (-) (-) Slight irritant

Safety DataTOXICITY Sheet IRRITATION zinc oxide Oral (rat) LD50: >5000 mg/kg[1] Eye (rabbit) : 500 mg/24 h - mild Skin (rabbit) : 500 mg/24 h- mild

TOXICITY IRRITATION

TOXICITY IRRITATION bisphenol A/ diglycidyl ether dermal (rat) LD50: >800 mg/kg[1] Eye (rabbit): 100mg - Mild resin, liquid Oral (rat) LD50: 13447 mg/kg[1]

TOXICITY IRRITATION [2] carbon black Dermal (rabbit) LD50: >3000 mg/kg Not Available

Oral (rat) LD50: >8000 mg/kg[1]

Oxiranes (including glycidyl ethers and alkyl oxides, and epoxides) exhibit many common characteristics with respect to animal toxicology. One such oxirane is ethyloxirane; data presented here may be taken as representative. for 1,2-butylene oxide (ethyloxirane): Ethyloxirane increased the incidence of tumours of the respiratory system in male and female rats exposed via inhalation. Significant increases in nasal papillary adenomas and combined alveolar/bronchiolar adenomas and carcinomas were observed in male rats exposed to 1200 mg/m3 ethyloxirane via Slow Cure, inhalation for 103 weeks. There was also a significant positive trend in the incidence of combined alveolar/bronchiolar adenomas and carcinomas. Nasal Thermally Conductive papillary adenomas were also observed in 2/50 high-dose female rats with none occurring in control or low-dose animals. In mice exposed chronically via Adhesive, Flowable (Part A) inhalation, one male mouse developed a squamous cell papilloma in the nasal cavity (300 mg/m3) but other tumours were not observed. Tumours were not observed in mice exposed chronically via dermal exposure. When trichloroethylene containing 0.8% ethyloxirane was administered orally to mice for up to 35 weeks, followed by 0.4% from weeks 40 to 69, squamous-cell carcinomas of the forestomach occurred in 3/49 males (p=0.029, age-adjusted) and 1/48 females at week 106. Trichloroethylene administered alone did not induce these tumours and they were not observed in control animals . Two structurally related substances, oxirane (ethylene oxide) and methyloxirane (propylene oxide), which are also direct-acting alkylating agents, have been classified as carcinogenic The material may cause skin irritation after prolonged or repeated exposure and may produce a contact dermatitis (nonallergic). This form of dermatitis is often ZINC OXIDE characterised by skin redness (erythema) and swelling epidermis. Histologically there may be intercellular oedema of the spongy layer (spongiosis) and intracellular oedema of the epidermis. The substance is classified by IARC as Group 3: NOT classifiable as to its carcinogenicity to humans. Evidence of carcinogenicity may be inadequate or limited in animal testing. In mice,dermal application of bisphenol A diglycidyl ether (BADGE) (1, 10, or 100mg/kg) for 13 weeks produced mild to moderate chronic active dermatitis. At thehigh dose, spongiosis and epidermal micro abscess formation were observed. Inrats, dermal application of BADGE (10, 100, or 1000 mg/kg) for 13 weeksresulted in a decrease in body weight at the high dose. The no-observableeffect level (NOEL) for dermal exposure was 100 mg/kg for both sexes. In aseparate study, application of BADGE (same doses) five times per week for ~13weeks not only caused a decrease in body weight but also produced BISPHENOL A/ chronicdermatitis at all dose levels in males and at >100 mg/kg in females (as wellas in a satellite group of females given 1000 mg/kg). DIGLYCIDYL ETHER Reproductiveand Developmental Toxicity: BADGE (50, 540, or 750 mg/kg)administered to rats via gavage for 14 weeks (P1) or 12 weeks (P2) RESIN, LIQUID produceddecreased body weight in all males at the mid dose and in both males andfemales at the high dose, but had no reproductive effects. The NOEL forreproductive effects was 750 mg/kg. Version No: 4.7 Carcinogenicity: IARC concluded that 'there is limitedPage 12evidence of 20 for thecarcinogenicity of bisphenol A diglycidyl ether in experimental animals.'ItsIssue Date:overall 29/07/2016 evaluation was 'Bisphenol A diglycidyl ether is notclassifiable as to its carcinogenicity to humans (Group 3). Print Date: 29/07/2016 In8329TFS alifetime tumourigenicity Slow Cure, study inThermally which 90-day-old Conductive C3H mice received Adhesive, threedermal Flowableapplications per (Part week ofA) BADGE (undiluted dose) for 23 months, only oneout of 32 animals developed a papilloma after 16 months. A retest, in whichskin paintings were done for 27 months, however, produced no tumours (Weil etal., 1963). In another lifetime skin-painting study, BADGE (dose n.p.) was alsoreported to be noncarcinogenic to the skin of C3H mice; it was, however, weaklycarcinogenic to the skin of C57BL/6 mice (Holland et al., 1979; cited by Canteret al., 1986). In a two-year bioassay, female Fisher 344 rats dermally exposedto BADGE (1, 100, or 1000 mg/kg) showed no evidence of dermal carcinogenicitybut did have low incidences of tumours in the oral cavity (U.S. EPA, 1997). Continued... Genotoxicity: In S. typhimurium strains TA100 and TA1535, BADGE (10-10,000ug/plate) was mutagenic with and without S9; negative results were obtained inTA98 and TA1537 (Canter et al., 1986; Pullin, 1977). In a spot test, BADGE(0.05 or 10.00 mg) failed to show mutagenicity in strains TA98 and TA100 (Wadeet al., 1979). Negative results were also obtained in the body fluid test usingurine of female BDF and ICR mice (1000 mg/kg BADGE), the mouse host-mediatedassay (1000 mg/kg), micronucleus test (1000 mg/kg), and dominant lethal assay(~3000 mg/kg). Immunotoxicity: Intracutaneous injection of diluted BADGE (0.1 mL) three timesper week on alternate days (total of 8 injections) followed by a three- weekincubation period and a challenge dose produced sensitisation in 19 of 20guinea pigs - Consumerexposure to BADGE is almost exclusively from migration of BADGE from cancoatings into food. Using a worst-case scenario that assumes BADGE migrates atthe same level into all types of food, the estimated per capita daily intakefor a 60-kg individual is approximately 0.16 ug/kg body weight/day. A review ofone- and two-generation reproduction studies and developmental investigationsfound no evidence of reproductive or endocrine toxicity, the upper ranges ofdosing being determined by maternal toxicity. The lack of endocrine toxicity inthe reproductive and developmental toxicological tests is supported by www.element14.com negativeresults from both in vivo and in vitro assays designed specifically to detectoestrogenic and androgenic properties of BADGE. An examination of data www.farnell.com fromsub-chronic and chronic toxicological studies support a NOAEL of 50 mg/ kg/bodyweight day from the 90-day study, and a NOAEL of 15 mg/kg body weigh/day (malerats) from the 2-year carcinogenicity study. Both NOAELS are consideredappropriate for risk assessment. Comparing the estimated daily www.newark.com human intake of0.16 ug/kg body weight/day with the NOAELS of 50 and 15 mg/kg body weight/dayshows human exposure to BADGE from can coatings is between 250,000 and100,000-fold lower than the NOAELs from the most sensitive toxicology tests.These large margins of safety together with lack of reproductive,developmental, endocrine and carcinogenic effects supports the continued use ofBADGE for use in articles intended to come into contact with foodstuffs. Page <13> 28/10/18 V1.0 Foetoxicity has been observed in animal studies Oral (rabbit, female) NOEL 180 mg/kg (teratogenicity; NOEL (maternal 60 mg/kg

CARBON BLACK WARNING: This substance has been classified by the IARC as Group 2B: Possibly Carcinogenic to Humans. Inhalation (rat) TCLo: 50 mg/m3/6h/90D-I Nil reported

Slow Cure, Thermally Conductive The following information refers to contact allergens as a group and may not be specific to this product. Adhesive, Flowable (Part A) Contact allergies quickly manifest themselves as contact eczema, more rarely as urticaria or Quincke's oedema. The pathogenesis of contact eczema involves & BISPHENOL F GLYCIDYL a cell-mediated (T lymphocytes) immune reaction of the delayed type. Other allergic skin reactions, e.g. contact urticaria, involve antibody-mediated immune ETHER/ FORMALDEHYDE reactions. The significance of the contact allergen is not simply determined by its sensitisation potential: the distribution of the substance and the opportunities COPOLYMER & 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 (C12-14)ALKYLGLYCIDYL sensitising potential with which few individuals come into contact. From a clinical point of view, substances are noteworthy if they produce an allergic test ETHER & BISPHENOL A/ reaction in more than 1% of the persons tested. DIGLYCIDYL ETHER RESIN, LIQUID The chemical structure of hydroxylated diphenylalkanes or bisphenols consists of two phenolic rings joined together through a bridging carbon. This class of Slow Cure, endocrine disruptors that mimic oestrogens is widely used in industry, particularly in plastics Thermally Conductive Bisphenol A (BPA) and some related compounds exhibit oestrogenic activity in human breast cancer cell line MCF-7, but there were remarkable differences in Adhesive, Flowable (Part A) activity. Several derivatives of BPA exhibited significant thyroid hormonal activity towards rat pituitary cell line GH3, which releases growth hormone in a thyroid & BISPHENOL F GLYCIDYL hormone-dependent manner. However, BPA and several other derivatives did not show such activity. Results suggest that the 4-hydroxyl group of the A-phenyl ETHER/ FORMALDEHYDE ring and the B-phenyl ring of BPA derivatives are required for these hormonal activities, and substituents at the 3,5-positions of the phenyl rings and the COPOLYMER & bridging alkyl moiety markedly influence the activities. BISPHENOL A/ Bisphenols promoted cell proliferation and increased the synthesis and secretion of cell type-specific proteins. When ranked by proliferative potency, the longer DIGLYCIDYL ETHER the alkyl substituent at the bridging carbon, the lower the concentration needed for maximal cell yield; the most active compound contained two propyl chains at RESIN, LIQUID the bridging carbon. Bisphenols with two hydroxyl groups in the para position and an angular configuration are suitable for appropriate hydrogen bonding to the acceptor site of the oestrogen receptor.

ALUMINIUM OXIDE & No significant acute toxicological data identified in literature search. CARBON BLACK

Legend: – Data available but does not fill the criteria for classification – Data required to make classification available – Data Not Available to make classification

SECTION 12 ECOLOGICAL INFORMATION

12.1. Toxicity

Continued... Version No: 4.7 Page 11 of 20 Issue Date: 29/07/2016 Print Date: 29/07/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part A)

TOXICITY IRRITATION aluminium oxide Oral (rat) LD50: >2000 mg/kg[1] Not Available

TOXICITY IRRITATION

zinc oxide Oral (rat) LD50: >5000 mg/kg[1] Eye (rabbit) : 500 mg/24 h - mild Skin (rabbit) : 500 mg/24 h- mild

TOXICITY IRRITATION

TOXICITY IRRITATION bisphenol A/ diglycidyl ether dermal (rat) LD50: >800 mg/kg[1] Eye (rabbit): 100mg - Mild resin, liquid Oral (rat) LD50: 13447 mg/kg[1]

TOXICITY IRRITATION [2] carbon black Dermal (rabbit) LD50: >3000 mg/kg Not Available

Oral (rat) LD50: >8000 mg/kg[1]

Oxiranes (including glycidyl ethers and alkyl oxides, and epoxides) exhibit many common characteristics with respect to animal toxicology. One such oxirane is ethyloxirane; data presented here may be taken as representative. for 1,2-butylene oxide (ethyloxirane): Ethyloxirane increased the incidence of tumours of the respiratory system in male and female rats exposed via inhalation. Significant increases in nasal papillary adenomas and combined alveolar/bronchiolar adenomas and carcinomas were observed in male rats exposed to 1200 mg/m3 ethyloxirane via Version No: 4.7 Slow Cure, Page 12 of 20 Issue Date: 29/07/2016 inhalation for 103 weeks. There was also a significant positive trend in the incidence of combined alveolar/bronchiolar adenomas and carcinomas. Nasal Thermally Conductive Print Date: 29/07/2016 papillary adenomas were also observed in 2/50 high-dose female rats with none occurring in control or low-dose animals. In mice exposed chronically via Adhesive, Flowable (Part A) 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part A) inhalation, one male mouse developed a squamous cell papilloma in the nasal cavity (300 mg/m3) but other tumours were not observed. Tumours were not observed in mice exposed chronically via dermal exposure. When trichloroethylene containing 0.8% ethyloxirane was administered orally to mice for up to 35 weeks, followed by 0.4% from weeks 40 to 69, squamous-cell carcinomas of the forestomach occurred in 3/49 males (p=0.029, age-adjusted) and 1/48 females exposedtoat week 106. BADGE Trichloroethylene (1, 100, or 1000 administered mg/kg) showed alone did no not evidence induce ofthese dermal tumours carcinogenicitybut and they were did not have observed low incidences in control ofanimals tumours . Two in the structurally oral cavity related (U.S. EPA, 1997).substances, oxirane (ethylene oxide) and methyloxirane (propylene oxide), which are also direct-acting alkylating agents, have been classified as carcinogenic Genotoxicity: In S. typhimurium strains TA100 and TA1535, BADGE (10-10,000ug/plate) was mutagenic with and without S9; negative results were obtained The material may cause skin irritation after prolonged or repeated exposure and may produce a contact dermatitis (nonallergic). This form of dermatitis is often inTA98 and TA1537 (Canter et al., 1986; Pullin, 1977). In a spot test, BADGE(0.05 or 10.00 mg) failed to show mutagenicity in strains TA98 and TA100 (Wadeet SafetyZINC OXIDE Datacharacterised by skin Sheetredness (erythema) and swelling epidermis. Histologically there may be intercellular oedema of the spongy layer (spongiosis) and al., 1979). Negative results were also obtained in the body fluid test usingurine of female BDF and ICR mice (1000 mg/kg BADGE), the mouse intracellular oedema of the epidermis. host-mediatedassay (1000 mg/kg), micronucleus test (1000 mg/kg), and dominant lethal assay(~3000 mg/kg). Immunotoxicity:The substance is classifiedIntracutaneous by IARC injection as Group of diluted 3: BADGE (0.1 mL) three timesper week on alternate days (total of 8 injections) followed by a three- weekincubationNOT classifiable period as to andits carcinogenicity a challenge dose to humans. produced sensitisation in 19 of 20guinea pigs -Evidence of carcinogenicity may be inadequate or limited in animal testing. ConsumerexposureIn mice,dermal application to BADGE of bisphenol is almost A diglycidyl exclusively ether from (BADGE) migration (1, of 10, BADGE or 100mg/kg) from cancoatings for 13 weeks into produced food. Using mild a to worst-case moderate scenariochronic active that assumes dermatitis. At BADGEthehigh dose,migrates spongiosis atthe same and level epidermal into all micro types abscess of food, theformation estimated were per observed. capita daily Inrats, intakefor dermal a 60-kgapplication individual of BADGE is approximately (10, 100, or0.16 1000 ug/kg mg/kg) body for weight/day. 13 A reviewweeksresulted ofone- and in a two-generation decrease in body reproduction weight at thestudies high anddose. developmental The no-observableeffect investigationsfound level (NOEL) no evidence for dermal of reproductive exposure was or endocrine100 mg/kg toxicity, for both the sexes. upper In rangesaseparate ofdosing study, beingapplication determined of BADGE by maternal (same doses) toxicity. five The times lack per of endocrine week for ~13weeks toxicity inthe not reproductive only caused anda decrease developmental in body toxicologicalweight but also tests produced is supported by BISPHENOL A/ negativeresultschronicdermatitis from at allboth dose in vivo levels and in inmales vitro assaysand at >100 designed mg/kg specifically in females to (as detectoestrogenic wellas in a satellite and groupandrogenic of females properties given of 1000 BADGE. mg/kg). An examination of data DIGLYCIDYL ETHER fromsub-chronicReproductiveand and Developmental chronic toxicological Toxicity studies: BADGE support (50, a NOAEL 540, or of750 50 mg/kg)administered mg/ kg/bodyweight dayto rats from via the gavage 90-day for study, 14 weeks and a(P1) NOAEL or 12 of weeks 15 mg/kg (P2) body RESIN, LIQUID weigh/dayproduceddecreased (malerats) body from weightthe 2-year in all carcinogenicity males at the mid study. dose Both and NOAELSin both males are consideredappropriateandfemales at the high fordose, risk but assessment. had no reproductive Comparing effects. the estimated The NOEL daily humanforreproductive intake of0.16 effects ug/kg was body 750 mg/kg.weight/day with the NOAELS of 50 and 15 mg/kg body weight/dayshows human exposure to BADGE from can coatings is betweenCarcinogenicity: 250,000 and100,000-fold IARC concluded lower that 'therethan the is limitedNOAELs evidence from the for most thecarcinogenicity sensitive toxicology of bisphenol tests.These A diglycidyl large margins ether in of experimental safety together animals.'Its with lack overallof reproductive,developmental,evaluation was 'Bisphenol A endocrinediglycidyl etherand carcinogenic is notclassifiable effects as supportsto its carcinogenicity the continued to use humans ofBADGE (Group for 3). use in articles intended to come into contact with foodstuffs.In alifetime tumourigenicity study in which 90-day-old C3H mice received threedermal applications per week of BADGE (undiluted dose) for 23 months, only Foetoxicityoneout of 32 has animals been observeddeveloped in a animalpapilloma studies after Oral16 months. (rabbit, Afemale) retest, NOELin whichskin 180 mg/kg paintings (teratogenicity; were done forNOEL 27 months, (maternal however, 60 mg/kg produced no tumours (Weil etal., 1963). In another lifetime skin-painting study, BADGE (dose n.p.) was alsoreported to be noncarcinogenic to the skin of C3H mice; it was, however, weaklycarcinogenic to the skin of C57BL/6 mice (Holland et al., 1979; cited by Canteret al., 1986). In a two-year bioassay, female Fisher 344 rats dermally CARBON BLACK WARNING: This substance has been classified by the IARC as Group 2B: Possibly Carcinogenic to Humans. Inhalation (rat) TCLo: 50 mg/m3/6h/90D-I Nil reported Continued... Slow Cure, Thermally Conductive The following information refers to contact allergens as a group and may not be specific to this product. Adhesive, Flowable (Part A) Contact allergies quickly manifest themselves as contact eczema, more rarely as urticaria or Quincke's oedema. The pathogenesis of contact eczema involves & BISPHENOL F GLYCIDYL a cell-mediated (T lymphocytes) immune reaction of the delayed type. Other allergic skin reactions, e.g. contact urticaria, involve antibody-mediated immune ETHER/ FORMALDEHYDE reactions. The significance of the contact allergen is not simply determined by its sensitisation potential: the distribution of the substance and the opportunities COPOLYMER & 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 (C12-14)ALKYLGLYCIDYL sensitising potential with which few individuals come into contact. From a clinical point of view, substances are noteworthy if they produce an allergic test ETHER & BISPHENOL A/ reaction in more than 1% of the persons tested. DIGLYCIDYL ETHER RESIN, LIQUID The chemical structure of hydroxylated diphenylalkanes or bisphenols consists of two phenolic rings joined together through a bridging carbon. This class of Slow Cure, endocrine disruptors that mimic oestrogens is widely used in industry, particularly in plastics Thermally Conductive Bisphenol A (BPA) and some related compounds exhibit oestrogenic activity in human breast cancer cell line MCF-7, but there were remarkable differences in Adhesive, Flowable (Part A) activity. Several derivatives of BPA exhibited significant thyroid hormonal activity towards rat pituitary cell line GH3, which releases growth hormone in a thyroid & BISPHENOL F GLYCIDYL hormone-dependent manner. However, BPA and several other derivatives did not show such activity. Results suggest that the 4-hydroxyl group of the A-phenyl ETHER/ FORMALDEHYDE ring and the B-phenyl ring of BPA derivatives are required for these hormonal activities, and substituents at the 3,5-positions of the phenyl rings and the COPOLYMER & bridging alkyl moiety markedly influence the activities. BISPHENOL A/ Bisphenols promoted cell proliferation and increased the synthesis and secretion of cell type-specific proteins. When ranked by proliferative potency, the longer DIGLYCIDYL ETHER the alkyl substituent at the bridging carbon, the lower the concentration needed for maximal cell yield; the most active compound contained two propyl chains at RESIN, LIQUID the bridging carbon. Bisphenols with two hydroxyl groups in the para position and an angular configuration are suitable for appropriate hydrogen bonding to the acceptor site of the oestrogen receptor.

ALUMINIUM OXIDE & No significant acute toxicological data identified in literature search. CARBON BLACK

Legend: – Data available but does not fill the criteria for classification – Data required to make classification available – Data Not Available to make classification

SECTION 12 ECOLOGICAL INFORMATION

12.1. Toxicity

Page <14> 28/10/18 V1.0 Version No: 4.7 Page 12 of 20 Issue Date: 29/07/2016 Print Date: 29/07/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part A)

exposedto BADGE (1, 100, or 1000 mg/kg) showed no evidence of dermal carcinogenicitybut did have low incidences of tumours in the oral cavity (U.S. EPA, 1997). Genotoxicity: In S. typhimurium strains TA100 and TA1535, BADGE (10-10,000ug/plate) was mutagenic with and without S9; negative results were obtained inTA98 and TA1537 (Canter et al., 1986; Pullin, 1977). In a spot test, BADGE(0.05 or 10.00 mg) failed to show mutagenicity in strains TA98 and TA100 (Wadeet al., 1979). Negative results were also obtained in the body fluid test usingurine of female BDF and ICR mice (1000 mg/kg BADGE), the mouse host-mediatedassay (1000 mg/kg), micronucleus test (1000 mg/kg), and dominant lethal assay(~3000 mg/kg). Immunotoxicity: Intracutaneous injection of diluted BADGE (0.1 mL) three timesper week on alternate days (total of 8 injections) followed by a three- weekincubation period and a challenge dose produced sensitisation in 19 of 20guinea pigs - Consumerexposure to BADGE is almost exclusively from migration of BADGE from cancoatings into food. Using a worst-case scenario that assumes BADGE migrates atthe same level into all types of food, the estimated per capita daily intakefor a 60-kg individual is approximately 0.16 ug/kg body weight/day. A review ofone- and two-generation reproduction studies and developmental investigationsfound no evidence of reproductive or endocrine toxicity, the upper ranges ofdosing being determined by maternal toxicity. The lack of endocrine toxicity inthe reproductive and developmental toxicological tests is supported by negativeresults from both in vivo and in vitro assays designed specifically to detectoestrogenic and androgenic properties of BADGE. An examination of data fromsub-chronic and chronic toxicological studies support a NOAEL of 50 mg/ kg/bodyweight day from the 90-day study, and a NOAEL of 15 mg/kg body weigh/day (malerats) from the 2-year carcinogenicity study. Both NOAELS are consideredappropriate for risk assessment. Comparing the estimated daily human intake of0.16 ug/kg body weight/day with the NOAELS of 50 and 15 mg/kg body weight/dayshows human exposure to BADGE from can coatings is between 250,000 and100,000-fold lower than the NOAELs from the most sensitive toxicology tests.These large margins of safety together with lack of reproductive,developmental, endocrine and carcinogenic effects supports the continued use ofBADGE for use in articles intended to come into contact with foodstuffs. Foetoxicity has been observed in animal studies Oral (rabbit, female) NOEL 180 mg/kg (teratogenicity; NOEL (maternal 60 mg/kg

CARBON BLACK WARNING: This substance has been classified by the IARC as Group 2B: Possibly Carcinogenic to Humans. Inhalation (rat) TCLo: 50 mg/m3/6h/90D-I Nil reported

ALUMINIUM OXIDE & No significant acute toxicological data identified in literature search. CARBON BLACK

Legend: – Data available but does not fill the criteria for classification – Data required to make classification available – Data Not Available to make classification

SECTION 12 ECOLOGICAL INFORMATION

12.1. Toxicity

Very toxic to aquatic organisms, may cause long-term adverse effects in the aquatic environment. Do NOT allow product to come in contact with surface waters or to intertidal areas below the mean high water mark. Do not contaminate water when cleaning equipment or disposing of equipment wash-waters. Wastes resulting from use of the product must be disposed of on site or at approved waste sites. For bisphenol A and related bisphenols:

In general, studies have shown that bisphenol A can affect growth, reproduction and development in aquatic organisms. Among freshwater organisms, fish appear to be the most sensitive species. Evidence of endocrine-related effects in fish, aquatic invertebrates, amphibians and reptiles has been reported at environmentally relevant exposure levels lower than those required for acute toxicity. There is a widespread variation in reported values for endocrine-related effects, but many fall in the range of 1 ug/L to 1 mg/L Bisphenol A, its derivatives and analogues, can be released from polymers, resins and certain substances by metabolic products As an environmental contaminant, bisphenol A interferes with nitrogen fixation at the roots of leguminous plants associated with the bacterial symbiont Sinorhizobium meliloti. Despite a half-life in the soil of only 1-10 days, its ubiquity makes it an important pollutant. According to Environment Canada, 'initial assessment shows that at low levels, bisphenol A can harm fish and organisms over time. Studies also indicate that it can currently be found in municipal wastewater.' However, a study conducted in the United States found that 91-98% of bisphenol A may be removed from water during treatment at municipal water treatment plants. A 2009 review of the biological impacts of plasticisers on wildlife published by the Royal Society with a focus on annelids (both aquatic and terrestrial), molluscs, crustaceans, insects, fish and amphibians concluded that bisphenol A has been shown to affect reproduction in all studied animal groups, to impair development in crustaceans and amphibians and to induce genetic aberrations. A large 2010 study of two rivers in Canada found that areas contaminated with hormone-like chemicals including bisphenol A showed females made up 85 per cent of the population of a certain fish, while females made up only 55 per cent in uncontaminated areas. Although abundant data are available on the toxicity of bisphenol-A (2,2-bis (4-hydroxydiphenyl)propane;(BPA) A variety of BPs were examined for their acute toxicity against Daphnia magna, mutagenicity, and oestrogenic activity using the Daphtoxkit (Creasel Ltd.), the umu test system, and the yeast two-hybrid system, respectively, in comparison with BPA. BPA was moderately toxic to D. magna (48-h EC50 was 10 mg/l) according to the current U.S. EPA acute toxicity evaluation standard, and it was weakly oestrogenic with 5 orders of magnitude lower activity than that of the natural estrogen 17 beta-oestradiol in the yeast screen, while no mutagenicity was observed. All seven BPs tested here showed moderate to slight acute toxicity, no mutagenicity, and weak oestrogenic activity as well as BPA. Some of the BPs showed considerably higher oestrogenic activity than BPA, and others exhibited much lower activity. Bisphenol S (bis(4- hydroxydiphenyl)sulfone) and bis(4-hydroxyphenyl)sulfide) showed oestrogenic activity. Biodegradation is a major mechanism for eliminating various environmental pollutants. Studies on the biodegradation of bisphenols have mainly focused on bisphenol A. A number of BPA-degrading bacteria have been isolated from enrichments of sludge from wastewater treatment plants. The first step in the biodegradation of BPA is the hydroxylation of the carbon atom of a methyl group or the quaternary carbon in the BPA molecule. Judging from these features of the biodegradation mechanisms, it is possible that the same mechanism used for BPA is used to biodegrade all bisphenols that have at least one methyl or methylene group bonded at the carbon atom between the two phenol groups. However, bisphenol F ([bis(4-hydroxyphenyl)methane; BPF), which has no substituent at the bridging carbon, is unlikely to be metabolised by such a mechanism. Nevertheless BPF is readily degraded by river water microorganisms under aerobic conditions. From this evidence, it was clear that a specific mechanism for biodegradation of BPF does exist in the natural ecosystem, Algae can enhance the photodegradation of bisphenols. The photodegradation rate of BPF increased with increasing algae concentration. Humic acid and Fe3+ ions also enhanced the photodegradation of BPF. The effect of pH value on the BPF photodegradation was also important. Significant environmental findings are limited. Oxiranes (including glycidyl ethers and alkyl oxides, and epoxides) exhibit common characteristics with respect to environmental fate and ecotoxicology. One such oxirane is ethyloxirane and data presented here may be taken as representative. for 1,2-butylene oxide (ethyloxirane): Environmental fate: Ethyloxirane is highly soluble in water and has a very low soil-adsorption coefficient, which suggests that if released to water, adsorption of ethyloxirane to sediment and suspended solids is not expected. Volatilisation of ethyloxirane from water surfaces would be expected based on the moderate estimated Henry's Law constant. If ethyloxirane is released to soil, it is expected to have low adsorption and thus very high mobility. Volatilisation from moist soil and dry soil surfaces is expected, based on its vapour pressure. It is expected that ethyloxirane exists solely as a vapour in ambient atmosphere, based on its very high vapour pressure. Ethyloxirane may also be removed from the atmosphere by wet deposition processes, considering its relatively high water solubility. Persistence: The half-life in air is about 5.6 days from the reaction of ethyloxirane with photochemically produced hydroxyl radicals which indicates that this chemical meets the persistence criterion in air (half-life of = 2 days)*. Ethyloxirane is hydrolysable, with a half-life of 6.5 days, and biodegradable up to 100% degradation and is not expected to persist in water. A further model-predicted biodegradation half-life of 15 days in water was obtained and used to predict the half-life of this chemical in soil and sediment by applying Boethling's extrapolation factors ( t1/2water : t1/2 soil : t1/2sediment = 1: 1: 4 ) (Boethling 1995). According to these values, it can be concluded that ethyloxirane does not meet the persistence criteria in water and soil (half-lives = 182 days) and sediments (half-life = 365 days). www.element14.comExperimental and modelled log Kow values of 0.68 and 0.86, respectively, indicate that the potential for bioaccumulation of ethyloxirane in organisms is likely to be low. Modelled bioaccumulation -factor (BAF) and bioconcentration -factor (BCF) values of 1 to 17 L/kg indicate that ethyloxirane does not meet the bioaccumulation criteria (BCF/BAF = 5000)* www.farnell.comEcotoxicity: www.newark.comExperimental ecotoxicological data for ethyloxirane (OECD 2001) indicate low to moderate toxicity to aquatic organisms. For fish and water flea, acute LC50/EC50 values vary within a narrow range of 70-215 mg/L; for algae, toxicity values exceed 500 mg/L, while for bacteria they are close to 5000 mg/L * Persistence and Bioaccumulation Regulations (Canada 2000). Page <15> 28/10/18 V1.0 Foraluminium and its compounds and salts: Despiteits prevalence in the environment, no known form of life uses aluminium saltsmetabolically. In keeping with its pervasiveness, aluminium is well toleratedby plants and animals.Owing to their prevalence, potential beneficial (orotherwise) biological roles of aluminium compounds are of continuing interest. Environmentalfate: Aluminiumoccurs in the environment in the form of silicates, oxides and hydroxides,combined with other elements such as sodium, fluorine and arsenic complexeswith organic matter. Acidificationof soils releases aluminium as a transportable solution. Mobilisation ofaluminium by acid rain results in aluminium becoming available for plantuptake. As anelement, aluminum cannot be degraded in the environment, but may undergovarious precipitation or ligand exchange reactions. Aluminum in compounds hasonly one oxidation state (+3), and would not undergo oxidation-reductionreactions under environmental conditions. Aluminum can be complexed by variousligands present in the environment (e.g., fulvic and humic acids).

Continued... Version No: 4.7 Page 13 of 20 Issue Date: 29/07/2016 Print Date: 29/07/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part A)

(C12-14)alkylglycidyl ether EC50 48 Crustacea 6.07mg/L 2 (C12-14)alkylglycidyl ether NOEC 48 Crustacea <10mg/L 2 bisphenol A/ diglycidyl ether LC50 96 Fish 1.2mg/L 2 resin, liquid bisphenol A/ diglycidyl ether EC50 48 Crustacea 1.1mg/L 2 resin, liquid bisphenol A/ diglycidyl ether EC50 48 Crustacea 1.7mg/L 2 resin, liquid bisphenol A/ diglycidyl ether NOEC 504 Crustacea 0.3mg/L 2 resin, liquid bisphenol A/ diglycidyl ether EC50 72 Algae or other aquatic plants 9.4mg/L 2 resin, liquid carbon black LC50 96 Fish >100mg/L 2 carbon black NOEC 720 Fish 17mg/L 2 carbon black EC50 48 Crustacea >100mg/L 2 carbon black EC50 384 Crustacea 4.9mg/L 2 carbon black EC50 96 Algae or other aquatic plants 95mg/L 2 Extracted from 1. IUCLID Toxicity Data 2. Europe ECHA Registered Substances - Ecotoxicological Information - Aquatic Toxicity 3. EPIWIN Suite V3.12 - Legend: Aquatic Toxicity Data (Estimated) 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

In general, studies have shown that bisphenol A can affect growth, reproduction and development in aquatic organisms. Among freshwater organisms, fish appear to be the most sensitive species. Evidence of endocrine-related effects in fish, aquatic invertebrates, amphibians and reptiles has been reported at environmentally relevant exposure levels lower than those required for acute toxicity. There is a widespread variation in reported values for endocrine-related effects, but many fall in the range of 1 ug/L to 1 mg/L Bisphenol A, its derivatives and analogues, can be released from polymers, resins and certain substances by metabolic products As an environmental contaminant, bisphenol A interferes with nitrogen fixation at the roots of leguminous plants associated with the bacterial symbiont Sinorhizobium meliloti. Despite a half-life in the soil of only 1-10 days, its ubiquity makes it an important pollutant. According to Environment Canada, 'initial assessment shows that at low levels, bisphenol A can harm fish and organisms over time. Studies also indicate that it can currently be found in municipal wastewater.' However, a study conducted in the United States found that 91-98% of bisphenol A may be removed from water during treatment at municipal water treatment plants. A 2009 review of the biological impacts of plasticisers on wildlife published by the Royal Society with a focus on annelids (both aquatic and terrestrial), molluscs, crustaceans, insects, fish and amphibians concluded that bisphenol A has been shown to affect reproduction in all studied animal groups, to impair development in crustaceans and amphibians and to induce genetic aberrations. A large 2010 study of two rivers in Canada found that areas contaminated with hormone-like chemicals including bisphenol A showed females made up 85 per cent of the population of a certain fish, while females made up only 55 per cent in uncontaminated areas. Although abundant data are available on the toxicity of bisphenol-A (2,2-bis (4-hydroxydiphenyl)propane;(BPA) A variety of BPs were examined for their acute toxicity against Daphnia magna, mutagenicity, and oestrogenic activity using the Daphtoxkit (Creasel Ltd.), the umu test system, and the yeast two-hybrid system, respectively, in comparison with BPA. BPA was moderately toxic to D. magna (48-h EC50 was 10 mg/l) according to the current U.S. EPA acute toxicity evaluation standard, and it was weakly oestrogenic with 5 orders of magnitude lower activity than that of the natural estrogen 17 beta-oestradiol in the yeast screen, while no mutagenicity was observed. All seven BPs tested here showed moderate to slight acute toxicity, no mutagenicity, and weak oestrogenic activity as well as BPA. Some of the BPs showed considerably higher oestrogenic activity than BPA, and others exhibited much lower activity. Bisphenol S (bis(4- hydroxydiphenyl)sulfone) and bis(4-hydroxyphenyl)sulfide) showed oestrogenic activity. Biodegradation is a major mechanism for eliminating various environmental pollutants. Studies on the biodegradation of bisphenols have mainly focused on bisphenol A. A number of BPA-degrading bacteria have been isolated from enrichments of sludge from wastewater treatment plants. The first step in the biodegradation of BPA is the hydroxylation of the carbon atom of a methyl group or the quaternary carbon in the BPA molecule. Judging from these features of the biodegradation mechanisms, it is possible that the same mechanism used for BPA is used to biodegrade all bisphenols that have at least one methyl or methylene group bonded at the carbon atom between the two phenol groups. However, bisphenol F ([bis(4-hydroxyphenyl)methane; BPF), which has no substituent at the bridging carbon, is unlikely to be metabolised by such a mechanism. Nevertheless BPF is readily degraded by river water microorganisms under aerobic conditions. From this evidence, it was clear that a specific mechanism for biodegradation of BPF does exist in the natural ecosystem, Algae can enhance the photodegradation of bisphenols. The photodegradation rate of BPF increased with increasing algae concentration. Humic acid and Fe3+ ions also enhanced the photodegradation of BPF. The effect of pH value on the BPF photodegradation was also important. Significant environmental findings are limited. Oxiranes (including glycidyl ethers and alkyl oxides, and epoxides) exhibit common characteristics with respect to environmental fate and ecotoxicology. One such oxirane is ethyloxirane and data presented here may be taken as representative. for 1,2-butylene oxide (ethyloxirane): Environmental fate: Ethyloxirane is highly soluble in water and has a very low soil-adsorption coefficient, which suggests that if released to water, adsorption of ethyloxirane to sediment and suspended solids is not expected. Volatilisation of ethyloxirane from water surfaces would be expected based on the moderate estimated Henry's Law constant. If ethyloxirane is released to soil, it is Safetyexpected to have low adsorption Dataand thus very high mobility. Sheet Volatilisation from moist soil and dry soil surfaces is expected, based on its vapour pressure. It is expected that ethyloxirane exists solely as a vapour in ambient atmosphere, based on its very high vapour pressure. Ethyloxirane may also be removed from the atmosphere by wet deposition processes, considering its relatively high water solubility. Persistence: The half-life in air is about 5.6 days from the reaction of ethyloxirane with photochemically produced hydroxyl radicals which indicates that this chemical meets the persistence criterion in air (half-life of = 2 days)*. Ethyloxirane is hydrolysable, with a half-life of 6.5 days, and biodegradable up to 100% degradation and is not expected to persist in water. A further model-predicted biodegradation half-life of 15 days in water was obtained and used to predict the half-life of this chemical in soil and sediment by applying Boethling's extrapolation factors ( t1/2water : t1/2 soil : t1/2sediment = 1: 1: 4 ) (Boethling 1995). According to these values, it can be concluded that ethyloxirane does not meet the persistence criteria in water and soil (half-lives = 182 days) and sediments (half-life = 365 days). Experimental and modelled log Kow values of 0.68 and 0.86, respectively, indicate that the potential for bioaccumulation of ethyloxirane in organisms is likely to be low. Modelled bioaccumulation -factor (BAF) and bioconcentration -factor (BCF) values of 1 to 17 L/kg indicate that ethyloxirane does not meet the bioaccumulation criteria (BCF/BAF = 5000)* Ecotoxicity: Experimental ecotoxicological data for ethyloxirane (OECD 2001) indicate low to moderate toxicity to aquatic organisms. For fish and water flea, acute LC50/EC50 values vary within a narrow range of 70-215 mg/L; for algae, toxicity values exceed 500 mg/L, while for bacteria they are close to 5000 mg/L

* Persistence and Bioaccumulation Regulations (Canada 2000). Foraluminium and its compounds and salts: Despiteits prevalence in the environment, no known form of life uses aluminium saltsmetabolically. In keeping with its pervasiveness, aluminium is well toleratedby plants and animals.Owing to their Versionprevalence, No: 4.7 potential beneficial (orotherwise) biological roles of aluminium compoundsPage are of14 continuing of 20 interest. Issue Date: 29/07/2016 Environmentalfate: Print Date: 29/07/2016 Aluminiumoccurs in the environment in8329TFS the form of silicates, Slow oxides Cure, and Thermally hydroxides,combined Conductive with other elements Adhesive, such as Flowablesodium, fluorine (Part and arsenic A) complexeswith organic matter. Acidificationof soils releases aluminium as a transportable solution. Mobilisation ofaluminium by acid rain results in aluminium becoming available for plantuptake. As anelement, aluminum cannot be degraded in the environment, but may undergovarious precipitation or ligand exchange reactions. Aluminum in compounds hasonly one oxidation state (+3), and would not undergo oxidation-reductionreactions under environmental conditions. Aluminum can be complexed by variousligands present in the environment (e.g., fulvic and humic acids). Thesolubility of aluminum in the environment will depend on the ligands presentand the pH. Thetrivalent aluminum ion is surrounded by six water molecules in solution. Thehydrated aluminum ion, [Al(H2O)6]3+, undergoes hydrolysis, in which a stepwisedeprotonation of the coordinatedContinued... water ligands forms bound hydroxide ligands(e.g., [Al(H2O)5(OH)]2+, [Al(H2O)4(OH)2]+). The speciation of aluminum in wateris pH dependent. The hydrated trivalent aluminum ion is the predominant form atpH levels below 4. Between pH 5 and 6, the predominant hydrolysis products areAl(OH)2+ and Al(OH)2+, while the solid Al(OH)3 is most prevalent between pH 5.2and 8.8. The soluble species Al(OH)4- is the predominant species above pH 9,and is the only species present above pH 10. Polymeric aluminum hydroxidesappear between pH 4.7 and 10.5, and increase in size until they are transformedinto colloidal particles of amorphous Al(OH)3, which crystallise to gibbsite inacid waters. Polymerisation is affected by the presence of dissolved silica;when enough silica is present, aluminum is precipitated as poorly crystallisedclay mineral species. Hydroxyaluminumcompounds are considered amphoteric (e.g., they can act as both acids and basesin solution). Because of this property, aluminum hydroxides can act as buffersand resist pH changes within the narrow pH range of 4-5. Monomericaluminum compounds, typified by aluminum fluoride, chloride, and sulfate, areconsidered reactive or labile compounds, whereas polymeric aluminum speciesreact much more slowly in the environment. Aluminum has a stronger attractionfor fluoride in an acidic environment compared to other inorganic ligand. Theadsorption of aluminum onto clay surfaces can be a significant factor incontrolling aluminum mobility in the environment, and these adsorptionreactions, measured in one study at pH 3.0-4.1, have been observed to be veryrapid. However, clays may act either as a sink or a source for soluble aluminumdepending on the degree of aluminum saturation on the clay surface. Withinthe pH range of 5-6, aluminum complexes with phosphate and is removed fromsolution. Because phosphate is a necessary nutrient in ecological systems, thisimmobilization of both aluminum and phosphate may result in depleted nutrientstates in surface water. Plantspecies and cultivars of the same species differ considerably in their abilityto take up and translocate aluminum to above-ground parts. Tea leaves maycontain very high concentrations of aluminum, >5,000 mg/kg in old leaves.Other plants that may contain high levels of aluminum include Lycopodium(Lycopodiaceae), a few ferns, Symplocos (Symplocaceae), and Orites(Proteaceae). Aluminum is often taken up and concentrated in root tissue. Insub-alpine ecosystems, the large root biomass of the Douglas fir, Abiesamabilis, takes up aluminum and immobilizes it, preventing largeaccumulation in above-ground tissue. It is unclear to what extent aluminum istaken up into root food crops and leafy vegetables. An uptake factor(concentration of aluminum in the plant/concentration of aluminum in soil) of0.004 for leafy vegetables and 0.00065 for fruits and tubers has been reported,but the pH and plant species from which these uptake factors were derived areunclear. Based upon these values, however, it is clear that aluminum is nottaken up in plants from soil, but is instead biodiluted. Aluminumconcentrations in rainbow trout from an alum-treated lake, an untreated lake,and a hatchery were highest in gill tissue and lowest in muscle. Aluminumresidue analyses in brook trout have shown that whole-body aluminum contentdecreases as the fish advance from larvae to juveniles. These results implythat the aging larvae begin to decrease their rate of aluminum uptake, toeliminate aluminum at a rate that exceeds uptake, or to maintain approximatelythe same amount of aluminum while the body mass increases. The decline inwhole-body aluminum residues in juvenile brook trout may be related to growthand dilution by edible muscle tissue that accumulated less aluminum than didthe other tissues. Thegreatest fraction of the gill-associated aluminum was not sorbed to the gilltissue, but to the gill mucus. It is thought that mucus appears to retardaluminum transport from solution to the membrane surface, thus delaying theacute biological response of the fish. It has been reported that concentrationsof aluminum in whole-body tissue of the Atlantic salmon exposed to highconcentrations of aluminum ranging from 3 ug/g (for fish exposed to 33 ug/L) to96 ug/g (for fish exposed to 264 ug/L) at pH 5.5. After 60 days of exposure,BCFs ranged from 76 to 190 and were directly related to the aluminum exposureconcentration. In acidic waters (pH 4.6-5.3) with low concentrations of calcium(0.5-1.5 mg Ca/L), labile aluminum between 25 and 75 ug/L is toxic. Becausealuminum is toxic to many aquatic species, it is not bioaccumulated to asignificant degree (BCF <300) in most fish and shellfish; therefore,consumption of contaminated fish does not appear to be a significant source ofaluminum exposure in humans. Bioconcentrationof aluminum has also been reported for several aquatic invertebrate species.BCF values ranging from 0.13 to 0.5 in the whole-body were reported for thesnail. Bioconcentration of aluminum has also been reported for aquatic insects. Ecotoxicity: Freshwaterspecies pH >6.5 Fish:Acute LC50 (48-96 h) 5 spp: 0.6 (Salmo salar) - 106 mg/L; Chronic NOEC(8-28 d): 7 spp,NOEC, 0.034-7.1 mg/L. The lowest measured chronic figure was an8-d LC50 of 0.17 mg/L for Micropterus sp. Amphibian:Acute LC50 (4 d): Bufo americanus, 0.86-1.66 mg/L; Chronic LC50 (8-d)2.28 mg/L CrustaceansLC50 (48 h): 1 sp 2.3-36 9 mg/L; Chronic NOEC (7-28 d) 3 spp, 0.136-1.72 mg/L AlgaeEC50 (96 h): population growth, 0.46-0.57 mg/L; 2 spp, chronic NOEC, 0.8-2.0mg/L Freshwaterspecies pH <6.5 (all between pH 4.5 and 6.0) Fish LC50(24-96 h): 4 spp, 0.015 (S. trutta) - 4.2 mg/L; chronic data on Salmotrutta, LC50 (21-42 d) 0.015- 0.105 mg/L AmphibiansLC50 (4-5 d): 2 spp, 0.540-2.670 m/L (absolute range 0.40-5.2 mg/L) Alga: 1sp NOEC growth 2.0 mg/L Amongfreshwater aquatic plants, single-celled plants are generally the mostsensitive to aluminium. Fish are generally more sensitive to aluminium thanaquatic invertebrates. Aluminium is a gill toxicant to fish, causing bothionoregulatory and respiratory effects. Thebioavailability and toxicity of aluminium is generally greatest in acidsolutions. Aluminium in acid habitats has been observed to be toxic to fish andphytoplankton. Aluminium is generally more toxic over the pH range 4.4.5.4,with a maximum toxicity occurring around pH 5.0.5.2. The inorganic single unitaluminium species (Al(OH)2 +) is thought to be the most toxic. Under very acidconditions, the toxic effects of the high H+ concentration appear to be moreimportant than the effects of low concentrations of aluminium; at approximatelyneutral pH values, the toxicity of aluminium is greatly reduced. The solubilityof aluminium is also enhanced under alkaline conditions, due to its amphotericcharacter, and some researchers found that the acute toxicity of aluminiumincreased from pH 7 to pH 9. However, the opposite relationship was found inother studies. The uptake and toxicity of aluminium in freshwater organismsgenerally decreases with increasing water hardness under acidic, neutral andalkaline conditions. Complexing agents such as fluoride, citrate and humicsubstances reduce the availability of aluminium to organisms, resulting inlower toxicity. Silicon can also reduce aluminium toxicity to fish. DrinkingWater Standards: aluminium:200 ug/l (UK max.) 200 ug/l(WHO guideline) chloride:400 mg/l (UK max.) 250 mg/l(WHO guideline) fluoride:1.5 mg/l (UK max.) www.element14.com1.5 mg/l(WHO guideline) nitrate:50 mg/l (UK max.) www.farnell.com50 mg/l(WHO guideline) sulfate:250 mg/l (UK max.) www.newark.comSoilGuideline: none available. AirQuality Standards: none available. For zinc and its compounds: Page <16> 28/10/18 V1.0 Environmental fate: Zinc is capable of forming complexes with a variety of organic andinorganic groups (ligands). Biological activity can affect the mobility of zincin the aquatic environment, although the biota contains relatively little zinccompared to the sediments. Zinc bioconcentrates moderately in aquaticorganisms; bioconcentration is higher in crustaceans and bivalve species thanin fish. Zinc does not concentrate appreciably in plants, and it does notbiomagnify significantly through terrestrial food chains. However biomagnification may be of concern if concentration ofzinc exceeds 1632 ppm in the top 12 inches of soil. Zinc can persist in water indefinitely and can be toxic to aquaticlife. The threshold concentration for fish is 0.1 ppm. Zinc may be concentratedin the aquatic food chain; it is concentrated over 200,000 times in oysters.Copper is synergistic but calcium is antagonistic to zinc toxicity in fish.Zinc can accumulate in freshwater animals at 5 -1,130 times the concentrationpresent in the water. Furthermore, although zinc actively bioaccumulates inaquatic systems, biota appears to represent a relatively minor sink compared tosediments. Steady-state zinc bioconcentration factors (BCFs) for 12 aquaticspecies range from 4 to 24,000. Crustaceans and fish can accumulate zinc fromboth water and food. A BCF of 1,000 was reported for both aquatic plants andfish, and a value of 10,000 was reported for aquatic invertebrates. The orderof enrichment of zinc in different aquatic organisms was as follows (zincconcentrations in µg/g dry weight appear in parentheses): fish (25), shrimp(50), mussel (60), periphyton (260), zooplankton (330), and oyster (3,300). Thehigh enrichment in oysters may be due to their ingestion of particulate mattercontaining higher concentrations of zinc than ambient water. Otherinvestigators have also indicated that organisms associated with sediments havehigher zinc concentrations than organisms living in the aqueous layer. Withrespect to bioconcentration from soil by terrestrial plants, invertebrates, andmammals, BCFs of 0.4, 8, and 0.6, respectively, have been reported. Theconcentration of zinc in plants depends on the plant species, soil pH, and thecomposition of the soil. Plant species do not concentrate zinc above the levels present insoil. In some fish, it has been observed that the level of zinc found intheir bodies did not directly relate to the exposure concentrations. Bioaccumulationof zinc in fish is inversely related to the aqueous exposure. This evidencesuggests that fish placed in environments with lower zinc concentrations cansequester zinc in their bodies. The concentration of zinc in drinking water may increase as aresult of the distribution system and household plumbing. Common pipingmaterials used in distribution systems often contain zinc, as well as othermetals and alloys. Trace metals may enter the water through corrosion productsor simply by the dissolution of small amounts of metals with which the watercomes in contact. Reactions with materials of the distribution system,particularly in soft low-pH waters, very often have produced concentrations ofzinc in tap water much greater than those in the raw or treated waters at theplant of origin. Zinc gives water a metallic taste at low levels. Overexposuresto zinc also have been associated with toxic effects. Ingestion of zinc orzinc-containing compounds has resulted in a variety of systemic effects in thegastrointestinal and hematological systems and alterations in the blood lipidprofile in humans and animals. In addition, lesions have been observed in

Continued... Version No: 4.7 Page 14 of 20 Issue Date: 29/07/2016 Print Date: 29/07/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part A)

Thesolubility of aluminum in the environment will depend on the ligands presentand the pH. Thetrivalent aluminum ion is surrounded by six water molecules in solution. Thehydrated aluminum ion, [Al(H2O)6]3+, undergoes hydrolysis, in which a stepwisedeprotonation of the coordinated water ligands forms bound hydroxide ligands(e.g., [Al(H2O)5(OH)]2+, [Al(H2O)4(OH)2]+). The speciation of aluminum in wateris pH dependent. The hydrated trivalent aluminum ion is the predominant form atpH levels below 4. Between pH 5 and 6, the predominant hydrolysis products areAl(OH)2+ and Al(OH)2+, while the solid Al(OH)3 is most prevalent between pH 5.2and 8.8. The soluble species Al(OH)4- is the predominant species above pH 9,and is the only species present above pH 10. Polymeric aluminum hydroxidesappear between pH 4.7 and 10.5, and increase in size until they are transformedinto colloidal particles of amorphous Al(OH)3, which crystallise to gibbsite inacid waters. Polymerisation is affected by the presence of dissolved silica;when enough silica is present, aluminum is precipitated as poorly crystallisedclay mineral species. Hydroxyaluminumcompounds are considered amphoteric (e.g., they can act as both acids and basesin solution). Because of this property, aluminum hydroxides can act as buffersand resist pH changes within the narrow pH range of 4-5. Monomericaluminum compounds, typified by aluminum fluoride, chloride, and sulfate, areconsidered reactive or labile compounds, whereas polymeric aluminum speciesreact much more slowly in the environment. Aluminum has a stronger attractionfor fluoride in an acidic environment compared to other inorganic ligand. Theadsorption of aluminum onto clay surfaces can be a significant factor incontrolling aluminum mobility in the environment, and these adsorptionreactions, measured in one study at pH 3.0-4.1, have been observed to be veryrapid. However, clays may act either as a sink or a source for soluble aluminumdepending on the degree of aluminum saturation on the clay surface. Withinthe pH range of 5-6, aluminum complexes with phosphate and is removed fromsolution. Because phosphate is a necessary nutrient in ecological systems, thisimmobilization of both aluminum and phosphate may result in depleted nutrientstates in surface water. Plantspecies and cultivars of the same species differ considerably in their abilityto take up and translocate aluminum to above-ground parts. Tea leaves maycontain very high concentrations of aluminum, >5,000 mg/kg in old leaves.Other plants that may contain high levels of aluminum include Lycopodium(Lycopodiaceae), a few ferns, Symplocos (Symplocaceae), and Orites(Proteaceae). Aluminum is often taken up and concentrated in root tissue. Insub-alpine ecosystems, the large root biomass of the Douglas fir, Abiesamabilis, takes up aluminum and immobilizes it, preventing largeaccumulation in above-ground tissue. It is unclear to what extent aluminum istaken up into root food crops and leafy vegetables. An uptake factor(concentration of aluminum in the plant/concentration of aluminum in soil) of0.004 for leafy vegetables and 0.00065 for fruits and tubers has been reported,but the pH and plant species from which these uptake factors were derived areunclear. Based upon these values, however, it is clear that aluminum is nottaken up in plants from soil, but is instead biodiluted. Aluminumconcentrations in rainbow trout from an alum-treated lake, an untreated lake,and a hatchery were highest in gill tissue and lowest in muscle. Aluminumresidue analyses in brook trout have shown that whole-body aluminum contentdecreases as the fish advance from larvae to juveniles. These results implythat the aging larvae begin to decrease their rate of aluminum uptake, toeliminate aluminum at a rate that exceeds uptake, or to maintain approximatelythe same amount of aluminum while the body mass increases. The decline inwhole-body aluminum residues in juvenile brook trout may be related to growthand dilution by edible muscle tissue that accumulated less aluminum than didthe other tissues. Thegreatest fraction of the gill-associated aluminum was not sorbed to the gilltissue, but to the gill mucus. It is thought that mucus appears to retardaluminum transport from solution to the membrane surface, thus delaying theacute biological response of the fish. It has been reported that concentrationsof aluminum in whole-body tissue of the Atlantic salmon exposed to highconcentrations of aluminum ranging from 3 ug/g (for fish exposed to 33 ug/L) to96 ug/g (for fish exposed to 264 ug/L) at pH 5.5. After 60 days of exposure,BCFs ranged from 76 to 190 and were directly related to the aluminum exposureconcentration. In acidic waters (pH 4.6-5.3) with low concentrations of calcium(0.5-1.5 mg Ca/L), labile aluminum between 25 and 75 ug/L is toxic. Becausealuminum is toxic to many aquatic species, it is not bioaccumulated to asignificant degree (BCF <300) in most fish and shellfish; therefore,consumption of contaminated fish does not appear to be a significant source ofaluminum exposure in humans. Bioconcentrationof aluminum has also been reported for several aquatic invertebrate species.BCF values ranging from 0.13 to 0.5 in the whole-body were reported for thesnail. Bioconcentration of aluminum has also been reported for aquatic insects. Ecotoxicity: Freshwaterspecies pH >6.5 Fish:Acute LC50 (48-96 h) 5 spp: 0.6 (Salmo salar) - 106 mg/L; Chronic NOEC(8-28 d): 7 spp,NOEC, 0.034-7.1 mg/L. The lowest measured chronic figure was an8-d LC50 of 0.17 mg/L for Micropterus sp. Amphibian:Acute LC50 (4 d): Bufo americanus, 0.86-1.66 mg/L; Chronic LC50 (8-d)2.28 mg/L CrustaceansLC50 (48 h): 1 sp 2.3-36 9 mg/L; Chronic NOEC (7-28 d) 3 spp, 0.136-1.72 mg/L AlgaeEC50 (96 h): population growth, 0.46-0.57 mg/L; 2 spp, chronic NOEC, 0.8-2.0mg/L Freshwaterspecies pH <6.5 (all between pH 4.5 and 6.0) Fish LC50(24-96 h): 4 spp, 0.015 (S. trutta) - 4.2 mg/L; chronic data on Salmotrutta, LC50 (21-42 d) 0.015- 0.105 mg/L AmphibiansLC50 (4-5 d): 2 spp, 0.540-2.670 m/L (absolute range 0.40-5.2 mg/L) Alga: 1sp NOEC growth 2.0 mg/L Amongfreshwater aquatic plants, single-celled plants are generally the mostsensitive to aluminium. Fish are generally more sensitive to aluminium thanaquatic invertebrates. Aluminium is a gill toxicant to fish, causing bothionoregulatory and respiratory effects. Thebioavailability and toxicity of aluminium is generally greatest in acidsolutions. Aluminium in acid habitats has been observed to be toxic to fish andphytoplankton. Aluminium is generally more toxic over the pH range 4.4.5.4,with a maximum toxicity occurring around pH 5.0.5.2. The inorganic single unitaluminium species (Al(OH)2 +) is thought to be the most toxic. Under very acidconditions, the toxic effects of the high H+ concentration appear to be moreimportant than the effects of low concentrations of aluminium; at approximatelyneutral pH values, the toxicity of aluminium is greatly reduced. The solubilityof aluminium is also enhanced under alkaline conditions, due to its amphotericcharacter, and some researchers found that the acute toxicity of aluminiumincreased from pH 7 to pH 9. However, the opposite relationship was found inother studies. The uptake and toxicity of aluminium in freshwater organismsgenerally decreases with increasing water hardness under acidic, neutral andalkaline conditions. Complexing agents such as fluoride, citrate and humicsubstances reduce the availability of aluminium to organisms, Safetyresulting inlower toxicity. Silicon Datacan also reduce aluminium Sheet toxicity to fish. DrinkingWater Standards: aluminium:200 ug/l (UK max.) 200 ug/l(WHO guideline) chloride:400 mg/l (UK max.) 250 mg/l(WHO guideline) fluoride:1.5 mg/l (UK max.) 1.5 mg/l(WHO guideline) nitrate:50 mg/l (UK max.) 50 mg/l(WHO guideline) sulfate:250 mg/l (UK max.) SoilGuideline: none available. AirQuality Standards: none available. For zinc and its compounds: Environmental fate: Zinc is capable of forming complexes with a variety of organic andinorganic groups (ligands). Biological activity can affect the mobility of zincin the aquatic environment, although the biota contains relatively little zinccompared to the sediments. Zinc bioconcentrates moderately in aquaticorganisms; bioconcentration is higher in crustaceans and bivalve species thanin fish. Zinc does not concentrate appreciably in plants, and it does notbiomagnify significantly through terrestrial food chains. However biomagnification may be of concern if concentration ofzinc exceeds 1632 ppm in the top 12 inches of soil. Zinc can persist in water indefinitely and can be toxic to aquaticlife. The threshold concentration for fish is 0.1 ppm. Zinc may be concentratedin the aquatic food chain; it is concentrated over 200,000 times in oysters.Copper is synergistic but calcium is antagonistic to zinc toxicity in fish.Zinc can accumulate in freshwater animals at 5 -1,130 times the concentrationpresent in the water. Furthermore, although zinc actively bioaccumulates inaquatic systems, biota appears to represent a relatively minor sink compared tosediments. Steady-state zinc bioconcentration factors (BCFs) for 12 aquaticspecies range from 4 to 24,000. Crustaceans and fish can accumulate zinc fromboth water and food. A BCF of 1,000 was reported for both aquatic plants andfish, and a value of 10,000 was reported for aquatic invertebrates. The orderof enrichment of zinc in different aquatic organisms was as follows (zincconcentrations in µg/g dry weight appear in parentheses): fish (25), shrimp(50), mussel (60), periphyton (260), zooplankton (330), and oyster (3,300). Thehigh enrichment in oysters may be due to their ingestion of particulate mattercontaining higher concentrations of zinc than ambient water. Otherinvestigators have also indicated that organisms associated with sediments havehigher zinc concentrations than organisms living in the aqueous layer. Withrespect to bioconcentration from soil by terrestrial plants, invertebrates, andmammals, BCFs of 0.4, 8, and 0.6, respectively, have been reported. Theconcentration of zinc in plants depends on the plant species, soil pH, and thecomposition of the soil. Plant species do not concentrate zinc above the levels present insoil. In some fish, it has been observed that the level of zinc found intheir bodies did not directly relate to the exposure concentrations. Bioaccumulationof zinc in fish is inversely related to the aqueous exposure. This evidencesuggests that fish placed in environments with lower zinc concentrations cansequester zinc in their bodies. Version No: 4.7 Page 15 of 20 Issue Date: 29/07/2016 The concentration of zinc in drinking water may increase as aresult of the distribution system and household plumbing. Common pipingmaterials used in distribution systems often contain zinc, as Print Date: 29/07/2016 well as othermetals and alloys. Trace metals8329TFS may enter Slow the water Cure, through Thermally corrosion productsor Conductive simply by theAdhesive, dissolution of Flowable small amounts (Part of metals A) with which the watercomes in contact. Reactions with materials of the distribution system,particularly in soft low-pH waters, very often have produced concentrations ofzinc in tap water much greater than those in the raw or treated waters at theplant of origin. Zinc gives water a metallic taste at low levels. Overexposuresto zinc also have been associated with toxic effects. Ingestion of zinc orzinc-containing compounds has resulted in a variety of systemic effects in thegastrointestinal and hematological systems and alterations in the blood lipidprofile in humans and animals. In addition, lesions have been observed in theliver, pancreas, and kidneys of animals. Environmental toxicity of zinc in water is dependent upon theconcentration of other minerals and the pH of the solution, which affect theligands that associate with zinc. Continued... Zinc occurs in the environment mainly in the +2 oxidation state.Sorption is the dominant reaction, resulting in the enrichment of zinc in suspendedand bed sediments. Zinc in aerobic waters is partitioned into sediments throughsorption onto hydrous iron and manganese oxides, clay minerals, and organicmaterial. The efficiency of these materials in removing zinc from solutionvaries according to their concentrations, pH, redox potential (Eh), salinity,nature and concentrations of complexing ligands, cation exchange capacity, andthe concentration of zinc. Precipitation of soluble zinc compounds appears tobe significant only under reducing conditions in highly polluted water.Generally, at lower pH values, zinc remains as the free ion. The free ion(Zn+2) tends to be adsorbed and transported by suspended solids in unpollutedwaters. Zinc is an essential nutrient that is present in all organisms.Although biota appears to be a minor reservoir of zinc relative to soils andsediments, microbial decomposition of biota in water can produce ligands, suchas humic acids, that can affect the mobility of zinc in the aquatic environmentthrough zinc precipitation and adsorption. The relative mobility of zinc in soil is determined by the samefactors that affect its transport in aquatic systems (i.e., solubility of thecompound, pH, and salinity) The redox status of the soil may shift zinc partitioning. Reductivedissolution of iron and manganese (hydr)oxides under suboxic conditions releasezinc into the aqueous phase; the persistence of suboxic conditions may thenlead to a repartitioning of zinc into sulfide and carbonate solids. Themobility of zinc in soil depends on the solubility of the speciated forms ofthe element and on soil properties such as cation exchange capacity, pH, redoxpotential, and chemical species present in soil; under anaerobic conditions,zinc sulfide is the controlling species. Since zinc sulfide is insoluble, the mobility of zinc in anaerobicsoil is low. In a study of the effect of pH on zinc solubility: When the pH is<7, an inverse relationship exists between the pH and the amount of zinc insolution. As negative charges on soil surfaces increase with increasing pH,additional sites for zinc adsorption are activated and the amount of zinc insolution decreases. The active zinc species in the adsorbed state is the singlycharged zinc hydroxide species (i.e., Zn[OH]+). Other investigators have alsoshown that the mobility of zinc in soil increases at lower soil pH underoxidizing conditions and at a lower cation exchange capacity of soil. On theother hand, the amount of zinc in solution generally increases when the pH is>7 in soils high in organic matter. This is a result of the release oforganically complexed zinc, reduced zinc adsorption at higher pH, or anincrease in the concentration of chelating agents in soil. For calcareoussoils, the relationship between zinc solubility and pH is nonlinear. At a highpH, zinc in solution is precipitated as Zn(OH)2, zinc carbonate (ZnCO3), orcalcium zincate. Clay and metal oxides are capable of sorbing zinc and tend toretard its mobility in soil. Zinc was more mobile at pH 4 than at pH 6.5 as aconsequence of sorption Zinc concentrations in the air are relatively low, except nearindustrial sources such as smelters. No estimate for the atmospheric lifetimeof zinc is available at this time, but the fact that zinc is transported longdistances in air indicates that its lifetime in air is at least on the order ofdays. There are few data regarding the speciation of zinc released to theatmosphere. Zinc is removed from the air by dry and wet deposition, but zincparticles with small diameters and low densities suspended in the atmospheretravel long distances from emission sources.

12.2. Persistence and degradability

Ingredient Persistence: Water/Soil Persistence: Air bisphenol A/ diglycidyl ether HIGH HIGH resin, liquid

12.3. Bioaccumulative potential

Ingredient Bioaccumulation zinc oxide LOW (BCF = 217) bisphenol A/ diglycidyl ether LOW (LogKOW = 2.6835) resin, liquid

12.4. Mobility in soil

Ingredient Mobility bisphenol A/ diglycidyl ether LOW (KOC = 51.43) resin, liquid

12.5.Results of PBT and vPvB assessment

www.element14.com P B T www.farnell.comRelevant available data Not Available Not Available Not Available www.newark.comPBT Criteria fulfilled? Not Available Not Available Not Available

Page <17> 28/10/18 V1.0 12.6. Other adverse effects No data available

SECTION 13 DISPOSAL CONSIDERATIONS

13.1. Waste treatment methods

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. Legislation addressing waste disposal requirements may differ by country, state and/ or territory. Each user must refer to laws operating in their area. In some areas, certain wastes must be tracked. A Hierarchy of Controls seems to be common - the user should investigate: Reduction Reuse Product / Packaging Recycling disposal Disposal (if all else fails) This material may be recycled if unused, or if it has not been contaminated so as to make it unsuitable for its intended use. If it has been contaminated, it may be possible to reclaim the product by filtration, distillation or some other means. Shelf life considerations should also be applied in making decisions of this type. Note that properties of a material may change in use, and recycling or reuse may not always be appropriate. DO NOT allow wash water from cleaning or process equipment to enter drains. It may be necessary to collect all wash water for treatment before disposal. In all cases disposal to sewer may be subject to local laws and regulations and these should be considered first. Where in doubt contact the responsible authority. Recycle wherever possible 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.

Continued... Version No: 4.7 Page 15 of 20 Issue Date: 29/07/2016 Print Date: 29/07/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part A)

theliver, pancreas, and kidneys of animals. Environmental toxicity of zinc in water is dependent upon theconcentration of other minerals and the pH of the solution, which affect theligands that associate with zinc. Zinc occurs in the environment mainly in the +2 oxidation state.Sorption is the dominant reaction, resulting in the enrichment of zinc in suspendedand bed sediments. Zinc in aerobic waters is partitioned into sediments throughsorption onto hydrous iron and manganese oxides, clay minerals, and organicmaterial. The efficiency of these materials in removing zinc from solutionvaries according to their concentrations, pH, redox potential (Eh), salinity,nature and concentrations of complexing ligands, cation exchange capacity, andthe concentration of zinc. Precipitation of soluble zinc compounds appears tobe significant only under reducing conditions in highly polluted water.Generally, at lower pH values, zinc remains as the free ion. The free ion(Zn+2) tends to be adsorbed and transported by suspended solids in unpollutedwaters. Zinc is an essential nutrient that is present in all organisms.Although biota appears to be a minor reservoir of zinc relative to soils andsediments, microbial decomposition of biota in water can produce ligands, suchas humic acids, that can affect the mobility of zinc in the aquatic environmentthrough zinc precipitation and adsorption. The relative mobility of zinc in soil is determined by the samefactors that affect its transport in aquatic systems (i.e., solubility of thecompound, pH, and salinity) The redox status of the soil may shift zinc partitioning. Reductivedissolution of iron and manganese (hydr)oxides under suboxic conditions releasezinc into the aqueous phase; the persistence of suboxic conditions may thenlead to a repartitioning of zinc into sulfide and carbonate solids. Themobility of zinc in soil depends on the solubility of the speciated forms ofthe element and on soil properties such as cation exchange capacity, pH, redoxpotential, and chemical species present in soil; under anaerobic conditions,zinc sulfide is the controlling species. Since zinc sulfide is insoluble, the mobility of zinc in anaerobicsoil is low. In a study of the effect of pH on zinc solubility: When the pH is<7, an inverse relationship exists between the pH and the amount of zinc insolution. As negative charges on soil surfaces increase with increasing pH,additional sites for zinc adsorption are activated and the amount of zinc insolution decreases. The active zinc species in the adsorbed state is the singlycharged zinc hydroxide species (i.e., Zn[OH]+). Other investigators have alsoshown that the mobility of zinc in soil increases at lower soil pH underoxidizing conditions and at a lower cation exchange capacity of soil. On theother hand, the amount of zinc in solution generally increases when the pH is>7 in soils high in organic matter. This is a result of the release oforganically complexed zinc, reduced zinc adsorption at higher pH, or anincrease in the concentration of chelating agents in soil. For calcareoussoils, the relationship between zinc solubility and pH is nonlinear. At a highpH, zinc in solution is precipitated as Zn(OH)2, zinc carbonate (ZnCO3), orcalcium zincate. Clay and metal oxides are capable of sorbing zinc and tend toretard its mobility in soil. Zinc was more mobile at pH 4 than at pH 6.5 as aconsequence of sorption Zinc concentrations in the air are relatively low, except nearindustrial sources such as smelters. No estimate for the atmospheric lifetimeof zinc is available at this time, but the fact that zinc is transported longdistances in air indicates that its lifetime in air is at least on the order ofdays. There are few data regarding the speciation of zinc released to theatmosphere. Zinc is removed from the air by dry and wet deposition, but zincparticles with small diameters and low densities suspended in the atmospheretravel long distances from emission sources.

12.2. Persistence and degradability

Ingredient Persistence: Water/Soil Persistence: Air bisphenol A/ diglycidyl ether HIGH HIGH resin, liquid

12.3. Bioaccumulative potential

Ingredient Bioaccumulation zinc oxide LOW (BCF = 217) bisphenol A/ diglycidyl ether LOW (LogKOW = 2.6835) resin, liquid Safety12.4. Mobility in soil Data Sheet Ingredient Mobility bisphenol A/ diglycidyl ether LOW (KOC = 51.43) resin, liquid

12.5.Results of PBT and vPvB assessment

P B T Relevant available data Not Available Not Available Not Available PBT Criteria fulfilled? Not Available Not Available Not Available

12.6. Other adverse effects No data available

SECTION 13 DISPOSAL CONSIDERATIONS

13.1. Waste treatment methods

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. Legislation addressing waste disposal requirements may differ by country, state and/ or territory. Each user must refer to laws operating in their area. In some areas, certain wastes must be tracked. A Hierarchy of Controls seems to be common - the user should investigate: Reduction Reuse Product / Packaging Recycling disposal Disposal (if all else fails) This material may be recycled if unused, or if it has not been contaminated so as to make it unsuitable for its intended use. If it has been contaminated, it may be possible to reclaim the product by filtration, distillation or some other means. Shelf life considerations should also be applied in making decisions of this type. Note that properties of a material may change in use, and recycling or reuse may not always be appropriate. DO NOT allow wash water from cleaning or process equipment to enter drains. It may be necessary to collect all wash water for treatment before disposal. In all cases disposal to sewer may be subject to local laws and regulations and these should be considered first. Version No: 4.7 Page 16 of 20 Issue Date: 29/07/2016 Where in doubt contact the responsible authority. Print Date: 29/07/2016 8329TFSRecycle wherever Slow possible Cure, or Thermally consult manufacturer Conductive for recycling Adhesive, options. Flowable (Part A) 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. Waste treatment options Not Available

Sewage disposal options Not Available Continued...

SECTION 14 TRANSPORT INFORMATION

Labels Required

For MC002977-25ML8329TFS-25ML, 8329TFS-50ML

NOT REGULATED by Ground ADR Special Provision 375 NOT REGULATED by Air IATA Special Provision A197 NOT REGULATED by Sea IMDG per 2.10.2.7 NOT REGUATED by ADN Special Provision 274 (The provision of 3.1.2.8 apply)

Land transport (ADR)

14.1.UN number 3082 14.2.UN proper shipping ENVIRONMENTALLY HAZARDOUS SUBSTANCE, LIQUID, N.O.S. (contains zinc oxide and bisphenol a/ diglycidyl ether resin, liquid) name

14.3. Transport hazard Class 9 class(es) Subrisk Not Applicable

14.4.Packing group III 14.5.Environmental hazard Not Applicable www.element14.com www.farnell.com Hazard identification (Kemler) 90 www.newark.com Classification code M6 14.6. Special precautions for Hazard Label 9 user Special provisions 274 335 375 601 Page <18> 28/10/18 V1.0 Limited quantity 5 L

Air transport (ICAO-IATA / DGR)

14.1. UN number 3082 14.2. UN proper shipping Environmentally hazardous substance, liquid, n.o.s. * (contains zinc oxide and bisphenol a/ diglycidyl ether resin, liquid) name

ICAO/IATA Class 9 14.3. Transport hazard ICAO / IATA Subrisk Not Applicable class(es) ERG Code 9L

14.4. Packing group III 14.5. Environmental hazard Not Applicable

Special provisions A97 A158 A197 Cargo Only Packing Instructions 964 Cargo Only Maximum Qty / Pack 450 L 14.6. Special precautions for Passenger and Cargo Packing Instructions 964 user Passenger and Cargo Maximum Qty / Pack 450 L Passenger and Cargo Limited Quantity Packing Instructions Y964 Passenger and Cargo Limited Maximum Qty / Pack 30 kg G

Sea transport (IMDG-Code / GGVSee)

14.1. UN number 3082 14.2. UN proper shipping ENVIRONMENTALLY HAZARDOUS SUBSTANCE, LIQUID, N.O.S. (contains zinc oxide and bisphenol a/ diglycidyl ether resin, liquid) name

14.3. Transport hazard IMDG Class 9 class(es) IMDG Subrisk Not Applicable

14.4. Packing group III

Continued... Version No: 4.7 Page 16 of 20 Issue Date: 29/07/2016 Print Date: 29/07/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part A)

Waste treatment options Not Available Sewage disposal options Not Available

SECTION 14 TRANSPORT INFORMATION

Labels Required

For 8329TFS-25ML, 8329TFS-50ML

Land transport (ADR)

14.1.UN number 3082 14.2.UN proper shipping ENVIRONMENTALLY HAZARDOUS SUBSTANCE, LIQUID, N.O.S. (contains zinc oxide and bisphenol a/ diglycidyl ether resin, liquid) Safetyname Data Sheet

14.3. Transport hazard Class 9 class(es) Subrisk Not Applicable

14.4.Packing group III 14.5.Environmental hazard Not Applicable

Hazard identification (Kemler) 90 Classification code M6 14.6. Special precautions for Hazard Label 9 user Special provisions 274 335 375 601 Limited quantity 5 L

Air transport (ICAO-IATA / DGR)

14.1. UN number 3082 14.2. UN proper shipping Environmentally hazardous substance, liquid, n.o.s. * (contains zinc oxide and bisphenol a/ diglycidyl ether resin, liquid) name

ICAO/IATA Class 9 14.3. Transport hazard ICAO / IATA Subrisk Not Applicable class(es) ERG Code 9L

14.4. Packing group III 14.5. Environmental hazard Not Applicable

Sea transport (IMDG-Code / GGVSee)

14.1. UN number 3082 14.2. UN proper shipping ENVIRONMENTALLY HAZARDOUS SUBSTANCE, LIQUID, N.O.S. (contains zinc oxide and bisphenol a/ diglycidyl ether resin, liquid) name

Version No: 4.7 Page 17 of 20 Issue Date: 29/07/2016 14.3. Transport hazard IMDG Class 9 Print Date: 29/07/2016 class(es) IMDG8329TFS Subrisk Slow Not Applicable Cure, Thermally Conductive Adhesive, Flowable (Part A)

14.4. Packing group III 14.5. Environmental hazard Marine Pollutant Continued...

EMS Number F-A, S-F 14.6. Special precautions for Special provisions 274 335 969 user Limited Quantities 5 L

Inland waterways transport (ADN)

14.1. UN number 3082 14.2. UN proper shipping ENVIRONMENTALLY HAZARDOUS SUBSTANCE, LIQUID, N.O.S. (contains zinc oxide and bisphenol a/ diglycidyl ether resin, liquid) name

14.3. Transport hazard 9 Not Applicable class(es)

14.4. Packing group III 14.5. Environmental hazard Not Applicable

www.element14.com Classification code M6 Special provisions 274; 335; 375; 601 www.farnell.com14.6. Special precautions for Limited quantity 5 L www.newark.comuser Equipment required PP Fire cones number 0 Page <19> 28/10/18 V1.0

Transport in bulk according to Annex II of MARPOL and the IBC code Not Applicable

SECTION 15 REGULATORY INFORMATION

15.1. Safety, health and environmental regulations / legislation specific for the substance or mixture

ALUMINIUM OXIDE(1344-28-1.) IS FOUND ON THE FOLLOWING REGULATORY LISTS EU REACH Regulation (EC) No 1907/2006 - Annex XVII - Restrictions on the manufacture, International Agency for Research on Cancer (IARC) - Agents Classified by the IARC placing on the market and use of certain dangerous substances, mixtures and articles Monographs European Customs Inventory of Chemical Substances ECICS (English) UK Workplace Exposure Limits (WELs) European Union - European Inventory of Existing Commercial Chemical Substances (EINECS) (English)

BISPHENOL F GLYCIDYL ETHER/ FORMALDEHYDE COPOLYMER(28064-14-4) IS FOUND ON THE FOLLOWING REGULATORY LISTS EU REACH Regulation (EC) No 1907/2006 - Annex XVII - Restrictions on the manufacture, placing on the market and use of certain dangerous substances, mixtures and articles

ZINC OXIDE(1314-13-2) IS FOUND ON THE FOLLOWING REGULATORY LISTS EU European Chemicals Agency (ECHA) Community Rolling Action Plan (CoRAP) List of European Union (EU) Annex I to Directive 67/548/EEC on Classification and Labelling of Substances Dangerous Substances - updated by ATP: 31 European Customs Inventory of Chemical Substances ECICS (English) European Union (EU) Regulation (EC) No 1272/2008 on Classification, Labelling and European Union - European Inventory of Existing Commercial Chemical Substances (EINECS) Packaging of Substances and Mixtures - Annex VI (English) International Agency for Research on Cancer (IARC) - Agents Classified by the IARC Monographs

(C12-14)ALKYLGLYCIDYL ETHER(68609-97-2) IS FOUND ON THE FOLLOWING REGULATORY LISTS EU European Chemicals Agency (ECHA) Community Rolling Action Plan (CoRAP) List of European Union - European Inventory of Existing Commercial Chemical Substances (EINECS) Substances (English) EU REACH Regulation (EC) No 1907/2006 - Annex XVII - Restrictions on the manufacture, European Union (EU) Annex I to Directive 67/548/EEC on Classification and Labelling of placing on the market and use of certain dangerous substances, mixtures and articles Dangerous Substances - updated by ATP: 31 European Customs Inventory of Chemical Substances ECICS (English) European Union (EU) Regulation (EC) No 1272/2008 on Classification, Labelling and European Trade Union Confederation (ETUC) Priority List for REACH Authorisation Packaging of Substances and Mixtures - Annex VI

BISPHENOL A/ DIGLYCIDYL ETHER RESIN, LIQUID(25068-38-6) IS FOUND ON THE FOLLOWING REGULATORY LISTS EU European Chemicals Agency (ECHA) Community Rolling Action Plan (CoRAP) List of European Union (EU) No-Longer Polymers List (NLP) (67/548/EEC) Substances European Union (EU) Regulation (EC) No 1272/2008 on Classification, Labelling and EU REACH Regulation (EC) No 1907/2006 - Annex XVII - Restrictions on the manufacture, Packaging of Substances and Mixtures - Annex VI placing on the market and use of certain dangerous substances, mixtures and articles European Union (EU) Annex I to Directive 67/548/EEC on Classification and Labelling of Dangerous Substances - updated by ATP: 31

CARBON BLACK(1333-86-4) IS FOUND ON THE FOLLOWING REGULATORY LISTS EU European Chemicals Agency (ECHA) Community Rolling Action Plan (CoRAP) List of European Trade Union Confederation (ETUC) Priority List for REACH Authorisation Substances European Union - European Inventory of Existing Commercial Chemical Substances (EINECS) EU REACH Regulation (EC) No 1907/2006 - Annex XVII - Restrictions on the manufacture, (English) placing on the market and use of certain dangerous substances, mixtures and articles International Agency for Research on Cancer (IARC) - Agents Classified by the IARC European Customs Inventory of Chemical Substances ECICS (English) Monographs European List of Notified Chemical Substances (ELINCS) UK Workplace Exposure Limits (WELs)

This safety data sheet is in compliance with the following EU legislation and its adaptations - as far as applicable - : 67/548/EEC, 1999/45/EC, 98/24/EC, 92/85/EC, 94/33/EC, 91/689/EEC,

Continued... Version No: 4.7 Page 17 of 20 Issue Date: 29/07/2016 Print Date: 29/07/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part A)

14.5. Environmental hazard Marine Pollutant

EMS Number F-A, S-F 14.6. Special precautions for Special provisions 274 335 969 user Limited Quantities 5 L

Inland waterways transport (ADN)

14.1. UN number 3082 14.2. UN proper shipping Safety DataENVIRONMENTALLY Sheet HAZARDOUS SUBSTANCE, LIQUID, N.O.S. (contains zinc oxide and bisphenol a/ diglycidyl ether resin, liquid) name

14.3. Transport hazard 9 Not Applicable class(es)

14.4. Packing group III 14.5. Environmental hazard Not Applicable

Classification code M6 Special provisions 274; 335; 375; 601 14.6. Special precautions for Limited quantity 5 L user Equipment required PP Fire cones number 0

Transport in bulk according to Annex II of MARPOL and the IBC code Not Applicable

SECTION 15 REGULATORY INFORMATION

15.1. Safety, health and environmental regulations / legislation specific for the substance or mixture

CARBON BLACK(1333-86-4) IS FOUND ON THE FOLLOWING REGULATORY LISTS EU European Chemicals Agency (ECHA) Community Rolling Action Plan (CoRAP) List of European Trade Union Confederation (ETUC) Priority List for REACH Authorisation Substances European Union - European Inventory of Existing Commercial Chemical Substances (EINECS) EU REACH Regulation (EC) No 1907/2006 - Annex XVII - Restrictions on the manufacture, (English) Versionplacing No: on 4.7 the market and use of certain dangerous substances, mixtures and articlesPage 18 of 20 International Agency for Research on Cancer (IARC) - Agents Classified Issueby the Date: IARC 29/07/2016 European Customs Inventory of Chemical Substances ECICS (English) Monographs Print Date: 29/07/2016 European List of Notified Chemical Substances8329TFS (ELINCS) Slow Cure, Thermally ConductiveUK Adhesive, Workplace Exposure Flowable Limits (WELs) (Part A)

This safety data sheet is in compliance with the following EU legislation and its adaptations - as far as applicable - : 67/548/EEC, 1999/45/EC, 98/24/EC, 92/85/EC, 94/33/EC, 91/689/EEC,

1999/13/EC, Commission Regulation (EU) 2015/830, Regulation (EC) No 1272/2008 and their amendments as well as the following British legislation: - The Control of Substances HazardousContinued... to Health Regulations (COSHH) 2002 - COSHH Essentials - The Management of Health and Safety at Work Regulations 1999

15.2. Chemical safety assessment For further information please look at the Chemical Safety Assessment and Exposure Scenarios prepared by your Supply Chain if available.

www.element14.comECHA SUMMARY

www.farnell.comIngredient CAS number Index No ECHA Dossier www.newark.comaluminium oxide 1344-28-1. Not Available 01-2119817795-27-XXXX, 01-2119529248-35-XXXX

Harmonisation (C&L Pictograms Signal Hazard Class and Category Code(s) Hazard Statement Code(s) Inventory) Page <20> Word Code(s) 28/10/18 V1.0 H370, H332, H335, H372, H341, H317, GHS08, Dgr, Wng, 1 Not Classified H350, H361, H220, H315, H319, H302, GHS09, GHS02 H225 Not Classified, STOT SE 3, Acute Tox. 4, STOT RE 1, Muta. 2, Skin Sens. 1, Carc. H370, H332, H335, H372, H341, H317, GHS08, Dgr, Wng, 2 1B, Repr. 2, Aquatic Chronic 3, Skin Irrit. 2, Eye Irrit. 2, STOT RE 2, Flam. Liq. 2, H350, H361, H220, H315, H319, H302, GHS09, GHS02 Aquatic Chronic 4 H225 Harmonisation Code 1 = The most prevalent classification. Harmonisation Code 2 = The most severe classification.

Ingredient CAS number Index No ECHA Dossier bisphenol F glycidyl ether/ 28064-14-4 Not Available Not Available formaldehyde copolymer

Harmonisation (C&L Pictograms Signal Word Hazard Statement Hazard Class and Category Code(s) Inventory) Code(s) Code(s) 1 Skin Irrit. 2, Skin Sens. 1, Eye Irrit. 2, Aquatic Chronic 2 GHS07, GHS09, Wng H315, H317, H319 Skin Irrit. 2, Skin Sens. 1, Eye Irrit. 2, Aquatic Chronic 2, Skin Sens. 1B, Not Classified, 2 GHS07, GHS09, Wng H315, H317, H319, H335 STOT SE 3 Harmonisation Code 1 = The most prevalent classification. Harmonisation Code 2 = The most severe classification.

Ingredient CAS number Index No ECHA Dossier zinc oxide 1314-13-2 030-013-00-7 01-2119463881-32-XXXX

Harmonisation (C&L Pictograms Signal Hazard Class and Category Code(s) Hazard Statement Code(s) Inventory) Word Code(s) H360, H335, H370, H372, H314, 1 Aquatic Acute 1 GHS09, Wng H318, H350, H300, H330, H317, H341 Aquatic Acute 1, Aquatic Chronic 1, Acute Tox. 4, Repr. 1A, STOT RE 2, Skin Irrit. 2, Eye H360, H335, H370, H372, H314, GHS09, Wng, GHS08, 2 Irrit. 2, STOT SE 3, STOT SE 1, Not Classified, STOT RE 1, Skin Corr. 1B, Eye Dam. 1, H318, H350, H300, H330, H317, Dgr, GHS05, GHS06 Carc. 1A, Acute Tox. 2, Skin Sens. 1, Muta. 2 H341 H360, H335, H370, H372, H314, 1 Aquatic Acute 1, Aquatic Chronic 1 GHS09, Wng H318, H350, H300, H330, H317, H341 H360, H335, H370, H372, H314, 2 Aquatic Acute 1, Aquatic Chronic 1 GHS09, Wng H318, H350, H300, H330, H317, H341 Harmonisation Code 1 = The most prevalent classification. Harmonisation Code 2 = The most severe classification.

Ingredient CAS number Index No ECHA Dossier (C12-14)alkylglycidyl ether 68609-97-2 603-103-00-4 01-2119485289-22-XXXX

Harmonisation (C&L Pictograms Signal Word Hazard Statement Hazard Class and Category Code(s) Inventory) Code(s) Code(s) 1 Skin Irrit. 2, Skin Sens. 1 GHS07, Wng H315, H317 Skin Irrit. 2, Skin Sens. 1, Aquatic Chronic 2, Not Classified, Acute Tox. 4, Eye Irrit. 2 GHS07, Wng, GHS09 H315, H317 2 Harmonisation Code 1 = The most prevalent classification. Harmonisation Code 2 = The most severe classification.

Ingredient CAS number Index No ECHA Dossier bisphenol A/ diglycidyl ether 25068-38-6 603-074-00-8 01-2119456619-26-XXXX resin, liquid

Continued... Version No: 4.7 Page 18 of 20 Issue Date: 29/07/2016 Print Date: 29/07/2016 Safety Data8329TFS Slow Sheet Cure, Thermally Conductive Adhesive, Flowable (Part A)

1999/13/EC, Commission Regulation (EU) 2015/830, Regulation (EC) No 1272/2008 and their amendments as well as the following British legislation: - The Control of Substances Hazardous to Health Regulations (COSHH) 2002 - COSHH Essentials - The Management of Health and Safety at Work Regulations 1999

15.2. Chemical safety assessment For further information please look at the Chemical Safety Assessment and Exposure Scenarios prepared by your Supply Chain if available.

ECHA SUMMARY

Ingredient CAS number Index No ECHA Dossier aluminium oxide 1344-28-1. Not Available 01-2119817795-27-XXXX, 01-2119529248-35-XXXX

Ingredient CAS number Index No ECHA Dossier bisphenol F glycidyl ether/ 28064-14-4 Not Available Not Available formaldehyde copolymer

Ingredient CAS number Index No ECHA Dossier zinc oxide 1314-13-2 030-013-00-7 01-2119463881-32-XXXX

Ingredient CAS number Index No ECHA Dossier (C12-14)alkylglycidyl ether 68609-97-2 603-103-00-4 01-2119485289-22-XXXX

Ingredient CAS number Index No ECHA Dossier bisphenol A/ diglycidyl ether 25068-38-6 603-074-00-8 01-2119456619-26-XXXX resin, liquid

Harmonisation (C&L Pictograms Signal Hazard Statement Hazard Class and Category Code(s) Inventory) Word Code(s) Code(s) 1 Skin Irrit. 2, Skin Sens. 1, Eye Irrit. 2, Aquatic Chronic 2 GHS07, GHS09, Wng H315, H317, H319 www.element14.com Skin Irrit. 2, Skin Sens. 1, Eye Irrit. 2, Aquatic Chronic 2, Not Classified, Acute Tox. 4, Aquatic GHS09, Wng, GHS08, H315, H317, H319, 2 www.farnell.com Chronic 3, Aquatic Chronic 4, Skin Corr. 1A, Aquatic Acute 1, Aquatic Chronic 1 Dgr, GHS07 H372 www.newark.com1 Skin Irrit. 2, Skin Sens. 1, Eye Irrit. 2, Aquatic Chronic 2 GHS07, GHS09, Wng H315, H317, H319 2 Skin Irrit. 2, Skin Sens. 1, Eye Irrit. 2, Aquatic Chronic 2, Skin Sens. 1B, Skin Sens. 1A, Not Classified GHS07, GHS09, Wng H315, H317, H319 1 Skin Irrit. 2, Skin Sens. 1A, Aquatic Chronic 2 Page <21> GHS07, GHS09, Wng H315,28/10/18 H317 V1.0

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1999/13/EC, Commission Regulation (EU) 2015/830, Regulation (EC) No 1272/2008 and their amendments as well as the following British legislation: - The Control of Substances Hazardous to Health Regulations (COSHH) 2002 - COSHH Essentials - The Management of Health and Safety at Work Regulations 1999

15.2. Chemical safety assessment For further information please look at the Chemical Safety Assessment and Exposure Scenarios prepared by your Supply Chain if available.

ECHA SUMMARY

Ingredient CAS number Index No ECHA Dossier aluminium oxide 1344-28-1. Not Available 01-2119817795-27-XXXX, 01-2119529248-35-XXXX

Ingredient CAS number Index No ECHA Dossier bisphenol F glycidyl ether/ 28064-14-4 Not Available Not Available formaldehyde copolymer

Ingredient CAS number Index No ECHA Dossier zinc oxide 1314-13-2 030-013-00-7 01-2119463881-32-XXXX

Ingredient CAS number Index No ECHA Dossier (C12-14)alkylglycidyl ether 68609-97-2 603-103-00-4 01-2119485289-22-XXXX

Harmonisation (C&L Pictograms Signal Word Hazard Statement Hazard Class and Category Code(s) Inventory) Code(s) Code(s) 1 Skin Irrit. 2, Skin Sens. 1 GHS07, Wng H315, H317 Skin Irrit. 2, Skin Sens. 1, Aquatic Chronic 2, Not Classified, Acute Tox. 4, Eye Irrit. 2 GHS07, Wng, GHS09 H315, H317 2 SafetyHarmonisation Code 1 = The mostData prevalent classification. Sheet Harmonisation Code 2 = The most severe classification. Ingredient CAS number Index No ECHA Dossier bisphenol A/ diglycidyl ether 25068-38-6 603-074-00-8 01-2119456619-26-XXXX resin, liquid

Harmonisation (C&L Pictograms Signal Hazard Statement Hazard Class and Category Code(s) Inventory) Word Code(s) Code(s) 1 Skin Irrit. 2, Skin Sens. 1, Eye Irrit. 2, Aquatic Chronic 2 GHS07, GHS09, Wng H315, H317, H319 Skin Irrit. 2, Skin Sens. 1, Eye Irrit. 2, Aquatic Chronic 2, Not Classified, Acute Tox. 4, Aquatic GHS09, Wng, GHS08, H315, H317, H319, 2 Version No: 4.7 Chronic 3, Aquatic Chronic 4, Skin Corr. 1A, AquaticPage Acute 19 of 1, 20 Aquatic Chronic 1 Dgr, GHS07 H372Issue Date: 29/07/2016 1 Skin Irrit. 2, Skin Sens. 1, Eye Irrit. 2, Aquatic Chronic 2 GHS07, GHS09, Wng H315,Print H317, Date: H319 29/07/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part A) 2 Skin Irrit. 2, Skin Sens. 1, Eye Irrit. 2, Aquatic Chronic 2, Skin Sens. 1B, Skin Sens. 1A, Not Classified GHS07, GHS09, Wng H315, H317, H319 1 Skin Irrit. 2, Skin Sens. 1A, Aquatic Chronic 2 GHS07, GHS09, Wng H315, H317 2 Skin Irrit. 2, Skin Sens. 1A, Aquatic Chronic 2 GHS07, GHS09, Wng H315, H317 Harmonisation Code 1 = The most prevalent classification. Harmonisation Code 2 = The most severe classification. Continued...

Ingredient CAS number Index No ECHA Dossier carbon black 1333-86-4 Not Available 01-2119384822-32-XXXX, 01-2119489801-30-XXXX, 01-2119475601-40-XXXX

Harmonisation (C&L Pictograms Signal Hazard Class and Category Code(s) Hazard Statement Code(s) Inventory) Word Code(s) GHS08, Wng, Dgr, H351, H335, H319, H372, 1 Not Classified GHS06, GHS02, GHS09 H251, H315, H228, H370, H332 Not Classified, Carc. 2, STOT SE 3, Eye Irrit. 2, STOT RE 2, STOT RE 1, Aquatic GHS08, Wng, Dgr, H351, H335, H319, H372, 2 Chronic 4, Self-heat. 1, Self-heat. 2, Skin Irrit. 2, STOT SE 1, Aquatic Chronic 1, Flam. GHS06, GHS02, GHS09 H251, H315, H228, H370, H332 Sol. 2, Acute Tox. 4 Not Classified, Carc. 2, STOT SE 3, Eye Irrit. 2, STOT RE 2, STOT RE 1, Aquatic GHS08, Wng, Dgr, H351, H335, H319, H372, 2 Chronic 4, Self-heat. 1, Self-heat. 2, Skin Irrit. 2, STOT SE 1, Aquatic Chronic 1, Flam. GHS06, GHS02, GHS09 H251, H315, H228, H370, H332 Sol. 2, Acute Tox. 4 Harmonisation Code 1 = The most prevalent classification. Harmonisation Code 2 = The most severe classification.

National Inventory Status Australia - AICS Y Canada - DSL Y Canada - NDSL N ((C12-14)alkylglycidyl ether; bisphenol A/ diglycidyl ether resin, liquid; aluminium oxide; bisphenol F glycidyl ether/ formaldehyde copolymer; carbon black) China - IECSC Y Europe - EINEC / ELINCS / N (bisphenol F glycidyl ether/ formaldehyde copolymer) NLP Japan - ENCS N ((C12-14)alkylglycidyl ether; bisphenol A/ diglycidyl ether resin, liquid) Korea - KECI Y New Zealand - NZIoC Y Philippines - PICCS Y USA - TSCA Y Y = All ingredients are on the inventory Legend: N = Not determined or one or more ingredients are not on the inventory and are not exempt from listing(see specific ingredients in brackets)

SECTION 16 OTHER INFORMATION

Full text Risk and Hazard codes

H220 Extremely flammable gas. H225 Highly flammable liquid and vapour. H228 Flammable solid. H251 Self-heating: may catch fire. H300 Fatal if swallowed. H302 Harmful if swallowed. H314 Causes severe skin burns and eye damage. H318 Causes serious eye damage. H330 Fatal if inhaled. H332 Harmful if inhaled. H335 May cause respiratory irritation. H341 Suspected of causing genetic defects. H350 May cause cancer. www.element14.comH351 Suspected of causing cancer. www.farnell.comH360 May damage fertility or the unborn child. www.newark.comH361 Suspected of damaging fertility or the unborn child. H370 Causes damage to organs. H372 Causes damage to organs. Page <22> 28/10/18 V1.0 H411 Toxic to aquatic life with long lasting effects.

Other information

Ingredients with multiple cas numbers

Name CAS No bisphenol F glycidyl ether/ 28064-14-4, 42616-71-7, 59029-73-1, 94422-39-6 formaldehyde copolymer zinc oxide 1314-13-2, 175449-32-8 bisphenol A/ diglycidyl ether 25068-38-6, 25085-99-8 resin, liquid

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2 Skin Irrit. 2, Skin Sens. 1A, Aquatic Chronic 2 GHS07, GHS09, Wng H315, H317 Harmonisation Code 1 = The most prevalent classification. Harmonisation Code 2 = The most severe classification.

Ingredient CAS number Index No ECHA Dossier carbon black 1333-86-4 Not Available 01-2119384822-32-XXXX, 01-2119489801-30-XXXX, 01-2119475601-40-XXXX

SECTION 16 OTHER INFORMATION

Full text Risk and Hazard codes

H220 Extremely flammable gas. H225 Highly flammable liquid and vapour. H228 Flammable solid. H251 Self-heating: may catch fire. H300 Fatal if swallowed. H302 Harmful if swallowed. H314 Causes severe skin burns and eye damage. SafetyH318 DataCauses serious eye damage.Sheet H330 Fatal if inhaled. H332 Harmful if inhaled. H335 May cause respiratory irritation. H341 Suspected of causing genetic defects. H350 May cause cancer. H351 Suspected of causing cancer. H360 May damage fertility or the unborn child. H361 Suspected of damaging fertility or the unborn child. H370 Causes damage to organs. H372 Causes damage to organs. H411 Toxic to aquatic life with long lasting effects.

Other information

Ingredients with multiple cas numbers

Name CAS No bisphenol F glycidyl ether/ 28064-14-4, 42616-71-7, 59029-73-1, 94422-39-6 Versionformaldehyde No: 4.7 copolymer Page 20 of 20 Issue Date: 29/07/2016 Print Date: 29/07/2016 zinc oxide 1314-13-2,8329TFS 175449-32-8 Slow Cure, Thermally Conductive Adhesive, Flowable (Part A) bisphenol A/ diglycidyl ether 25068-38-6, 25085-99-8 resin, liquid 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. Continued... A list of reference resources used to assist the committee may be found at: www.chemwatch.net

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.

For detailed advice on Personal Protective Equipment, refer to the following EU CEN Standards: EN 166 Personal eye-protection EN 340 Protective clothing EN 374 Protective gloves against chemicals and micro-organisms EN 13832 Footwear protecting against chemicals EN 133 Respiratory protective devices

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 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

www.element14.com www.farnell.com www.newark.com

Page <23> 28/10/18 V1.0

end of SDS Slow Cure, Thermally Conductive Adhesive, Flowable (Part B) SafetyMG Chemicals Slow UK SlowLimited Cure,Data Cure, Thermally Thermally Sheet Conductive Conductive Adhesive, Adhesive, Flowable Flowable (Part (Part B) B)Chemwatch Hazard Alert Code: 2 VersionMG Chemicals MGNo: 1.2 Chemicals UK Limited UK Limited ChemwatchChemwatch HazardIssue Hazard Date:Alert 01/04/2016 Code: Alert Code:2 2 Safety Data Sheet (Conforms to Regulations (EC) No 2015/830) Print Date: 01/04/2016 VersionVersion No: 1.2 No: 1.2 Issue Date:Issue 01/04/2016 Date: 01/04/2016 Initial Date: 01/04/2016 Safety DataSafety Sheet Data (Conforms Sheet (Conforms to Regulations to Regulations (EC) No (EC) 2015/830) No 2015/830) Print Date:Print 01/04/2016 Date: 01/04/2016 L.REACH.GBR.EN Initial Date:Initial 01/04/2016 Date: 01/04/2016 Slow Cure, Thermally Conductive Adhesive, Flowable (Part B) L.REACH.GBR.ENL.REACH.GBR.EN SECTION 1 IDENTIFICATION OF THE SUBSTANCE / MIXTURE AND OF THE COMPANY / UNDERTAKING MG Chemicals UK Limited Chemwatch Hazard Alert Code: 2 SECTIONSECTION 1 IDENTIFICATION 1 IDENTIFICATION OF THE OF SUBSTANCE THE SUBSTANCE / MIXTURE / MIXTURE AND OFAND THE OF COMPANYTHE COMPANY / UNDERTAKING / UNDERTAKING 1.1.ProductVersion Identifier No: 1.2 Issue Date: 01/04/2016 Safety Data Sheet (Conforms to Regulations (EC) No 2015/830) Print Date: 01/04/2016 1.1.Product1.1.Product IdentifierProduct Identifier name Slow Cure, Thermally Conductive Adhesive, Flowable (Part B) Initial Date: 01/04/2016 L.REACH.GBR.EN ProductSynonymsProduct name nameMC002977 Slow Cure, Slow Thermally Part Cure, B Thermally Conductive Conductive Adhesive, Adhesive, Flowable Flowable (Part B) (Part B) Proper shippingSynonyms nameSynonymsENVIRONMENTALLYMC002977 Part HAZARDOUS B Part B SUBSTANCE, SOLID, N.O.S. (contains zinc oxide) SECTION 1 IDENTIFICATION OF THE SUBSTANCE / MIXTURE AND OF THE COMPANY / UNDERTAKING ProperOther Propershipping means shipping name of nameENVIRONMENTALLYENVIRONMENTALLY HAZARDOUS HAZARDOUS SUBSTANCE, SUBSTANCE, SOLID, SOLID,N.O.S. (containsN.O.S. (contains zinc oxide) zinc oxide) Not Available identification Other meansOther meansof of 1.1.Product IdentifierNot AvailableNot Available identificationidentification 1.2. Relevant identified usesProduct of name the substance Slowor mixture Cure, Thermally and uses Conductive advised Adhesive, against Flowable (Part B)

1.2. RelevantRelevant1.2. Relevant identified identified identified uses usesSynonymsThermally ofuses the of substance conductive the substance adhesive or mixture for or bonding mixture Part and B and uses thermaland adviseduses management advised against against

RelevantUsesRelevant advised identifiedProper identifiedagainst uses shipping usesThermallyNot name for useThermally conductive as ENVIRONMENTALLYa spray conductive adhesive coating adhesive for bonding HAZARDOUS for bonding and thermal and SUBSTANCE, thermalmanagement management SOLID, N.O.S. (contains zinc oxide) Other means of Uses advisedUses advised against againstNot for useNot asfor aNotuse spray Availableas acoating spray coating 1.3. Details of the supplieridentification of the safety data sheet

1.3.Registered Details1.3. Details of company the of supplier thename supplier of the of safety the safety data sheet data sheet 1.2. Relevant identified uses of the substance or mixture and uses advised against RegisteredRegistered company Addresscompany name namePremier Farnell plc Relevant identified uses Thermally conductive adhesive for bonding and thermal management TeAddresslephoneAddress150 Armley Road, Leeds, LS12 2QQ Uses advised against Not for use as a spray coating TelephoneFaxTelephone+44 (0) 870 129 8608 WebsiteFax Fax-Not Available www.mgchemicals.com 1.3. Details of the supplier of the safety data sheet WebsiteEmailWebsite-Not AvailableNot Available www.mgchemicals.comwww.mgchemicals.com Registered company name Email Email Address 1.4. Emergency telephone number Telephone 1.4.Association Emergency1.4. Emergency / Organisation telephone telephone numberPremier number Farnell plc Fax AssociationEmergencyAssociation / Organisation telephone / Organisation +44+(44) 1865870-8200418 407333 numbers Website Not Available www.mgchemicals.com EmergencyEmergency telephone telephone +(44) 870-8200418+(44) 870-8200418 Other emergency telephonenumbersnumbers Email NA+(1) 703-527-3887 numbers Other emergencyOther emergency telephone telephone +(1) 703-527-3887+(1) 703-527-3887 1.4. Emergencynumbersnumbers telephone number

Association / Organisation SECTION 2 HAZARDSEmergency IDENTIFICATION telephone +(44) 870-8200418 SECTIONSECTION 2 HAZARDS 2 HAZARDS IDENTIFICATIONnumbers IDENTIFICATION 2.1.ClassificationOther emergencyof the substance telephone or mixture +(1) 703-527-3887 2.1.Classification2.1.Classification of the of substance thenumbers substance or mixture or mixture Considered a dangerous mixture according to Directive 1999/45/EC, Reg. (EC) No 1272/2008 (if applicable) and their amendments. Classified as Dangerous Goods for transport purposes.

ConsideredClassificationConsidered a dangerous according a dangerous mixture to mixtureaccording according to Directive to Directive 1999/45/EC, 1999/45/EC, Reg. (EC) Reg. No (EC) 1272/2008 No 1272/2008 (if applicable) (if applicable) and their and amendments. their amendments. Classified Classified as Dangerous as Dangerous Goods forGoods transport for transport purposes. purposes. regulation (EC) No Skin Corrosion/Irritation Category 2, Skin Sensitizer Category 1, Eye Irritation Category 2, Chronic Aquatic Hazard Category 1 ClassificationClassification according according to to 1272/2008SECTION [CLP] 2 [1]HAZARDS IDENTIFICATION regulationregulation (EC) No (EC) NoSkin Corrosion/IrritationSkin Corrosion/Irritation Category Category 2, Skin Sensitizer2, Skin Sensitizer Category Category 1, Eye Irritation1, Eye Irritation Category Category 2, Chronic 2, Chronic Aquatic AquaticHazard HazardCategory Category 1 1 [1] 1272/20081272/2008 [CLP] [CLP] 1.[1] Classified by Chemwatch; 2. Classification drawn from EC Directive 67/548/EEC - Annex I ; 3. Classification drawn from EC Directive 1272/2008 - Annex Legend: 2.1.Classification VIof the substance or mixture 1. Classified1. Classified by Chemwatch; by Chemwatch; 2. Classification 2. Classification drawn from drawn EC from Directive EC Directive 67/548/EEC 67/548/EEC - Annex - IAnnex ; 3. Classification I ; 3. Classification drawn from drawn EC from Directive EC Directive 1272/2008 1272/2008 - Annex - Annex Legend:Legend: VI VI Considered a dangerous mixture according to Directive 1999/45/EC, Reg. (EC) No 1272/2008 (if applicable) and their amendments. Classified as Dangerous Goods for transport purposes. 2.2. Label elements Classification according to 2.2. Label2.2. Labelelements elementsregulation (EC) No Skin Corrosion/Irritation Category 2, Skin Sensitizer Category 1, Eye Irritation Category 2, Chronic Aquatic Hazard Category 1 1272/2008 [CLP] [1] CLP label elements 1. Classified by Chemwatch; 2. Classification drawn from EC Directive 67/548/EEC - Annex I ; 3. Classification drawn from EC Directive 1272/2008 - Annex Legend: CLP labelCLP elements label elements VI

2.2.SIGNAL Label WORD elementsWARNING

SIGNALSIGNAL WORD WORDWARNINGWARNING Hazard statement(s) CLP label elements HazardHazard statement(s) statement(s)H315 Causes skin irritation.

H315H317 H315CausesMay causeCauses skin an irritation. allergic skin irritation. skin reaction. H319H317 H317CausesMay causeMay serious an cause allergic eye an irritation. allergicskin reaction. skin reaction. SIGNAL WORD WARNING H410H319 H319VeryCauses toxicCauses serious to aquatic seriouseye irritation.life eyewith irritation. long lasting effects. H410 Very toxicVery to toxicaquatic to aquaticlife with lifelong with lasting long effects.lasting effects. Hazard statement(s)H410 Continued... www.element14.com H315 Causes skin irritation. Continued...Continued... www.farnell.com H317 May cause an allergic skin reaction. www.newark.com H319 Causes serious eye irritation. H410 Very toxic to aquatic life with long lasting effects.

Page <24> 28/10/18 V1.0Continued... VersionSafety No: 1.2 Data SheetPage 2 of 22 Issue Date: 01/04/2016 Print Date: 01/04/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part B)

Supplementary statement(s) Not Applicable

Precautionary statement(s) Prevention

P280 Wear protective gloves/protective clothing/eye protection/face protection. P261 Avoid breathing dust/fume/gas/mist/vapours/spray. P273 Avoid release to the environment. P272 Contaminated work clothing should not be allowed out of the workplace.

Precautionary statement(s) Response

Precautionary statement(s) Storage Not Applicable

Precautionary statement(s) Disposal

P501 Dispose of contents/container in accordance with local regulations.

2.3. Other hazards Inhalation and/or ingestion may produce health damage*.

Cumulative effects may result following exposure*.

May produce discomfort of the respiratory system*.

Possible respiratory sensitizer*.

REACh - Art.57-59: The mixture does not contain Substances of Very High Concern (SVHC) at the SDS print date.

SECTION 3 COMPOSITION / INFORMATION ON INGREDIENTS

3.1.Substances See 'Composition on ingredients' in Section 3.2

3.2.Mixtures

1.CAS No 2.EC No %[weight] Name Classification according to regulation (EC) No 1272/2008 [CLP] 3.Index No 4.REACH No 1.1344-28-1. 2.215-691-6 3.Not Available 39 aluminium oxide Not Applicable 4.01-2119817795-27-XXXX, 01-2119529248-35-XXXX 1.1314-13-2 2.215-222-5 25 zinc oxide Acute Aquatic Hazard Category 1, Chronic Aquatic Hazard Category 1; H410 [3] 3.030-013-00-7 4.01-2119463881-32-XXXX 1.68541-13-9 2.Not Available linoleic acid/4,7,10-trioxa- 18 Skin Corrosion/Irritation Category 2, Serious Eye Damage Category 1; H315, H318 [1] 3.Not Available 1,13-tridecanediamine polyamid 4.Not Available 1.68082-29-1 2.500-191-5 9 tall oil/ triethylenetetramine polyamides Not Applicable 3.Not Available 4.Not Available 1.4246-51-9 2.224-207-2 diethylene glycol, di(3-aminopropyl) Metal Corrosion Category 1, Skin Corrosion/Irritation Category 1A, Serious Eye Damage 3 3.Not Available ether Category 1, Chronic Aquatic Hazard Category 3; H290, H314, H318, H412 [1] www.element14.com4.Not Available www.farnell.com1.108-65-6 2.203-603-9 propylene glycol monomethyl ether www.newark.com 1 Flammable Liquid Category 3; H226 [3] 3.607-195-00-7 acetate, alpha-isomer 4.01-2119475791-29-XXXX 1.112-24-3 Page <25> 28/10/18 V1.0 2.203-950-6 Acute Toxicity (Dermal) Category 4, Skin Corrosion/Irritation Category 1B, Skin Sensitizer 0.8 triethylenetetramine 3.612-059-00-5 Category 1, Chronic Aquatic Hazard Category 3; H312, H314, H317, H412 [3] 4.Not Available

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Supplementary statement(s) Not Applicable

Precautionary statement(s) Prevention

Precautionary statement(s) Response

Precautionary statement(s) Storage Not Applicable

Precautionary statement(s) Disposal

P501 Dispose of contents/container in accordance with local regulations.

2.3. Other hazards Inhalation and/or ingestion may produce health damage*.

Cumulative effects may result following exposure*.

May produce discomfort of the respiratory system*.

Possible respiratory sensitizer*.

REACh - Art.57-59: The mixture does not contain Substances of Very High Concern (SVHC) at the SDS print date.

SECTION 3 COMPOSITION / INFORMATION ON INGREDIENTS

3.1.Substances See 'Composition on ingredients' in Section 3.2

3.2.Mixtures

1.CAS No 2.EC No %[weight] Name Classification according to regulation (EC) No 1272/2008 [CLP] 3.Index No 4.REACH No 1.1344-28-1. 2.215-691-6 3.Not Available 39 aluminium oxide Not Applicable 4.01-2119817795-27-XXXX, 01-2119529248-35-XXXX 1.1314-13-2 2.215-222-5 25 zinc oxide Acute Aquatic Hazard Category 1, Chronic Aquatic Hazard Category 1; H410 [3] 3.030-013-00-7 4.01-2119463881-32-XXXX 1.68541-13-9 2.Not Available linoleic acid/4,7,10-trioxa- 18 Skin Corrosion/Irritation Category 2, Serious Eye Damage Category 1; H315, H318 [1] 3.Not Available 1,13-tridecanediamine polyamid Safety4.Not Available Data Sheet 1.68082-29-1 2.500-191-5 9 tall oil/ triethylenetetramine polyamides Not Applicable 3.Not Available 4.Not Available 1.4246-51-9 2.224-207-2 diethylene glycol, di(3-aminopropyl) Metal Corrosion Category 1, Skin Corrosion/Irritation Category 1A, Serious Eye Damage 3 3.Not Available ether Category 1, Chronic Aquatic Hazard Category 3; H290, H314, H318, H412 [1] 4.Not Available 1.108-65-6 2.203-603-9 propylene glycol monomethyl ether 1 Flammable Liquid Category 3; H226 [3] 3.607-195-00-7 acetate, alpha-isomer Version4.01-2119475791-29-XXXX No: 1.2 Page 3 of 22 Issue Date: 01/04/2016 1.112-24-3 Print Date: 01/04/2016 2.203-950-6 8329TFS Slow Cure, Thermally ConductiveAcute ToxicityAdhesive, (Dermal) Flowable Category 4, Skin (Part Corrosion/Irritation B) Category 1B, Skin Sensitizer 0.8 triethylenetetramine 3.612-059-00-5 Category 1, Chronic Aquatic Hazard Category 3; H312, H314, H317, H412 [3] 4.Not Available 1.1333-86-4 Continued... 2.215-609-9 3.Not Available 0.5 carbon black Carcinogenicity Category 2; H351 [1] 4.01-2119384822-32-XXXX, 01-2119489801-30-XXXX, 01-2119475601-40-XXXX

Legend: 1. Classified by Chemwatch; 2. Classification drawn from EC Directive 67/548/EEC - Annex I ; 3. Classification drawn from EC Directive 1272/2008 - Annex VI 4. Classification drawn from C&L

SECTION 4 FIRST AID MEASURES

4.1. Description of first aid measures

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. If this product comes in contact with the eyes: Wash out immediately with fresh 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. Seek medical attention without delay; if pain persists or recurs seek medical attention. Removal of contact lenses after an eye injury should only be undertaken by skilled personnel. If fumes or combustion products are inhaled remove from contaminated area. General 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. If swallowed do NOT induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain open airway and prevent aspiration. Observe the patient carefully. Never give liquid to a person showing signs of being sleepy or with reduced awareness; i.e. becoming unconscious. Give water to rinse out mouth, then provide liquid slowly and as much as casualty can comfortably drink. Seek medical advice. If this product comes in contact with the eyes: Wash out immediately with fresh running water. Eye Contact Ensure complete irrigation of the eye by keeping eyelids apart and away from eye and moving the eyelids by occasionally lifting the upper and lower lids. Seek medical attention without delay; if pain persists or recurs seek medical attention. Removal of contact lenses after an eye injury should only be undertaken by skilled personnel. If skin contact occurs: Immediately remove all contaminated clothing, including footwear. Skin Contact Flush skin and hair with running water (and soap if available). Seek medical attention in event of irritation. 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. Inhalation 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.

If swallowed do NOT induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain open airway and prevent aspiration. Observe the patient carefully. Ingestion Never give liquid to a person showing signs of being sleepy or with reduced awareness; i.e. becoming unconscious. Give water to rinse out mouth, then provide liquid slowly and as much as casualty can comfortably drink. Seek medical advice.

4.2 Most important symptoms and effects, both acute and delayed See Section 11

www.element14.com4.3. Indication of any immediate medical attention and special treatment needed www.farnell.comTreat symptomatically. Manifestation of aluminium toxicity include hypercalcaemia, anaemia, Vitamin D refractory osteodystrophy and a progressive encephalopathy (mixed dysarthria-apraxia of speech, asterixis, www.newark.comtremulousness, myoclonus, dementia, focal seizures). Bone pain, pathological fractures and proximal myopathy can occur. Symptoms usually develop insidiously over months to years (in chronic renal failure patients) unless dietary aluminium loads are excessive. Serum aluminium levels above 60 ug/ml indicate increased absorption. Potential toxicity occurs above 100 ug/ml and clinical symptoms are present when levels exceed 200 ug/ml. Deferoxamine has been used to treat dialysis encephalopathy and osteomalacia. CaNa2EDTAPage <26> is less effective in chelating aluminium. 28/10/18 V1.0 [Ellenhorn and Barceloux: Medical Toxicology]

Copper, magnesium, aluminium, antimony, iron, manganese, nickel, zinc (and their compounds) in welding, brazing, galvanising or smelting operations all give rise to thermally produced particulates of smaller dimension than may be produced if the metals are divided mechanically. Where insufficient ventilation or respiratory protection is available these particulates may produce 'metal fume fever' in workers from an acute or long term exposure. Onset occurs in 4-6 hours generally on the evening following exposure. Tolerance develops in workers but may be lost over the weekend. (Monday Morning Fever) Pulmonary function tests may indicate reduced lung volumes, small airway obstruction and decreased carbon monoxide diffusing capacity but these abnormalities resolve after several months. Although mildly elevated urinary levels of heavy metal may occur they do not correlate with clinical effects. The general approach to treatment is recognition of the disease, supportive care and prevention of exposure. Seriously symptomatic patients should receive chest x-rays, have arterial blood gases determined and be observed for the development of tracheobronchitis and pulmonary edema.

[Ellenhorn and Barceloux: Medical Toxicology]

SECTION 5 FIREFIGHTING MEASURES

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1.1333-86-4 2.215-609-9 3.Not Available 0.5 carbon black Carcinogenicity Category 2; H351 [1] 4.01-2119384822-32-XXXX, 01-2119489801-30-XXXX, 01-2119475601-40-XXXX

Legend: 1. Classified by Chemwatch; 2. Classification drawn from EC Directive 67/548/EEC - Annex I ; 3. Classification drawn from EC Directive 1272/2008 - Annex VI 4. Classification drawn from C&L

SECTION 4 FIRST AID MEASURES

4.1. Description of first aid measures

If swallowed do NOT induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain open airway and prevent aspiration. Safety DataObserve the patient Sheet carefully. Ingestion Never give liquid to a person showing signs of being sleepy or with reduced awareness; i.e. becoming unconscious. Give water to rinse out mouth, then provide liquid slowly and as much as casualty can comfortably drink. Seek medical advice.

4.2 Most important symptoms and effects, both acute and delayed See Section 11

Copper, magnesium, aluminium, antimony, iron, manganese, nickel, zinc (and their compounds) in welding, brazing, galvanising or smelting operations all give rise to thermally produced particulates of smaller dimension than may be produced if the metals are divided mechanically. Where insufficient ventilation or respiratory protection is available these particulates may produce 'metal fume fever' in workers from an acute or long term exposure. Onset occurs in 4-6 hours generally on the evening following exposure. Tolerance develops in workers but may be lost over the weekend. (Monday Morning Fever) Pulmonary function tests may indicate reduced lung volumes, small airway obstruction and decreased carbon monoxide diffusing capacity but these abnormalities resolve after several months. Although mildly elevated urinary levels of heavy metal may occur they do not correlate with clinical effects. The general approach to treatment is recognition of the disease, supportive care and prevention of exposure. Seriously symptomatic patients should receive chest x-rays, have arterial blood gases determined and be observed for the development of tracheobronchitis and pulmonary edema. Version No: 1.2 Page 4 of 22 Issue Date: 01/04/2016 [Ellenhorn and Barceloux: Medical Toxicology] Print Date: 01/04/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part B)

SECTION 5 FIREFIGHTING MEASURES

5.1. Extinguishing media

Foam. Continued... Dry chemical powder. BCF (where regulations permit). Carbon dioxide. Water spray or fog - Large fires only.

5.2. 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

5.3. Advice for firefighters

Alert Fire Brigade and tell them location and nature of hazard. Wear full body protective clothing with breathing apparatus. Prevent, by any means available, spillage from entering drains or water course. Use water delivered as a fine spray to control fire and cool adjacent area. Fire Fighting Avoid spraying water onto liquid pools. 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. 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). Fire/Explosion Hazard May emit acrid smoke. Mists containing combustible materials may be explosive. Combustion products include:, carbon dioxide (CO2), nitrogen oxides (NOx), other pyrolysis products typical of burning organic material When aluminium oxide dust is dispersed in air, firefighters should wear protection against inhalation of dust particles, which can also contain hazardous substances from the fire absorbed on the alumina particles.

SECTION 6 ACCIDENTAL RELEASE MEASURES

6.1. Personal precautions, protective equipment and emergency procedures See section 8

6.2. Environmental precautions See section 12

6.3. Methods and material for containment and cleaning up

Environmental hazard - contain spillage. Clean up all spills immediately. Avoid breathing vapours and contact with skin and eyes. Minor Spills Control personal contact with the substance, by using protective equipment. Contain and absorb spill with sand, earth, inert material or vermiculite. Wipe up. www.element14.com Place in a suitable, labelled container for waste disposal. www.farnell.com Environmental hazard - contain spillage. www.newark.com Moderate hazard. Clear area of personnel and move upwind. Alert Fire Brigade and tell them location and nature of hazard. Wear breathing apparatus plus protective gloves.Page <27> 28/10/18 V1.0 Prevent, by any means available, spillage from entering drains or water course. No smoking, naked lights or ignition sources. Major Spills Increase ventilation. Stop leak if safe to do so. Contain spill with sand, earth or vermiculite. Collect recoverable product into labelled containers for recycling. Absorb remaining product with sand, earth or vermiculite. Collect solid residues and seal in labelled drums for disposal. Wash area and prevent runoff into drains. If contamination of drains or waterways occurs, advise emergency services.

6.4. Reference to other sections Personal Protective Equipment advice is contained in Section 8 of the SDS.

SECTION 7 HANDLING AND STORAGE

7.1. Precautions for safe handling

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5.1. Extinguishing media Foam. Dry chemical powder. BCF (where regulations permit). Carbon dioxide. Water spray or fog - Large fires only.

5.2. 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

5.3. Advice for firefighters

SECTION 6 ACCIDENTAL RELEASE MEASURES

6.1. Personal precautions, protective equipment and emergency procedures SafetySee section 8 Data Sheet

6.2. Environmental precautions See section 12

6.3. Methods and material for containment and cleaning up

Environmental hazard - contain spillage. Clean up all spills immediately. Avoid breathing vapours and contact with skin and eyes. Minor Spills Control personal contact with the substance, by using protective equipment. Contain and absorb spill with sand, earth, inert material or vermiculite. Wipe up. Place in a suitable, labelled container for waste disposal. Environmental hazard - contain spillage. Moderate hazard. Clear area of personnel and move upwind. 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 course. No smoking, naked lights or ignition sources. Major Spills Increase ventilation. Stop leak if safe to do so. Contain spill with sand, earth or vermiculite. Collect recoverable product into labelled containers for recycling. Absorb remaining product with sand, earth or vermiculite. Collect solid residues and seal in labelled drums for disposal. Wash area and prevent runoff into drains. If contamination of drains or waterways occurs, advise emergency services.

6.4. Reference to other sections Personal Protective Equipment advice is contained in Section 8 of the SDS.

SECTION 7 HANDLING AND STORAGE

7.1. Precautions for safe handling

Always wash hands with soap and water after handling. Continued... Work clothes should be laundered separately. 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. DO NOT allow clothing wet with material to stay in contact with skin Fire and explosion See section 5 protection Store in original containers. Keep containers securely sealed. Store in a cool, dry, well-ventilated area. Other information 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.

7.2. Conditions for safe storage, including any incompatibilities

7.3. Specific end use(s) See section 1.2

SECTION 8 EXPOSURE CONTROLS / PERSONAL PROTECTION

8.1. Control parameters

DERIVED NO EFFECT LEVEL (DNEL) Not Available

PREDICTED NO EFFECT LEVEL (PNEC) Not Available

OCCUPATIONAL EXPOSURE LIMITS (OEL) INGREDIENT DATA Source Ingredient Material name TWA STEL Peak Notes UK Workplace Exposure Limits Aluminium oxides inhalable dust / Aluminium 10 mg/m3 / 4 Not Not aluminium oxide Not Available (WELs) oxides respirable dust mg/m3 Available Available UK Workplace Exposure Limits propylene glycol monomethyl ether 274 mg/m3 / 548 mg/m3 / Not 1-Methoxypropyl acetate Sk (WELs) acetate, alpha-isomer 50 ppm 100 ppm Available European Union (EU) First List of Indicative Occupational propylene glycol monomethyl ether 275 mg/m3 / 550 mg/m3 / Not 2-Methoxy-1-methylethylacetate Skin Exposure Limit Values acetate, alpha-isomer 50 ppm 100 ppm Available (IOELVs) (English) EU Consolidated List of Indicative Occupational propylene glycol monomethyl ether 275 mg/m3 / 550 mg/m3 / Not 1-Methoxypropyl-2-acetate Skin Exposure Limit Values acetate, alpha-isomer 50 ppm 100 ppm Available (IOELVs) UK Workplace Exposure Limits Not Not carbon black Carbon black 3.5 mg/m3 7 mg/m3 (WELs) Available Available

EMERGENCY LIMITS Ingredient Material name TEEL-1 TEEL-2 TEEL-3 aluminium oxide Aluminum oxide; (Alumina) 1.5 mg/m3 15 mg/m3 25 mg/m3 zinc oxide Zinc oxide 10 mg/m3 15 mg/m3 2500 mg/m3

Continued... Version No: 1.2 Page 5 of 22 Issue Date: 01/04/2016 Print Date: 01/04/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part B)

Always wash hands with soap and water after handling. Work clothes should be laundered separately. 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. DO NOT allow clothing wet with material to stay in contact with skin Fire and explosion See section 5 protection Store in original containers. Keep containers securely sealed. Store in a cool, dry, well-ventilated area. Other information 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.

7.2. Conditions for safe storage, including any incompatibilities

7.3. Specific end use(s) See section 1.2

SECTION 8 EXPOSURE CONTROLS / PERSONAL PROTECTION

8.1. Control parameters

DERIVED NO EFFECT LEVEL (DNEL) Not Available

PREDICTED NO EFFECT LEVEL (PNEC) Not Available

VersionEMERGENCY No: 1.2 LIMITS Page 6 of 22 Issue Date: 01/04/2016 Print Date: 01/04/2016 Ingredient Material8329TFS name Slow Cure, Thermally Conductive Adhesive, Flowable (PartTEEL-1 B) TEEL-2 TEEL-3 aluminium oxide Aluminum oxide; (Alumina) 1.5 mg/m3 15 mg/m3 25 mg/m3 zinc oxide Zinc oxide 10 mg/m3 15 mg/m3 2500 mg/m3 diethylene glycol, Diethylene glycol di(3-aminopropyl) ether; (Polyglycol diamine) 13 mg/m3 140 mg/m3 850 mg/m3 di(3-aminopropyl) ether Continued... propylene glycol monomethyl Propylene glycol monomethyl ether acetate, alpha-isomer; (1-Methoxypropyl-2-acetate) Not Available Not Available Not Available ether acetate, alpha-isomer triethylenetetramine Triethylenetetramine 3 ppm 5.7 ppm 83 ppm carbon black Carbon black 9 mg/m3 99 mg/m3 590 mg/m3

Ingredient Original IDLH Revised IDLH aluminium oxide Not Available Not Available zinc oxide 2,500 mg/m3 500 mg/m3 linoleic acid/4,7,10-trioxa- 1,13-tridecanediamine Not Available Not Available polyamid tall oil/ triethylenetetramine Not Available Not Available polyamides diethylene glycol, Not Available Not Available www.element14.comdi(3-aminopropyl) ether www.farnell.compropylene glycol monomethyl Not Available Not Available www.newark.comether acetate, alpha-isomer triethylenetetramine Not Available Not Available carbon black N.E. mg/m3 / N.E. ppm Page <29> 1,750 mg/m3 28/10/18 V1.0

8.2. Exposure controls

8.2.1. Appropriate Type of Contaminant: Air Speed: engineering controls 0.25-0.5 m/s (50-100 solvent, vapours, degreasing etc., evaporating from tank (in still air). f/min.) aerosols, fumes from pouring operations, intermittent container filling, low speed conveyer transfers, welding, spray drift, plating 0.5-1 m/s (100-200 acid fumes, pickling (released at low velocity into zone of active generation) f/min.) direct spray, spray painting in shallow booths, drum filling, conveyer loading, crusher dusts, gas discharge (active generation into 1-2.5 m/s (200-500 zone of rapid air motion) f/min.) grinding, abrasive blasting, tumbling, high speed wheel generated dusts (released at high initial velocity into zone of very high rapid 2.5-10 m/s (500-2000 air motion). 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

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diethylene glycol, Diethylene glycol di(3-aminopropyl) ether; (Polyglycol diamine) 13 mg/m3 140 mg/m3 850 mg/m3 di(3-aminopropyl) ether propylene glycol monomethyl Propylene glycol monomethyl ether acetate, alpha-isomer; (1-Methoxypropyl-2-acetate) Not Available Not Available Not Available ether acetate, alpha-isomer triethylenetetramine Triethylenetetramine 3 ppm 5.7 ppm 83 ppm carbon black Carbon black 9 mg/m3 99 mg/m3 590 mg/m3

Ingredient Original IDLH Revised IDLH Safetyaluminium oxide DataNot Available Sheet Not Available zinc oxide 2,500 mg/m3 500 mg/m3 linoleic acid/4,7,10-trioxa- 1,13-tridecanediamine Not Available Not Available polyamid tall oil/ triethylenetetramine Not Available Not Available polyamides diethylene glycol, Not Available Not Available di(3-aminopropyl) ether propylene glycol monomethyl Not Available Not Available ether acetate, alpha-isomer triethylenetetramine Not Available Not Available carbon black N.E. mg/m3 / N.E. ppm 1,750 mg/m3

8.2. Exposure controls

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

Continued...

www.element14.com www.farnell.com www.newark.com

Page <30> 28/10/18 V1.0 Version No: 1.2 Page 6 of 22 Issue Date: 01/04/2016 Print Date: 01/04/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part B)

Ingredient Original IDLH Revised IDLH aluminium oxide Not Available Not Available zinc oxide 2,500 mg/m3 500 mg/m3 linoleic acid/4,7,10-trioxa- 1,13-tridecanediamine Not Available Not Available polyamid tall oil/ triethylenetetramine Not Available Not Available polyamides diethylene glycol, Not Available Not Available di(3-aminopropyl) ether propylene glycol monomethyl Not Available Not Available ether acetate, alpha-isomer triethylenetetramine Not Available Not Available carbon black N.E. mg/m3 / N.E. ppm 1,750 mg/m3

8.2. Exposure 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 VersionSafety No: 1.2 Data'removes' air in the workSheet environment. Ventilation canPage remove 7 of 22 or dilute an air contaminant if designed properly. The design of a ventilation systemIssue must Date: match 01/04/2016 the particular process and chemical or contaminant in use. Print Date: 01/04/2016 Employers8329TFS may needSlow to useCure, multiple Thermally types of controls Conductive to prevent employee Adhesive, overexposure. Flowable (Part B)

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. An2: approvedContaminants self containedof low toxicity breathing or of nuisance apparatus value (SCBA) only. may be required in some situations. 2: Contaminants of high toxicity Provide adequate ventilation in warehouse or closed storage area. Air contaminants generated in the workplace possess varying 'escape' velocities which, in turn,3: Intermittent, determine thelow 'captureproduction. velocities' of fresh circulating air required to effectively remove the contaminant.3: High production, heavy use 4: Large hood or large air mass in motion 4: Small hood-local control only 8.2.1. Appropriate Type of Contaminant: Air Speed: engineering controls Simple theory shows that air velocity falls rapidly with distance away from the opening of a simple extraction pipe. Velocity generally decreases0.25-0.5 with m/s the (50-100 square solvent, vapours, degreasing etc., evaporating from tank (in still air). of distance from the extraction point (in simple cases). Therefore the air speed at the extraction point should be adjusted, accordingly, afterf/min.) 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 solventsaerosols, generated fumes from in a pouringtank 2 meters operations, distant intermittent from the extraction container point. filling, Other low speed mechanical conveyer considerations, transfers, welding, producing spray performance drift, plating deficits 0.5-1within m/s the (100-200extraction apparatus,acid fumes, make pickling it essential (released that at theoretical low velocity air intovelocities zone ofare active multiplied generation) by factors of 10 or more when extraction systems are installed or used.f/min.) direct spray, spray painting in shallow booths, drum filling, conveyer loading, crusher dusts, gas discharge (active generation into 1-2.5 m/s (200-500 zone of rapid air motion) f/min.) 8.2.2. Personal protection grinding, abrasive blasting, tumbling, high speed wheel generated dusts (released at high initial velocity into zone of very high rapid 2.5-10 m/s (500-2000 air motion). f/min.)

Within each range the appropriate value depends on: Safety glasses with side shields. LowerChemical end of goggles.the range Upper end of the range Contact lenses may pose a special hazard; soft contact lenses may absorb and concentrate irritants. A written policy document, describing the wearing of 1: Roomlenses air or currents restrictions minimal on use, or favourableshould be createdto capture for each workplace or task. This should include a 1:review Disturbing of lens room absorption air currents and adsorption for the class of Eye and face protection chemicals in use and an account of injury experience. Medical and first-aid personnel should be trained in their removal and suitable equipment should be readily available. In the event of chemical exposure, begin eye irrigation immediately and remove contact lens as soon as practicable. Lens shouldContinued... 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 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. The selection of suitable gloves does not only depend on the material, but also on further marks of quality which vary from manufacturer to manufacturer. Where the chemical is a preparation of several substances, the resistance of the glove material can not be calculated in advance and has therefore to be checked prior to the application. The exact break through time for substances has to be obtained from the manufacturer of the protective gloves and.has to be observed when making a final choice. Suitability and durability of glove type is dependent on usage. Important factors in the selection of gloves include: Hands/feet protection frequency and duration of contact, chemical resistance of glove material, glove thickness and dexterity Select gloves tested to a relevant standard (e.g. Europe EN 374, US F739, AS/NZS 2161.1 or national equivalent). When prolonged or frequently repeated contact may occur, a glove with a protection class of 5 or higher (breakthrough time greater than 240 minutes according to EN 374, AS/NZS 2161.10.1 or national equivalent) is recommended. When only brief contact is expected, a glove with a protection class of 3 or higher (breakthrough time greater than 60 minutes according to EN 374, AS/NZS 2161.10.1 or national equivalent) is recommended. Some glove polymer types are less affected by movement and this should be taken into account when considering gloves for long-term use. Contaminated gloves should be replaced. Gloves must only be worn on clean hands. After using gloves, hands should be washed and dried thoroughly. Application of a non-perfumed moisturiser is recommended.

Body protection See Other protection below Overalls. P.V.C. apron. Other protection Barrier cream. Skin cleansing cream. Eye wash unit.

Thermal hazards Not Available

Recommended material(s) Respiratory protection GLOVE SELECTION INDEX Type AK-P Filter of sufficient capacity. (AS/NZS 1716 & 1715, EN 143:2000 & 149:2001, ANSI Glove selection is based on a modified presentation of the: Z88 or national equivalent) 'Forsberg Clothing Performance Index'. Where the concentration of gas/particulates in the breathing zone,approaches or exceeds the The effect(s) of the following substance(s) are taken into account in the computer- 'Exposure Standard' (or ES), respiratoryprotection is required. generated selection: Degree of protection varies with both face-piece and Class offilter; the nature of protection Slow Cure, Thermally Conductive Adhesive, Flowable (Part B) varies with Type of filter.

Material CPI Required Minimum Half-Face Full-Face Powered Air BUTYL A Protection Factor Respirator Respirator Respirator AK-AUS / Class AK-PAPR-AUS / NEOPRENE A up to 10 x ES - 1 P2 Class 1 P2 NITRILE A up to 50 x ES Air-line* - - PE/EVAL/PE A up to 100 x ES - AK-3 P2 - www.element14.comVITON A www.farnell.com 100+ x ES - Air-line** - * CPI - Chemwatch Performance Index www.newark.comA: Best Selection * - Continuous-flow; ** - Continuous-flow or positivepressure demand B: Satisfactory; may degrade after 4 hours continuous immersion A(All classes) = Organic vapours, B AUS or B1 = Acid gasses, B2 =Acid gas or hydrogen C: Poor to Dangerous Choice for other than short term immersion cyanide(HCN), B3 = Acid gas or hydrogen cyanide(HCN), E =Sulfur dioxide(SO2), G = NOTE: As a series of factors will influence the actual performance of the glove, a final Page <31>Agricultural chemicals, K = Ammonia(NH3), Hg =Mercury, NO = Oxides of28/10/18 nitrogen, MB = V1.0 selection must be based on detailed observation. - Methyl bromide, AX = Low boiling pointorganic compounds(below 65 degC) * 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

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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

8.2.2. Personal protection

Body protection See Other protection below Overalls. P.V.C. apron. SafetyOther protection DataBarrier cream. Sheet Skin cleansing cream. Eye wash unit.

Thermal hazards Not Available

Material CPI Required Minimum Half-Face Full-Face Powered Air BUTYL A Protection Factor Respirator Respirator Respirator AK-AUS / Class AK-PAPR-AUS / NEOPRENE A up to 10 x ES - 1 P2 Class 1 P2 NITRILE A up to 50 x ES Air-line* - - PE/EVAL/PE A up to 100 x ES - AK-3 P2 - VITON A 100+ x ES - Air-line** - * CPI - Chemwatch Performance Index A: Best Selection * - Continuous-flow; ** - Continuous-flow or positivepressure demand B: Satisfactory; may degrade after 4 hours continuous immersion A(All classes) = Organic vapours, B AUS or B1 = Acid gasses, B2 =Acid gas or hydrogen VersionC: Poor No: to1.2 Dangerous Choice for other than short term immersion Page 8 of 22 cyanide(HCN), B3 = Acid gas or hydrogen cyanide(HCN), E =Sulfur dioxide(SO2),Issue Date: G = 01/04/2016 NOTE: As a series of factors will influence the actual performance of the glove, a final Agricultural chemicals, K = Ammonia(NH3), Hg =Mercury, NO = Oxides ofPrint nitrogen, Date: MB 01/04/2016 = selection must be based on detailed observation.8329TFS - Slow Cure, Thermally ConductiveMethyl Adhesive, bromide, AX =Flowable Low boiling pointorganic (Part B) compounds(below 65 degC) * 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. Continued...

8.2.3. Environmental exposure controls See section 12

SECTION 9 PHYSICAL AND CHEMICAL PROPERTIES

9.1. Information on basic physical and chemical properties

Appearance grey

Physical state Liquid Relative density (Water = 1) 2.0 Partition coefficient Odour Not Available Not Available n-octanol / water Auto-ignition temperature Odour threshold Not Available Not Available (°C) Decomposition pH (as supplied) Not Available Not Available temperature Melting point / freezing Not Available Viscosity (cSt) >20.5 point (°C) Initial boiling point and >145 Molecular weight (g/mol) Not Available boiling range (°C) Flash point (°C) >110 Taste Not Available Evaporation rate Not Available Explosive properties Not Available Flammability Not Applicable Oxidising properties Not Available Surface Tension (dyn/cm or Upper Explosive Limit (%) Not Available Not Available mN/m) Lower Explosive Limit (%) Not Available Volatile Component (%vol) Not Available Vapour pressure (kPa) Not Available Gas group Not Available Solubility in water (g/L) Immiscible pH as a solution (1%) Not Available Vapour density (Air = 1) Not Available VOC g/L Not Available

9.2. Other information Not Available

SECTION 10 STABILITY AND REACTIVITY

10.1.Reactivity See section 7.2 Unstable in the presence of incompatible materials. www.element14.com10.2.Chemical stability Product is considered stable. Hazardous polymerisation will not occur. www.farnell.com 10.3. Possibility of See section 7.2 www.newark.comhazardous reactions 10.4. Conditions to avoid See section 7.2 10.5. Incompatible materials See section 7.2 Page <32> 28/10/18 V1.0 10.6. Hazardous See section 5.3 decomposition products

SECTION 11 TOXICOLOGICAL INFORMATION

11.1. Information on toxicological effects

Inhalation of vapours or aerosols (mists, fumes), generated by the material during the course of normal handling, may be damaging to the health of the individual. Limited evidence or practical experience suggests that the material may produce irritation of the respiratory system, in a significant 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.

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be unsuitable following long-term or frequent use. A qualified practitioner should be consulted.

8.2.3. Environmental exposure controls See section 12

SECTION 9 PHYSICAL AND CHEMICAL PROPERTIES

9.1. Information on basic physical and chemical properties

Appearance grey

Physical state Liquid Relative density (Water = 1) 2.0 Partition coefficient Odour Not Available Not Available n-octanol / water Auto-ignition temperature Odour threshold Not Available Not Available (°C) Decomposition pH (as supplied) Not Available Not Available temperature Melting point / freezing Not Available Viscosity (cSt) >20.5 point (°C) Initial boiling point and >145 Molecular weight (g/mol) Not Available boiling range (°C) Flash point (°C) >110 Taste Not Available Evaporation rate Not Available Explosive properties Not Available Flammability Not Applicable Oxidising properties Not Available Surface Tension (dyn/cm or Upper Explosive Limit (%) Not Available Not Available mN/m) Lower Explosive Limit (%) Not Available Volatile Component (%vol) Not Available Vapour pressure (kPa) Not Available Gas group Not Available Solubility in water (g/L) Immiscible pH as a solution (1%) Not Available SafetyVapour density (Air = 1) DataNot Available Sheet VOC g/L Not Available 9.2. Other information Not Available

SECTION 10 STABILITY AND REACTIVITY

10.1.Reactivity See section 7.2 Unstable in the presence of incompatible materials. 10.2.Chemical stability Product is considered stable. Hazardous polymerisation will not occur.

10.3. Possibility of See section 7.2 hazardous reactions 10.4. Conditions to avoid See section 7.2 10.5. Incompatible materials See section 7.2 10.6. Hazardous See section 5.3 decomposition products

SECTION 11 TOXICOLOGICAL INFORMATION

11.1. Information on toxicological effects

Inhalation of freshly formed metal oxide particles sized below 1.5 microns and generally between 0.02 to 0.05 microns may result in 'metal fume fever'. Symptoms may be delayed for up to 12 hours and begin with the sudden onset of thirst, and a sweet, metallic or foul taste in the mouth. Other symptoms include upper respiratory tract irritation accompanied by coughing and a dryness of the mucous membranes, lassitude and a generalised feeling of malaise. Mild to Inhaled severe headache, nausea, occasional vomiting, fever or chills, exaggerated mental activity, profuse sweating, diarrhoea, excessive urination and prostration may also occur. Tolerance to the fumes develops rapidly, but is quickly lost. All symptoms usually subside within 24-36 hours following removal from exposure. Zinc is necessary for normal fetal growth and development. Fetal damage may result from zinc deficiency. Only one report in the literature suggested adverse developmental effects in humans due to exposure to excessive levels of zinc. Four women were given zinc supplements of 0.6 mg zinc/kg/day as zinc sulfate Version No: 1.2 during the third trimester of pregnancy. Three of thePage women 9 of had22 premature deliveries, and one delivered a stillborn infant. However, the significanceIssue Date: of these 01/04/2016 results cannot be determined because very few details were given regarding the study protocol, reproductive histories, and the nutritional status of the women. Print Date: 01/04/2016 Other8329TFS human studies Slow have Cure, found noThermally developmental Conductive effects in the newborns Adhesive, of mothers Flowable consuming 0.3 (Part mg zinc/kg/day B) as zinc sulfate or zinc citrate or 0.06 mg zinc/kg/day as zinc aspartate during the last two trimesters. There has been a suggestion that increased serum zinc levels in pregnant women may be associated with an increase in neural tube defects, but others have failed to confirm this association. The developmental toxicity of zinc in experimental animals has been evaluated in a number of investigations. Exposure to high levels of zinc in the diet prior to and/or during gestation has been associated with increased fetal resorptions, reduced fetal weights, altered tissue concentrations of fetal iron and copper, and reduced growth in the offspring. Animal studies suggest that exposure to very high levels of dietary zinc is associated with reduced fetal weight, alopecia, decreased hematocrit, and copper deficiency in offspring. For example, second generation mice exposed to zinc carbonate during gestation and lactation (260 mg/kg/day in the maternalContinued... diet), and then continued on that diet for 8 weeks, had reduced body weight, alopecia, and signs of copper deficiency (e.g., lowered hematocrit and occasional achromotrichia [loss of hair colour]. Similarly, mink kits from dams that ingested a time-weighted-average dose of 20.8 mg zinc/kg/day as zinc sulfate also had alopecia and achromotrichia. It is likely that the alopecia resulted from zinc-induced copper deficiency, which is known to cause alopecia in monkeys. However, no adverse effects were observed in parental mice or mink. No effects on reproduction were reported in rats exposed to 50 mg zinc/kg/day as zinc carbonate; however, increased stillbirths were observed in rats exposed to 250 mg zinc/kg/day. Welding or flame cutting of metals with zinc or zinc dust coatings may result in inhalation of zinc oxide fume; high concentrations of zinc oxide fume may result in 'metal fume fever'; also known as 'brass chills', an industrial disease of short duration. [I.L.O] Symptoms include malaise, fever, weakness, nausea and may appear quickly if operations occur in enclosed or poorly ventilated areas. Genotoxicity studies conducted in a variety of test systems have failed to provide evidence for mutagenicity of zinc. However, there are indications of weak clastogenic effects following zinc exposure. Accidental ingestion of the material may be damaging to the health of the individual. Ingestion Acute toxic responses to aluminium are confined to the more soluble forms.

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fetal resorptions, reduced fetal weights, altered tissue concentrations of fetal iron and copper, and reduced growth in the offspring. Animal studies suggest that exposure to very high levels of dietary zinc is associated with reduced fetal weight, alopecia, decreased hematocrit, and copper deficiency in offspring. For example, second generation mice exposed to zinc carbonate during gestation and lactation (260 mg/kg/day in the maternal diet), and then continued on that diet for 8 weeks, had reduced body weight, alopecia, and signs of copper deficiency (e.g., lowered hematocrit and occasional achromotrichia [loss of hair colour]. Similarly, mink kits from dams that ingested a time-weighted-average dose of 20.8 mg zinc/kg/day as zinc sulfate also had alopecia and achromotrichia. It is likely that the alopecia resulted from zinc-induced copper deficiency, which is known to cause alopecia in monkeys. However, no adverse effects were observed in parental mice or mink. No effects on reproduction were reported in rats exposed to 50 mg zinc/kg/day as zinc carbonate; however, increased stillbirths were observed in rats exposed to 250 mg zinc/kg/day. Welding or flame cutting of metals with zinc or zinc dust coatings may result in inhalation of zinc oxide fume; high concentrations of zinc oxide fume may result in 'metal fume fever'; also known as 'brass chills', an industrial disease of short duration. [I.L.O] Symptoms include malaise, fever, weakness, nausea and may appear quickly if operations occur in enclosed or poorly ventilated areas. Genotoxicity studies conducted in a variety of test systems have failed to provide evidence for mutagenicity of zinc. However, there are indications of weak clastogenic effects following zinc exposure. Accidental ingestion of the material may be damaging to the health of the individual. Ingestion Acute toxic responses to aluminium are confined to the more soluble forms.

Slow Cure, TOXICITY IRRITATION Thermally Conductive Adhesive, Flowable (Part B) Not Available Not Available

TOXICITY IRRITATION aluminium oxide Oral (rat) LD50: >2000 mg/kg[1] Not Available

TOXICITY IRRITATION

zinc oxide Oral (rat) LD50: >5000 mg/kg[1] Eye (rabbit) : 500 mg/24 h - mild Skin (rabbit) : 500 mg/24 h- mild

linoleic acid/4,7,10-trioxa- TOXICITY IRRITATION 1,13-tridecanediamine polyamid Not Available Not Available

TOXICITY IRRITATION [2] tall oil/ triethylenetetramine Oral (rat) LD50: >5000 mg/kg*d * [Gibson-Homans Co.] polyamides **[Devoe] Nil reported

diethylene glycol, TOXICITY IRRITATION di(3-aminopropyl) ether Dermal (rabbit) LD50: 2500 mg/kg[2] Nil reported

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TOXICITY IRRITATION

zinc oxide Oral (rat) LD50: >5000 mg/kg[1] Eye (rabbit) : 500 mg/24 h - mild Skin (rabbit) : 500 mg/24 h- mild

linoleic acid/4,7,10-trioxa- TOXICITY IRRITATION 1,13-tridecanediamine polyamid Not Available Not Available

TOXICITY IRRITATION [2] tall oil/ triethylenetetramine Oral (rat) LD50: >5000 mg/kg*d * [Gibson-Homans Co.] polyamides **[Devoe] Nil reported VersionVersion No:No: 1.21.2 PagePage 1111 ofof 2222 IssueIssue Date:Date: 01/04/201601/04/2016 PrintPrint Date:Date: 01/04/201601/04/2016 8329TFS8329TFS SlowSlow Cure,Cure, ThermallyThermally ConductiveConductive Adhesive,Adhesive, FlowableFlowable (Part(Part B)B) diethylene glycol, TOXICITY IRRITATION di(3-aminopropyl) ether Dermal (rabbit) LD50: 2500 mg/kg[2] Nil reported OralOral (rat)(rat) LD50:LD50: 42904290 mg/kgdmg/kgd[2][2] Continued...

TOXICITYTOXICITY IRRITATIONIRRITATION

propylenepropylene glycolglycol dermaldermal (rat)(rat) LD50:LD50: >2000>2000 mg/kgmg/kg[1][1] ** [CCINFO][CCINFO] monomethylmonomethyl etherether acetate,acetate, [2][2] www.element14.comalpha-isomeralpha-isomer InhalationInhalation (rat)(rat) LC50:LC50: 43454345 ppm/6hppm/6h NilNil reportedreported www.farnell.com OralOral (rat)(rat) LD50:LD50: >14.1>14.1 mlml[1][1] www.newark.com

TOXICITYTOXICITY IRRITATIONIRRITATION

DermalDermal (rabbit)(rabbit) LD50:LD50: 805805 mg/kgEmg/kgE[2][2] Page <35> EyeEye (rabbit):20(rabbit):20 mg/24mg/24 hh -- moderatemoderate 28/10/18 V1.0

triethylenetetraminetriethylenetetramine OralOral (rat)(rat) LD50:LD50: 25002500 mg/kgEmg/kgE[2][2] EyeEye (rabbit);(rabbit); 4949 mgmg -- SEVERESEVERE SkinSkin (rabbit):(rabbit): 490490 mgmg openopen SEVERESEVERE SkinSkin (rabbit):(rabbit): 55 mg/24mg/24 SEVERESEVERE

TOXICITYTOXICITY IRRITATIONIRRITATION [2][2] carboncarbon blackblack DermalDermal (rabbit)(rabbit) LD50:LD50: >3000>3000 mg/kgmg/kg NotNot AvailableAvailable

OralOral (rat)(rat) LD50:LD50: >8000>8000 mg/kgmg/kg[1][1]

Legend:Legend: 1.1. ValueValue obtainedobtained fromfrom EuropeEurope ECHAECHA RegisteredRegistered SubstancesSubstances -- AcuteAcute toxicitytoxicity 2.*2.* ValueValue obtainedobtained fromfrom manufacturer'smanufacturer's SDS.SDS. UnlessUnless otherwiseotherwise specifiedspecified datadata extractedextracted fromfrom RTECSRTECS -- RegisterRegister ofof ToxicToxic EffectEffect ofof chemicalchemical SubstancesSubstances

TheThe followingfollowing informationinformation refersrefers toto contactcontact allergensallergens asas aa groupgroup andand maymay notnot bebe specificspecific toto thisthis product.product. ContactContact allergiesallergies quicklyquickly manifestmanifest themselvesthemselves asas contactcontact eczema,eczema, moremore rarelyrarely asas urticariaurticaria oror Quincke'sQuincke's oedema.oedema. TheThe pathogenesispathogenesis ofof contactcontact eczemaeczema involvesinvolves aa cell-mediatedcell-mediated (T(T lymphocytes)lymphocytes) immuneimmune reactionreaction ofof thethe delayeddelayed type.type. OtherOther allergicallergic skinskin reactions,reactions, e.g.e.g. contactcontact urticaria,urticaria, involveinvolve antibody-mediatedantibody-mediated immuneimmune reactions.reactions. TheThe significancesignificance ofof thethe contactcontact allergenallergen isis notnot simplysimply determineddetermined byby itsits sensitisationsensitisation potential:potential: thethe distributiondistribution ofof thethe substancesubstance andand thethe opportunitiesopportunities forfor contactcontact withwith itit areare equallyequally important.important. AA weaklyweakly sensitisingsensitising substancesubstance whichwhich isis widelywidely distributeddistributed cancan bebe aa moremore importantimportant allergenallergen thanthan oneone withwith strongerstronger sensitisingsensitising potentialpotential withwith whichwhich fewfew individualsindividuals comecome intointo contact.contact. FromFrom aa clinicalclinical pointpoint ofof view,view, substancessubstances areare noteworthynoteworthy ifif theythey produceproduce anan allergicallergic testtest reactionreaction inin moremore thanthan 1%1% ofof thethe personspersons tested.tested. ForFor FattyFatty NitrogenNitrogen DerivedDerived (FND)Amides(FND)Amides (including(including severalseveral highhigh molecularmolecular weightweight alkylalkyl aminoamino acidacid amides)amides) TheThe chemicalschemicals inin thethe FattyNitrogenFattyNitrogen DerivedDerived (FND)(FND) AmidesAmides ofof surfactantssurfactants areare similarsimilar toto thethe classclass ingeneralingeneral asas toto physical/chemicphysical/chemicalal properties,properties, environmentalenvironmental fatefate andand toxicity.toxicity. HumanexposureHumanexposure toto thesethese chemicalschemicals isis substantiallysubstantially documented.documented. SomeSome typicaltypical applicationsapplications ofof FNDAmidesFNDAmides are:are: masonrymasonry cementcement additive;additive; curingagentcuringagent forfor epoxyepoxy resins;resins; closedclosed hydrocarbonhydrocarbon systemssystems inin oiloil fieldfield production,refineriesproduction,refineries andand chemicalchemical plants;plants; andand slipslip andand antiblockingantiblocking additivesadditives forpolymers.forpolymers. TheThe safetysafety ofof thethe FNDFND AmidesAmides tohumanstohumans isis recognisedrecognised byby thethe U.S.U.S. FDA,FDA, whichwhich hashas approvedapproved stearamide,stearamide, oleamideand/oroleamideand/or erucamideerucamide forfor adhesives;adhesives; coatingscoatings forfor articlesarticles inin foodfood contact;contact; coatingsforcoatingsfor polyolefinpolyolefin films;films; defoamingdefoaming agentsagents forfor manufacturemanufacture ofof paperpaper andand paperboard;animalpaperboard;animal glueglue (defoamer(defoamer inin foodfood packaging);packaging); inin EVAEVA copolymerscopolymers forfor foodfood packaging;lubricantspackaging;lubricants forfor manufacturemanufacture ofof metallicmetallic foodfood packaging;packaging; irradiationirradiation ofof preparedfoods;preparedfoods; releaserelease agentsagents inin manufacturemanufacture ofof foodfood packagingpackaging materials,materials, foodfood contactsurfacecontactsurface ofof paperpaper andand paperboard;paperboard; cellophanecellophane inin foodfood packaging;packaging; closureclosure sealinggaskets;sealinggaskets; andand releaserelease agentsagents inin polymericpolymeric resinsresins andand petroleumpetroleum wax.wax. TheThe loworderloworder ofof toxicitytoxicity indicatesindicates thatthat thethe useuse ofof FNDFND AmidesAmides doesdoes notnot posepose asignificantasignificant hazardhazard toto humanhuman health.health. TheThe differencesdifferences inin chainchain length,degreelength,degree ofof saturationsaturation ofof thethe carboncarbon chains,chains, sourcesource ofof thethe naturalnatural oils,oils, oradditionoraddition ofof anan aminoamino groupgroup inin thethe chainchain wouldwould notnot bebe expectedexpected toto havehave anan impactonimpacton thethe toxicitytoxicity profile.profile. ThisThis conclusionconclusion isis supportedsupported byby aa numbernumber ofof studiesstudies intheinthe FNDFND familyfamily ofof chemicalschemicals (amines,(amines, cationics,cationics, andand amidesamides asas separatecategories)separatecategories) thatthat showshow nono differencesdifferences inin thethe lengthlength oror degreedegree ofof saturationsaturation oftheofthe alkylalkyl substituentssubstituents andand isis alsoalso supportedsupported byby thethe limitedlimited toxicitytoxicity ofof theselong-chaintheselong-chain substitutedsubstituted chemicalschemicals TheThe FattyFatty nitrogen-derivednitrogen-derived amides(FNDamides(FND amides)amides) comprisecomprise fourfour categories:categories: SlowSlow Cure,Cure,·· SubcategorySubcategory I:I: SubstitutedSubstituted AmidesAmides ThermallyThermally ConductiveConductive·· SubcategorySubcategory II:II: FattyFatty AcidAcid ReactionReaction ProductsProducts withwith AminoAmino Compounds(Note:Compounds(Note: SubcategorySubcategory IIII chemicals,chemicals, inin manymany cases,cases, containcontain SubcategorySubcategory II chemicalsaschemicalsas Adhesive,Adhesive, FlowableFlowable (Part(Part B)B) majormajor components)components) ·· SubcategorySubcategory III:III: ImidazoleImidazole DerivativesDerivatives ·· SubcategorySubcategory IV:IV: FNDFND AmphotericsAmphoterics AcuteAcute Toxicity:Toxicity: TheThe lowacutelowacute oraloral toxicitytoxicity ofof thethe FNDFND AmidesAmides isis wellwell establishedestablished acrossacross allSubcategoriesallSubcategories byby thethe availableavailable data.data. TheThe limitedlimited acuteacute toxicitytoxicity ofof thesechemicalsthesechemicals isis alsoalso confirmedconfirmed byby fourfour acuteacute dermaldermal andand twotwo acuteacute inhalationstudiesinhalationstudies RepeatedRepeated DoseDose andand ReproductiveToxicity:ReproductiveToxicity: TwoTwo subchronicsubchronic toxicitytoxicity studiesstudies demonstratingdemonstrating lowlow toxicitytoxicity areavailableareavailable forfor SubcategorySubcategory II chemicals.chemicals. InIn addition,addition, aa 5-day5-day repeatedrepeated dosedose studyforstudyfor aa thirdthird chemicalchemical confirmedconfirmed thethe minimalminimal toxicitytoxicity ofof thesethese chemicals.chemicals. SincetheSincethe SubcategorySubcategory II chemicalschemicals areare majormajor componentscomponents ofof manymany SubcategorySubcategory IIchemicals,IIchemicals, andand basedbased onon thethe lowlow repeat-doserepeat-dose toxicitytoxicity ofof thethe aminoamino compounds(e.g.compounds(e.g. diethanolamine,diethanolamine, triethanolamine)triethanolamine) usedused forfor producingproducing thethe SubcategorySubcategory IIderivatives,IIderivatives, thethe SubcategorySubcategory II repeat-doserepeat-dose toxicitytoxicity studiesstudies adequatelyadequately supportSubcategorysupportSubcategory II.II. TwoTwo subchronicsubchronic toxicitytoxicity studiesinstudiesin SubcategorySubcategory IIIIII confirmedconfirmed thethe lowlow orderorder ofof repeatrepeat dosedose toxicitytoxicity forfor thethe FNDAmidesFNDAmides ImidazoleImidazole derivatives.derivatives. ForFor SubcategorySubcategory IV,IV, twotwo subchronicsubchronic toxicitystudiestoxicitystudies forfor oneone ofof thethe chemicalschemicals indicatedindicated aa lowlow orderorder ofof repeat-doserepeat-dose toxicitytoxicity fortheforthe FNDFND amphotericamphoteric saltssalts similarsimilar toto thatthat seenseen inin thethe otherother categories.categories. GeneticGenetic ToxicityToxicity inin vitrovitro::BasedBased onon thethe lacklack ofof effecteffect ofof oneone oror moremore chemicalschemicals inin eachsubcategory,eachsubcategory, adequateadequate datadata forfor mutagenicmutagenic activityactivity asas measuredmeasured byby thethe SalmonellaSalmonellareversereverse mutationmutation assayassay existexist forfor allall ofof thethe subcategories.subcategories. DevelopmentalDevelopmental Toxicity:Toxicity: AdevelopmentalAdevelopmental toxicitytoxicity studystudy inin SubcategorySubcategory II andand inin SubcategorySubcategory IVIV andand aa thirdstudythirdstudy forfor aa chemicalchemical inin SubcategorySubcategory IIIIII areare available.available. TheThe studiesstudies indicatetheseindicatethese chemicalschemicals areare notnot developmentaldevelopmental toxicants,toxicants, asas expectedexpected basedbased onon theirstructures,theirstructures, molecularmolecular weights,weights, physicalphysical propertiesproperties andand knowledgeknowledge ofof similarchemicals.similarchemicals. AsAs aboveabove forfor repeat-doserepeat-dose toxicity,toxicity, thethe datadata forfor SubcategorySubcategory II areadequateareadequate toto supportsupport SubcategorySubcategory II.II. InIn evaluatingevaluating potentialpotential toxicityoftoxicityof thethe FNDFND AmidesAmides chemicals,chemicals, itit isis alsoalso usefuluseful toto reviewreview thethe availableavailable datadata fortheforthe relatedrelated FNDFND CationicCationic andand FNDFND AminesAmines CategoryCategory chemicals.chemicals. AcuteAcute oraloral toxicitystudiestoxicitystudies (approximately(approximately 8080 studiesstudies forfor 4040 chemicalschemicals inin thethe threethree categories)providecategories)provide LD50LD50 valuesvalues fromfrom approximatelyapproximately 400400 toto 10,00010,000 mg/kgmg/kg withwith nono apparentorganapparentorgan specificspecific toxicity.toxicity. Similarly,Similarly, repeatedrepeated dosedose toxicitytoxicity studies(approximatelystudies(approximately 3535 studiesstudies forfor 1515 chemicals)chemicals) provideprovide NOAELsNOAELs betweenbetween 1010 andand 100mg/kg/day100mg/kg/day forfor ratsrats andand slightlyslightly lowerlower forfor dogs.dogs. MoreMore thanthan 6060 geneticgenetic toxicitystudiestoxicitystudies ((inin vitrovitro bacterialbacterial andand mammalianmammalian cellscells asas wellwell asas inin vivovivo studies)indicatedstudies)indicated nono mutagenicmutagenic activityactivity amongamong moremore thanthan 3030 chemicalschemicals tested.tested. ForreproductiveForreproductive evaluations,evaluations, 1414 studiesstudies evaluatedevaluated reproductivereproductive endpointsendpoints and/orreproductiveand/orreproductive organsorgans forfor 1111 chemicals,chemicals, andand 1515 studiesstudies evaluatedevaluated developmentaltoxicitydevelopmentaltoxicity forfor 1313 chemicalschemicals indicatingindicating nono reproductivereproductive oror developmentaldevelopmental effectsforeffectsfor thethe FNDFND groupgroup asas aa whole.whole.

ALUMINIUMALUMINIUM OXIDEOXIDE NoNo significantsignificant acuteacute toxicologicaltoxicological datadata identifiedidentified inin literatureliterature search.search. TheThe materialmaterial maymay causecause skinskin irritationirritation afterafter prolongedprolonged oror repeatedrepeated exposureexposure andand maymay produceproduce aa contactcontact dermatitisdermatitis (nonallergic).(nonallergic). ThisThis formform ofof dermatitisdermatitis isis oftenoften ZINCZINC OXIDEOXIDE characterisedcharacterised byby skinskin rednessredness (erythema)(erythema) andand swellingswelling epidermis.epidermis. HistologicallyHistologically therethere maymay bebe intercellularintercellular oedemaoedema ofof thethe spongyspongy layerlayer (spongiosis)(spongiosis) andand intracellularintracellular oedemaoedema ofof thethe epidermis.epidermis.

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Oral (rat) LD50: 4290 mg/kgd[2]

TOXICITY IRRITATION

propylene glycol dermal (rat) LD50: >2000 mg/kg[1] * [CCINFO] monomethyl ether acetate, [2] alpha-isomer Inhalation (rat) LC50: 4345 ppm/6h Nil reported

Oral (rat) LD50: >14.1 ml[1]

TOXICITY IRRITATION

Dermal (rabbit) LD50: 805 mg/kgE[2] Eye (rabbit):20 mg/24 h - moderate

triethylenetetramine Oral (rat) LD50: 2500 mg/kgE[2] Eye (rabbit); 49 mg - SEVERE Skin (rabbit): 490 mg open SEVERE Skin (rabbit): 5 mg/24 SEVERE

TOXICITY IRRITATION [2] carbon black Dermal (rabbit) LD50: >3000 mg/kg Not Available

Oral (rat) LD50: >8000 mg/kg[1]

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Oral (rat) LD50: 4290 mg/kgd[2]

TOXICITY IRRITATION

propylene glycol dermal (rat) LD50: >2000 mg/kg[1] * [CCINFO] monomethyl ether acetate, [2] alpha-isomer Inhalation (rat) LC50: 4345 ppm/6h Nil reported

Oral (rat) LD50: >14.1 ml[1]

TOXICITY IRRITATION

Dermal (rabbit) LD50: 805 mg/kgE[2] Eye (rabbit):20 mg/24 h - moderate

triethylenetetramine Oral (rat) LD50: 2500 mg/kgE[2] Eye (rabbit); 49 mg - SEVERE Version No: 1.2 Page 11 of 22 Issue Date: 01/04/2016 Skin (rabbit): 490 mg open SEVERE Print Date: 01/04/2016 8329TFS Slow Cure, Thermally Conductive Adhesive,Skin Flowable (rabbit): 5 mg/24 (Part SEVERE B)

TOXICITY IRRITATION Oral (rat) LD50: 4290 mg/kgd[2] [2] carbon black Dermal (rabbit) LD50: >3000 mg/kg Not Available

Oral (rat) LD50: >8000 mg/kg[1] TOXICITY IRRITATION

propylene glycol dermal (rat) LD50: >2000 mg/kg[1] * [CCINFO] monomethyl ether acetate, 1. Value obtained from Europe ECHA Registered Substances - Acute toxicity 2.* Value obtained from manufacturer's SDS. Unless otherwise specified data Legend: [2] alpha-isomer extractedInhalation from (rat) RTECS LC50: 4345 - Register ppm/6h of Toxic Effect of chemical Substances Nil reported

Oral (rat) LD50: >14.1 ml[1]

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 TOXICITYcell-mediated (T lymphocytes) immune reaction of the delayed type. Other allergicIRRITATION 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 Dermal (rabbit) LD50: 805 mg/kgE[2] Eye (rabbit):20 mg/24 h - moderate 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 triethylenetetramine sensitisingOral (rat) LD50:potential 2500 with mg/kgE which few[2] individuals come into contact. From a clinical pointEye of(rabbit); view, substances49 mg - SEVERE are noteworthy if they produce an allergic test reaction in more than 1% of the persons tested. For Fatty Nitrogen Derived (FND)Amides (including several high molecular weightSkin alkyl (rabbit): amino 490 acid mg amides) open SEVERE The chemicals in the FattyNitrogen Derived (FND) Amides of surfactants are similarSkin to (rabbit): the class 5 mg/24ingeneral SEVERE as to physical/chemical properties, environmental fate and toxicity. Humanexposure to these chemicals is substantially documented. Some typical applications of FNDAmides are: masonry cement additive; curingagent for epoxy resins; closed hydrocarbon systems in oil field production,refineries and chemical plants; and slip and antiblockingTOXICITY additives forpolymers. IRRITATION The safety of the FND Amides tohumans[2] is recognised by the U.S. FDA, which has approved stearamide, oleamideand/or erucamide for adhesives; coatings carbon black Dermal (rabbit) LD50: >3000 mg/kg Not Available for articles in food contact; coatingsfor polyolefin films; defoaming agents for manufacture of paper and paperboard;animal glue (defoamer in food packaging); inOral EVA (rat) copolymers LD50: >8000 for food mg/kg packaging;lubricants[1] for manufacture of metallic food packaging; irradiation of preparedfoods; release agents in manufacture of food packaging materials, food contactsurface of paper and paperboard; cellophane in food packaging; closure sealinggaskets; and release agents in polymeric resins and petroleum wax. The loworder of toxicity indicates that the use of FND Amides does not pose asignificant hazard to human health. The differences in chain length,degree of saturation of the carbon chains, source of the natural oils, oraddition of an amino group in the chain would not be Legend: 1. Value obtained from Europe ECHA Registered Substances - Acute toxicity 2.* Value obtained from manufacturer's SDS. Unless otherwise specified data extractedexpected tofrom have RTECS an impacton - Register the oftoxicity Toxic profile. Effect ofThis chemical conclusion Substances is supported by a number of studies inthe FND family of chemicals (amines, cationics, and amides as separatecategories) that show no differences in the length or degree of saturation ofthe alkyl substituents and is also supported by the limited toxicity of theselong-chain substituted chemicals The Fatty nitrogen-derived amides(FND amides) comprise four categories: The following information refers to contact allergens as a group and may not be specific to this product. Slow Cure,· Subcategory I: Substituted Amides Contact allergies quickly manifest themselves as contact eczema, more rarely as urticaria or Quincke's oedema. The pathogenesis of contact eczema involves Thermally Conductive· Subcategory II: Fatty Acid Reaction Products with Amino Compounds(Note: Subcategory II chemicals, in many cases, contain Subcategory I chemicalsas a cell-mediated (T lymphocytes) immune reaction of the delayed type. Other allergic skin reactions, e.g. contact urticaria, involve antibody-mediated immune Adhesive, Flowable (Part B) major components) · reactions.Subcategory The III: significance Imidazole Derivativesof the contact allergen is not simply determined by its sensitisation potential: the distribution of the substance and the opportunities · forSubcategory contact with IV: it FNDare equally Amphoterics important. A weakly sensitising substance which is widely distributed can be a more important allergen than one with stronger Acutesensitising Toxicity: potential The with lowacute which oralfew toxicityindividuals of the come FND into Amides contact. is well From established a clinical point across of allSubcategoriesview, substances byare the noteworthy available ifdata. they The produce limited an acute allergic toxicity test of thesechemicalsreaction in more isthan also 1% confirmed of the persons by four tested. acute dermal and two acute inhalationstudies ForRepeated Fatty Nitrogen Dose and Derived ReproductiveToxicity: (FND)Amides (including Two subchronicseveral high toxicity molecular studies weight demonstrating alkyl amino low acid toxicity amides) areavailable for Subcategory I chemicals. In addition, aThe 5-day chemicals repeated in dosethe FattyNitrogen studyfor a third Derived chemical (FND) confirmed Amides the of minimalsurfactants toxicity are ofsimilar these to chemicals. the class ingeneralSincethe Subcategoryas to physical/chemic I chemicalsal properties, are major components environmental of manyfate and Subcategory toxicity. Humanexposure IIchemicals, and to thesebased chemicals on the low is repeat-dose substantially toxicity documented. of the amino compounds(e.g. diethanolamine, triethanolamine) used for producing the SubcategorySome typical IIderivatives,applications ofthe FNDAmides Subcategory are: I repeat-dose toxicity studies adequately supportSubcategory II. masonryTwo subchronic cement toxicity additive; studiesin curingagent Subcategory for epoxy III resins;confirmed closed the hydrocarbonlow order of repeat systems dose in oil toxicity field production,refineriesfor the FNDAmides Imidazoleand chemical derivatives. plants; andFor Subcategoryslip and IV, antiblockingtwo subchronic additives toxicitystudies forpolymers. for one of the chemicals indicated a low orderThe safety of repeat-dose of the FND toxicity Amides forthe tohumans FND amphoteric is recognised salts by similarthe U.S. to FDA,that seen which in has the approvedother categories. stearamide, oleamideand/or erucamide for adhesives; coatings Geneticfor articles Toxicity in food incontact; vitro: Basedcoatingsfor on the polyolefin lack of effect films; of defoaming one or more agents chemicals for manufacture in eachsubcategory, of paper and adequate paperboard;animal data for mutagenic glue (defoamer activity as inmeasured food packaging); by the Salmonellain EVA copolymersreverse mutationfor food packaging;lubricantsassay exist for all of the for subcategories.manufacture of metallic food packaging; irradiation of preparedfoods; release agents in manufacture of food packaging materials, food contactsurface of paper and paperboard; cellophane in food packaging; closure sealinggaskets; and release agents in Developmental Toxicity: Adevelopmental toxicity study in Subcategory I and in Subcategory IV and a thirdstudy for a chemical in Subcategory III are available. Safety Datapolymeric resins and petroleumSheet wax. The loworder of toxicity indicates that the use of FND Amides does not pose asignificant hazard to human health. The studies indicatethese chemicals are not developmental toxicants, as expected based on theirstructures, molecular weights, physical properties and The differences in chain length,degree of saturation of the carbon chains, source of the natural oils, oraddition of an amino group in the chain would not be knowledge of similarchemicals. As above for repeat-dose toxicity, the data for Subcategory I areadequate to support Subcategory II. expected to have an impacton the toxicity profile. This conclusion is supported by a number of studies inthe FND family of chemicals (amines, cationics, and In evaluating potential toxicityof the FND Amides chemicals, it is also useful to review the available data forthe related FND Cationic and FND Amines amides as separatecategories) that show no differences in the length or degree of saturation ofthe alkyl substituents and is also supported by the limited toxicity Category chemicals. Acute oral toxicitystudies (approximately 80 studies for 40 chemicals in the three categories)provide LD50 values from approximately 400 of theselong-chain substituted chemicals to 10,000 mg/kg with no apparentorgan specific toxicity. Similarly, repeated dose toxicity studies(approximately 35 studies for 15 chemicals) provide NOAELs The Fatty nitrogen-derived amides(FND amides) comprise four categories: between 10 and 100mg/kg/day for rats and slightly lower for dogs. More than 60 genetic toxicitystudies (in vitro bacterial and mammalian cells as well as in · Subcategory I: Substituted Amides Slow Cure, vivo studies)indicated no mutagenic activity among more than 30 chemicals tested. Forreproductive evaluations, 14 studies evaluated reproductive endpoints · Subcategory II: Fatty Acid Reaction Products with Amino Compounds(Note: Subcategory II chemicals, in many cases, contain Subcategory I chemicalsas Thermally Conductive and/orreproductive organs for 11 chemicals, and 15 studies evaluated developmentaltoxicity for 13 chemicals indicating no reproductive or developmental major components) Adhesive, Flowable (Part B) effectsfor the FND group as a whole. Version No: 1.2 · Subcategory III: Imidazole Derivatives Page 12 of 22 Issue Date: 01/04/2016 ALUMINIUM OXIDE· NoSubcategory significant IV: acute FND toxicological Amphoterics data identified in literature search. Print Date: 01/04/2016 Acute8329TFS Toxicity: Slow The lowacute Cure, oral Thermally toxicity of the FND Conductive Amides is well Adhesive,established across Flowable allSubcategories (Part by B) the available data. The limited acute toxicity of The material may cause skin irritation after prolonged or repeated exposure and may produce a contact dermatitis (nonallergic). This form of dermatitis is often thesechemicals is also confirmed by four acute dermal and two acute inhalationstudies ZINC OXIDE characterised by skin redness (erythema) and swelling epidermis. Histologically there may be intercellular oedema of the spongy layer (spongiosis) and Repeated Dose and ReproductiveToxicity: Two subchronic toxicity studies demonstrating low toxicity areavailable for Subcategory I chemicals. In addition, intracellular oedema of the epidermis. a 5-day repeated dose studyfor a third chemical confirmed the minimal toxicity of these chemicals. Sincethe Subcategory I chemicals are major components of manyNo significant Subcategory acute IIchemicals, toxicological and data based identified on the in low literature repeat-dose search. toxicity of the amino compounds(e.g. diethanolamine, triethanolamine) used for producing the SubcategoryFor Fatty Nitrogen IIderivatives, Derived the (FND)Amides Subcategory (including I repeat-dose several toxicity high studies molecular adequately weight supportSubcategoryalkyl amino acid amides) II. Continued... TwoThe chemicalssubchronic in toxicity the FattyNitrogen studiesin Subcategory Derived (FND) III confirmed Amides theof surfactants low order of are repeat similar dose to thetoxicity class for ingeneral the FNDAmides as to physical/chemic Imidazole derivatives.al properties, For Subcategory environmental IV, twofate subchronicand toxicity. toxicitystudiesHumanexposure for toone these of the chemicals chemicals is substantiallyindicated a low documented. orderSome of typical repeat-dose applications toxicity of FNDAmidesforthe FND amphoteric are: salts similar to that seen in the other categories. masonryGenetic Toxicitycement additive;in vitro :curingagentBased on the for lack epoxy of effect resins; of closedone or morehydrocarbon chemicals systems in eachsubcategory, in oil field production,refineries adequate data for and mutagenic chemical activity plants; as and measured slip and by the antiblockingSalmonellareverse additives mutation forpolymers. assay exist for all of the subcategories. TheDevelopmental safety of the FNDToxicity: Amides Adevelopmental tohumans is recognisedtoxicity study by in the Subcategory U.S. FDA, whichI and in has Subcategory approved stearamide,IV and a thirdstudy oleamideand/or for a chemical erucamide in Subcategory for adhesives; III are coatings available. forThe articles studies in indicatethese food contact; chemicals coatingsfor are polyolefin not developmental films; defoaming toxicants, agents as expectedfor manufacture based onof papertheirstructures, and paperboard;animal molecular weights, glue physical(defoamer properties in food packaging);and knowledgein EVA copolymers of similarchemicals. for food packaging;lubricants As above for repeat-dose for manufacture toxicity, theof metallic data for food Subcategory packaging; I areadequate irradiation of to preparedfoods; support Subcategory release II. agents in manufacture of Infood evaluating packaging potential materials, toxicityof food contactsurfacethe FND Amides of chemicals,paper and paperboard;it is also useful cellophane to review in the food available packaging; data closureforthe related sealinggaskets; FND Cationic and andrelease FND agents Amines in polymericCategory chemicals.resins and Acutepetroleum oral wax.toxicitystudies The loworder (approximately of toxicity indicates 80 studies that for the 40 use chemicals of FND inAmides the three does categories)provide not pose asignificant LD50 hazard values to from human approximately health. 400 toThe 10,000 differences mg/kg inwith chain no apparentorganlength,degree of specific saturation toxicity. of the Similarly, carbon repeatedchains, source dose toxicityof the naturalstudies(approximately oils, oraddition of35 an studies amino for group 15 chemicals) in the chain provide would NOAELsnot be betweenexpected 10to haveand 100mg/kg/day an impacton the for toxicityrats and profile. slightly This lower conclusion for dogs. is More supported than 60 by genetic a number toxicitystudies of studies inthe (in vitro FND bacterial family of and chemicals mammalian (amines, cells cationics, as well as and in amidesvivo studies)indicated as separatecategories) no mutagenic that showactivity no among differences more inthan the 30length chemicals or degree tested. of saturation Forreproductive ofthe alkyl evaluations, substituents 14 studies and is alsoevaluated supported reproductive by the limited endpoints toxicity and/orreproductiveof theselong-chain substitutedorgans for 11chemicals chemicals, and 15 studies evaluated developmentaltoxicity for 13 chemicals indicating no reproductive or developmental effectsforThe Fatty thenitrogen-derived FND group as amides(FND a whole. amides) comprise four categories: · Subcategory I: Substituted Amides ALUMINIUM OXIDE· NoSubcategory significant II: acute Fatty toxicological Acid Reaction data Products identified with in Amino literature Compounds(Note: search. Subcategory II chemicals, in many cases, contain Subcategory I chemicalsas majorThe material components) may cause skin irritation after prolonged or repeated exposure and may produce a contact dermatitis (nonallergic). This form of dermatitis is often LINOLEIC ACID/4,7,10- · characterisedSubcategory III: by Imidazole skin redness Derivatives (erythema) and swelling epidermis. Histologically there may be intercellular oedema of the spongy layer (spongiosis) and ZINCTRIOXA- OXIDE · intracellularSubcategory oedema IV: FND of Amphoterics the epidermis. 1,13-TRIDECANEDIAMINE Acute Toxicity: The lowacute oral toxicity of the FND Amides is well established across allSubcategories by the available data. The limited acute toxicity of POLYAMID thesechemicals is also confirmed by four acute dermal and two acute inhalationstudies Continued... Repeated Dose and ReproductiveToxicity: Two subchronic toxicity studies demonstrating low toxicity areavailable for Subcategory I chemicals. In addition, a 5-day repeated dose studyfor a third chemical confirmed the minimal toxicity of these chemicals. Sincethe Subcategory I chemicals are major components of many Subcategory IIchemicals, and based on the low repeat-dose toxicity of the amino compounds(e.g. diethanolamine, triethanolamine) used for producing the Subcategory IIderivatives, the Subcategory I repeat-dose toxicity studies adequately supportSubcategory II. Two subchronic toxicity studiesin Subcategory III confirmed the low order of repeat dose toxicity for the FNDAmides Imidazole derivatives. For Subcategory IV, two subchronic toxicitystudies for one of the chemicals indicated a low order of repeat-dose toxicity forthe FND amphoteric salts similar to that seen in the other categories. Genetic Toxicity in vitro:Based on the lack of effect of one or more chemicals in eachsubcategory, adequate data for mutagenic activity as measured by the Salmonellareverse mutation assay exist for all of the subcategories. Developmental Toxicity: Adevelopmental toxicity study in Subcategory I and in Subcategory IV and a thirdstudy for a chemical in Subcategory III are available. The studies indicatethese chemicals are not developmental toxicants, as expected based on theirstructures, molecular weights, physical properties and knowledge of similarchemicals. As above for repeat-dose toxicity, the data for Subcategory I areadequate to support Subcategory II. In evaluating potential toxicityof the FND Amides chemicals, it is also useful to review the available data forthe related FND Cationic and FND Amines Category chemicals. Acute oral toxicitystudies (approximately 80 studies for 40 chemicals in the three categories)provide LD50 values from approximately 400 to 10,000 mg/kg with no apparentorgan specific toxicity. Similarly, repeated dose toxicity studies(approximately 35 studies for 15 chemicals) provide NOAELs between 10 and 100mg/kg/day for rats and slightly lower for dogs. More than 60 genetic toxicitystudies (in vitro bacterial and mammalian cells as well as in vivo studies)indicated no mutagenic activity among more than 30 chemicals tested. Forreproductive evaluations, 14 studies evaluated reproductive endpoints and/orreproductive organs for 11 chemicals, and 15 studies evaluated developmentaltoxicity for 13 chemicals indicating no reproductive or developmental effectsfor the FND group as a whole.

The repair process (which initially developed to protect mammalian lungs from foreign matter and antigens) may, however, cause further damage to the lungs (fibrosis for example) when activated by hazardous chemicals. Often, this results in an impairment of gas exchange, the primary function of the lungs. Therefore prolonged exposure to respiratory irritants may cause sustained breathing difficulties.

Continued... Version No: 1.2 Page 12 of 22 Issue Date: 01/04/2016 Print Date: 01/04/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part B)

No significant acute toxicological data identified in literature search. For Fatty Nitrogen Derived (FND)Amides (including several high molecular weight alkyl amino acid amides) The chemicals in the FattyNitrogen Derived (FND) Amides of surfactants are similar to the class ingeneral as to physical/chemical properties, environmental fate and toxicity. Humanexposure to these chemicals is substantially documented. Some typical applications of FNDAmides are: masonry cement additive; curingagent for epoxy resins; closed hydrocarbon systems in oil field production,refineries and chemical plants; and slip and antiblocking additives forpolymers. The safety of the FND Amides tohumans is recognised by the U.S. FDA, which has approved stearamide, oleamideand/or erucamide for adhesives; coatings for articles in food contact; coatingsfor polyolefin films; defoaming agents for manufacture of paper and paperboard;animal glue (defoamer in food packaging); in EVA copolymers for food packaging;lubricants for manufacture of metallic food packaging; irradiation of preparedfoods; release agents in manufacture of food packaging materials, food contactsurface of paper and paperboard; cellophane in food packaging; closure sealinggaskets; and release agents in polymeric resins and petroleum wax. The loworder of toxicity indicates that the use of FND Amides does not pose asignificant hazard to human health. The differences in chain length,degree of saturation of the carbon chains, source of the natural oils, oraddition of an amino group in the chain would not be expected to have an impacton the toxicity profile. This conclusion is supported by a number of studies inthe FND family of chemicals (amines, cationics, and amides as separatecategories) that show no differences in the length or degree of saturation ofthe alkyl substituents and is also supported by the limited toxicity of theselong-chain substituted chemicals The Fatty nitrogen-derived amides(FND amides) comprise four categories: · Subcategory I: Substituted Amides · Subcategory II: Fatty Acid Reaction Products with Amino Compounds(Note: Subcategory II chemicals, in many cases, contain Subcategory I chemicalsas major components) LINOLEIC ACID/4,7,10- · Subcategory III: Imidazole Derivatives TRIOXA- · Subcategory IV: FND Amphoterics 1,13-TRIDECANEDIAMINE Acute Toxicity: The lowacute oral toxicity of the FND Amides is well established across allSubcategories by the available data. The limited acute toxicity of POLYAMID thesechemicals is also confirmed by four acute dermal and two acute inhalationstudies Repeated Dose and ReproductiveToxicity: Two subchronic toxicity studies demonstrating low toxicity areavailable for Subcategory I chemicals. In addition, a 5-day repeated dose studyfor a third chemical confirmed the minimal toxicity of these chemicals. Sincethe Subcategory I chemicals are major components of many Subcategory IIchemicals, and based on the low repeat-dose toxicity of the amino compounds(e.g. diethanolamine, triethanolamine) used for producing the Subcategory IIderivatives, the Subcategory I repeat-dose toxicity studies adequately supportSubcategory II. Two subchronic toxicity studiesin Subcategory III confirmed the low order of repeat dose toxicity for the FNDAmides Imidazole derivatives. For Subcategory IV, two subchronic toxicitystudies for one of the chemicals indicated a low order of repeat-dose toxicity forthe FND amphoteric salts similar to that seen in the other categories. Genetic Toxicity in vitro:Based on the lack of effect of one or more chemicals in eachsubcategory, adequate data for mutagenic activity as measured by the Salmonellareverse mutation assay exist for all of the subcategories. Developmental Toxicity: Adevelopmental toxicity study in Subcategory I and in Subcategory IV and a thirdstudy for a chemical in Subcategory III are available. The studies indicatethese chemicals are not developmental toxicants, as expected based on theirstructures, molecular weights, physical properties and knowledge of similarchemicals. As above for repeat-dose toxicity, the data for Subcategory I areadequate to support Subcategory II. In evaluating potential toxicityof the FND Amides chemicals, it is also useful to review the available data forthe related FND Cationic and FND Amines Category chemicals. Acute oral toxicitystudies (approximately 80 studies for 40 chemicals in the three categories)provide LD50 values from approximately 400 to 10,000 mg/kg with no apparentorgan specific toxicity. Similarly, repeated dose toxicity studies(approximately 35 studies for 15 chemicals) provide NOAELs between 10 and 100mg/kg/day for rats and slightly lower for dogs. More than 60 genetic toxicitystudies (in vitro bacterial and mammalian cells as well as in vivo studies)indicated no mutagenic activity among more than 30 chemicals tested. Forreproductive evaluations, 14 studies evaluated reproductive endpoints and/orreproductive organs for 11 chemicals, and 15 studies evaluated developmentaltoxicity for 13 chemicals indicating no reproductive or developmental effectsfor the FND group as a whole.

The repair process (which initially developed to protect mammalian lungs from foreign matter and antigens) may, however, cause further damage to the lungs (fibrosis for example) when activated by hazardous chemicals. Often, this results in an impairment of gas exchange, the primary function of the lungs. Safety DataTherefore prolonged exposureSheet to respiratory irritants may cause sustained breathing difficulties.

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 epidermis. Histologically there may be intercellular oedema of the spongy layer (spongiosis) and Version No: 1.2 intracellular oedema of the epidermis. Page 13 of 22 Issue Date: 01/04/2016 for propylene glycol ethers (PGEs): Print Date: 01/04/2016 Typical8329TFS propylene Slow glycol Cure,ethers include Thermally propylene glycolConductive n-butylether Adhesive,(PnB); dipropylene Flowable glycol n-butyl (Part ether (DPnB);B) dipropylene glycol methylether acetate (DPMA); tripropylene glycol methyl ether (TPM). Testing of a wide variety of propylene glycol ethers Testing of awide variety of propylene glycol ethers has shown that propylene glycol-basedethers are less toxic than some ethers of the ethylene series. The commontoxicities associated with the lower molecular weight homologues of theethylene series, such as As a group PGEs exhibits low acute toxicity by the oral, dermal,and inhalation routes. Rat oral LD50s range from >3,000 mg/kg (PnB) to>5,000 mg/kg adverse effects on reproductive organs, the developingembryo and fetus, blood (haemolytic effects), or thymus, are not seen with thecommercial-grade (DPMA). Dermal LD50s are all > 2,000 mg/kg (PnB, & DPnB;where no deaths occurred), and ranging up to >15,000 mg/kg (TPM). InhalationLC50 values propylene glycol ethers. In the ethylene series, metabolism ofthe terminal hydroxyl group produces an alkoxyacetic acid. The reproductive anddevelopmental were higher than 5,000 mg/m3 for DPMA (4-hour exposure), and TPM(1-hour exposure). For DPnB the 4-hour LC50 is >2,040 mg/m3. For PnB, the4-hour toxicities of the lower molecular weight homologues in theethylene series are due specifically to the formation of methoxyacetic andethoxyacetic acids. LC50 was >651 ppm (>3,412 mg/m3), representing the highestpractically attainable vapor level. No deaths occurred at these concentrations.PnB and TPM are Longer chain length homologues in the ethylene series are notassociated with the reproductive toxicity but can cause haemolysis in sensitivespecies, also moderately irritating to eyes while the remaining categorymembers are only slightly irritating to nonirritating. PnB is moderatelyirritating to skin while the through formation of an alkoxyacetic acid. The predominant alphaisomer of all the PGEs (thermodynamically favored during manufacture of PGEs)is a PROPYLENE GLYCOL remaining category members are slightly tonon-irritating secondary alcohol incapable of forming an alkoxypropionic acid. In contrastbeta-isomers are able to form the alkoxypropionic acids and these are linked MONOMETHYL ETHER None are skin sensitisers. toteratogenic effects (and possibly haemolytic effects). ACETATE, ALPHA-ISOMER In repeated dose studies ranging in duration from 2 to 13 weeks,few adverse effects were found even at high exposure levels and effects thatdid occur were mild This alpha isomer comprises greater than 95% of the isomericmixture in the commercial product. in nature. By the oral route of administration, NOAELs of350 mg/kg-d (PnB – 13 wk) and 450 mg/kg-d (DPnB – 13 wk) were observed forliver and kidney weight Because the alpha isomer cannot form an alkoxypropionic acid, thisis the most likely reason for the lack of toxicity shown by the PGEs asdistinct from the lower increases (without accompanying histopathology). LOAELsfor these two chemicals were 1000 mg/kg-d (highest dose tested). molecular weight ethylene glycol ethers. Moreimportantly, however, very extensive empirical test data show that this classof commercial-grade glycol ether Dermal repeated-dose toxicity tests have been performed for manyPGEs. For PnB, no effects were seen in a 13-wk study at doses as high as 1,000mg/kg-d. A Version No: presents a low toxicity hazard. PGEs, whethermono,Page di- or tripropyleneof glycol-based (and no matter what the alcohol group),show a very similarIssue pattern Date: of low to 1.2 dose of 273 mg/kg-d constituted a LOAEL (increased organ13 weightswithout22 histopathology) in a 13-week dermal study for DPnB. For TPM, increasedkidney01/04/2016 non-detectable toxicity of any type atdoses or exposure levels greatly exceeding those showing pronounced effectsfrom the ethylene series. One of the primary weights (no histopathology) and transiently decreased body weights werefound at a dose of 2,895 mg/kg-d in a 90-day study in rabbits. By inhalation,noPrint Date: effects 01/04/2016 metabolites8329TFS of the Slow propyleneglycol Cure, Thermallyethers is propylene Conductive glycol, which is Adhesive, of low toxicity and Flowable completelymetabolised (Part B) in the body. were observed in 2-week studies in rats at the highest testedconcentrations of 3244 mg/m3 (600 ppm) for PnB and 2,010 mg/m3 (260 ppm) forDPnB. TPM As a class, the propylene glycol ethers are rapidly absorbed anddistributed throughout the body when introduced by inhalation or oral exposure.Dermal caused increased liver weights without histopathology by inhalationin a 2-week study at a LOAEL of 360 mg/m3 (43 ppm). In this study, the highesttested TPM absorption is somewhat slower but subsequent distribution is rapid. Mostexcretion for PGEs is via the urine and expired air. A small portion isexcreted in the concentration, 1010 mg/m3 (120 ppm), also caused increased liverweights without accompanying histopathology. Although no repeated-dose studiesare faeces. available for the oral route for TPM, or for any route for DPMA, it isanticipated that these chemicals would behave similarly to other categorymembers. As a group PGEs exhibits low acute toxicity by the oral, dermal,and inhalation routes. Rat oral LD50s range from >3,000 mg/kg (PnB) to>5,000 mg/kg One and two-generation reproductive toxicity testing has beenconducted in mice, rats, and rabbits via the oral or inhalation routes ofexposure on PM and PMA. (DPMA). Dermal LD50s are all > 2,000 mg/kg (PnB, & DPnB;where no deaths occurred), and ranging up to >15,000 mg/kg (TPM). InhalationLC50 values In an inhalation rat study using PM, the NOAEL forparental toxicity is 300 ppm (1106 mg/m3) with decreases in body and organweights occurring at the LOAEL were higher than 5,000 mg/m3 for DPMA (4-hour exposure), and TPM(1-hour exposure). For DPnB the 4-hour LC50 is >2,040 mg/m3. For PnB, the4-hourContinued... of 1000 ppm (3686 mg/m3). For offspring toxicitythe NOAEL is 1000 ppm (3686 mg/m3), with decreased body weights occurring at3000 ppm (11058 mg/m3). LC50 was >651 ppm (>3,412 mg/m3), representing the highestpractically attainable vapor level. No deaths occurred at these concentrations.PnB and TPM are For PMA, the NOAEL for parental and offspring toxicityis 1000 mg/kg/d. in a two generation gavage study in rats. No adverse effectswere found on reproductive moderately irritating to eyes while the remaining categorymembers are only slightly irritating to nonirritating. PnB is moderatelyirritating to skin while the organs, fertility rates, or other indices commonlymonitored in such studies. In addition, there is no evidence fromhistopathological data from repeated-dose remaining category members are slightly tonon-irritating studies for the category members thatwould indicate that these chemicals would pose a reproductive hazard to humanhealth. None are skin sensitisers. In developmental toxicity studies many PGEs have been tested byvarious routes of exposure and in various species at significant exposurelevels and show no In repeated dose studies ranging in duration from 2 to 13 weeks,few adverse effects were found even at high exposure levels and effects thatdid occur were mild frank developmental effects. Due to the rapid hydrolysis ofDPMA to DPM, DPMA would not be expected to show teratogenic effects. At highdoses where in nature. By the oral route of administration, NOAELs of350 mg/kg-d (PnB – 13 wk) and 450 mg/kg-d (DPnB – 13 wk) were observed forliver and kidney weight maternal toxicity occurs (e.g., significant body weight loss), anincreased incidence of some anomalies such as delayed skeletal ossification orincreased 13th increases (without accompanying histopathology). LOAELsfor these two chemicals were 1000 mg/kg-d (highest dose tested). ribs, have been reported. Commercially available PGEs showed noteratogenicity. Dermal repeated-dose toxicity tests have been performed for manyPGEs. For PnB, no effects were seen in a 13-wk study at doses as high as 1,000mg/kg-d. A The weight of the evidence indicates that propylene glycol ethersare not likely to be genotoxic. In vitro, negative results havebeen seen in a number of assays for dose of 273 mg/kg-d constituted a LOAEL (increased organ weightswithout histopathology) in a 13-week dermal study for DPnB. For TPM, increasedkidney PnB, DPnB, DPMA and TPM. Positive resultswere only seen in 3 out of 5 chromosome aberration assays in mammalian cellswith DPnB. However, negative weights (no histopathology) and transiently decreased body weights werefound at a dose of 2,895 mg/kg-d in a 90-day study in rabbits. By inhalation,no effects results were seen in a mouse micronucleus assaywith DPnB and PM. Thus, there is no evidence to suggest these PGEs would begenotoxic in vivo. In a 2-year were observed in 2-week studies in rats at the highest testedconcentrations of 3244 mg/m3 (600 ppm) for PnB and 2,010 mg/m3 (260 ppm) forDPnB. TPM bioassaycaused increased on PM, there liver weightswere nostatistically without histopathology significant byincreases inhalationin in tumors a 2-week in rats study and at mice. a LOAEL of 360 mg/m3 (43 ppm). In this study, the highesttested TPM Aconcentration, BASF report 1010(in ECETOC mg/m3 (120) showed ppm), that also inhalation caused increased exposure liverweightsto 545 ppm withoutPGMEA accompanying (beta isomer) washistopathology. associated Although with a teratogenic no repeated-dose response studiesare in rabbits; but availableexposure forto 145 the ppmoral routeand 36 for ppm TPM, had or no for adverse any route effects. for DPMA, it isanticipated that these chemicals would behave similarly to other categorymembers. OneThe betaand two-generationisomer of PGMEA reproductive comprises toxicity only 10% testing of thehas commercial beenconducted material, in mice, the remainingrats, and rabbits 90% is via alpha the isomer.oral or inhalation Hazard appears routes ofexposure low but emphasizes on PM and the PMA. needIn an inhalationfor care in rat handling study using this chemical. PM, the NOAEL [I.C.I] forparental toxicity is 300 ppm (1106 mg/m3) with decreases in body and organweights occurring at the LOAEL of 1000 ppm (3686 mg/m3). For offspring toxicitythe NOAEL is 1000 ppm (3686 mg/m3), with decreased body weights occurring at3000 ppm (11058 mg/m3). AFor BASF PMA, report the NOAEL (in ECETOC for parental ) showed and thatoffspring inhalation toxicityis exposure 1000 mg/kg/d.to 545 ppm in a PGMEA two generation (beta isomer) gavage was study associated in rats. No with adverse a teratogenic effectswere response found in on rabbits; reproductive but organs,exposure fertility to 145 rates, ppm orand other 36 ppmindices had commonlymonitored no adverse effects. Thein such beta studies. isomer Inof addition,PGMEA comprisesthere is no onlyevidence 10% offromhistopathological the commercial material, data fromthe remaining repeated-dose 90% is alphastudies isomer. for the Hazardcategory appears members low thatwould but emphasizes indicate thethat need these for chemicals care in handling would pose this chemical.a reproductive [I.C.I] hazard *Shin-Etsu to humanhealth. SDS InThe developmental following information toxicity studies refers manyto contact PGEs allergens have been as atested group byvarious and may routes not be of specific exposure to this and product. in various species at significant exposurelevels and show no frankContact developmental allergies quickly effects. manifest Due to themselves the rapid hydrolysis as contact ofDPMA eczema, to more DPM, rarely DPMA as would urticaria not or be Quincke's expected oedema. to show teratogenicThe pathogenesis effects. ofAt contact highdoses eczema where involves maternala cell-mediated toxicity (T occurs lymphocytes) (e.g., significant immune body reaction weight of the loss), delayed anincreased type. Other incidence allergic of skin some reactions, anomalies e.g. such contact as delayedurticaria, skeletal involve ossificationantibody-mediated orincreased immune 13th ribs,reactions. have beenThe significance reported. Commercially of the contact available allergen PGEs is not showed simply determined noteratogenicity. by its sensitisation potential: the distribution of the substance and the opportunities Thefor contact weight withof the it areevidence equally indicates important. that A propylene weakly sensitising glycol ethersare substance not likelywhich to is be widely genotoxic. distributed In vitro can, negative be a more results important havebeen allergen seen than in a one number with strongerof assays for PnB,sensitising DPnB, potential DPMA andwith TPM. which Positive few individuals resultswere come only into seen contact. in 3 outFrom of 5a chromosomeclinical point of aberration view, substances assays in are mammalian noteworthy cellswith if they produceDPnB. However, an allergic negative test resultsreaction were in more seen than in a 1% mouse of the micronucleus persons tested. assaywith DPnB and PM. Thus, there is no evidence to suggest these PGEs would begenotoxic in vivo. In a 2-year bioassayHandling onethyleneamine PM, there were products nostatistically is complicated significant by their increases tendency in tumorsto react in with rats other and mice.chemicals, such as carbon dioxide in the air, which results in the formation Aof BASFsolid carbamates. report (in ECETOC Because ) showedof their abilitythat inhalation to produce exposure chemical to burns,545 ppm skin PGMEA rashes, (betaand asthma-like isomer) was symptoms, associated ethyleneamines with a teratogenic also response require substantial in rabbits; butcare exposurein handling. to 145 Higher ppm molecular and 36 ppm weight had noethyleneamines adverse effects. are often handled at elevated temperatures further increasing the possibility of vapor exposure to these Thecompounds. beta isomer of PGMEA comprises only 10% of the commercial material, the remaining 90% is alpha isomer. Hazard appears low but emphasizes the needBecause for care of the in fragility handling of eyethis tissue,chemical. almost [I.C.I] any eye contact with any ethyleneamine may cause irreparable damage, even blindness. A single, short exposure to ethyleneamines, may cause severe skin burns, while a single, prolonged exposure may result in the material being absorbed through the skin in harmful Aamounts. BASF report Exposures (in ECETOC have caused ) showed allergic that skininhalation reactions exposure in some to 545individuals. ppm PGMEA Single (betadose isomer)oral toxicity was of associated ethyleneamines with a teratogenicis low. The oralresponse LD50 infor rabbits; rats is inbut the exposurerange of 1000 to 145 to ppm4500 and mg/kg 36 ppmfor the had ethyleneamines. no adverse effects. The beta isomer of PGMEA comprises only 10% of the commercial material, the remaining 90% is alphaIn general, isomer. the Hazard low-molecular appears weight low but polyamines emphasizes have the been need positive for care in in the handling Ames assay, this chemical. increase [I.C.I] sister *Shin-Etsu chromatid SDSexchange in Chinese hamster ovary (CHO) cells, and are positive for unscheduled DNA synthesis although they are negative in the mouse micronucleus assay. It is believed that the positive results are The following information refers to contact allergens as a group and may not be specific to this product. based on its ability to chelate copper 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 The material may produce severe irritation to the eye causing pronounced inflammation. Repeated or prolonged exposure to irritants may produce 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 conjunctivitis. sensitising potential with which few individuals come into contact. From a clinical point of view, substances are noteworthy if they produce an allergic test The material may produce severe skin irritation after prolonged or repeated exposure, and may produce a contact dermatitis (nonallergic). This form of reaction in more than 1% of the persons tested. dermatitis is often characterised by skin redness (erythema) thickening of the epidermis. Handling ethyleneamine products is complicated by their tendency to react with other chemicals, such as carbon dioxide in the air, which results in the formation TRIETHYLENETETRAMINE Histologically there may be intercellular oedema of the spongy layer (spongiosis) and intracellular oedema of the epidermis. Prolonged contact is unlikely, of solid carbamates. Because of their ability to produce chemical burns, skin rashes, and asthma-like symptoms, ethyleneamines also require substantial care given the severity of response, but repeated exposures may produce severe ulceration. in handling. Higher molecular weight ethyleneamines are often handled at elevated temperatures further increasing the possibility of vapor exposure to these For alkyl polyamines: compounds. The alkyl polyamines cluster consists of organic compounds containing two terminal primary amine groups and at least one secondary amine group.Typically Because of the fragility of eye tissue, almost any eye contact with any ethyleneamine may cause irreparable damage, even blindness. A single, short exposure to these substances are derivatives of ethylenediamine, propylenediamine or hexanediamine. The molecular weight range for the entire cluster is relatively narrow, ethyleneamines, may cause severe skin burns, while a single, prolonged exposure may result in the material being absorbed through the skin in harmful ranging from 103 to 232 amounts. Exposures have caused allergic skin reactions in some individuals. Single dose oral toxicity of ethyleneamines is low. The oral LD50 for rats is in the Acute toxicity of the alkyl polyamines cluster is low to moderate via oral exposure and a moderate to high via dermal exposure. Cluster members have been range of 1000 to 4500 mg/kg for the ethyleneamines. shown to be eye irritants, skin irritants, and skin sensitisers in experimental animals. Repeated exposure in rats via the oral route indicates a range of toxicity In general, the low-molecular weight polyamines have been positive in the Ames assay, increase sister chromatid exchange in Chinese hamster ovary (CHO) from low to high hazard. Most cluster members gave positive results in tests for potential genotoxicity. cells, and are positive for unscheduled DNA synthesis although they are negative in the mouse micronucleus assay. It is believed that the positive results are Limited carcinogenicity studies on several members of the cluster showed no evidence of carcinogenicity. Unlike aromatic amines, aliphatic amines are not based on its ability to chelate copper www.element14.com expected to be potential carcinogens because they are not expected to undergo metabolic activation, nor would activated intermediates be stable enough to www.farnell.com reach target macromolecules. Polyamines potentiate NMDA induced whole-cell currents in cultured striatal neurons www.newark.com The material may produce severe irritation to the eye causing pronounced inflammation. Repeated or prolonged exposure to irritants may produce conjunctivitis. Asthma-like symptoms may continue for months or even years after exposure to the material ceases. This may be due to a non-allergenic condition known as The material may produce severe skin irritation after prolonged or repeated exposure, and may produce a contact dermatitis (nonallergic). This form of reactive airways dysfunction syndrome (RADS) which can occur following exposure to high levels of highly irritating compound. Key criteria for the diagnosis dermatitis is often characterised by skin redness (erythema) thickening of the epidermis. of RADS include the absence of preceding respiratoryPage disease, <38> in a non-atopic individual, with abrupt onset of persistent asthma-like symptoms28/10/18 within minutes V1.0 TRIETHYLENETETRAMINE Histologically there may be intercellular oedema of the spongy layer (spongiosis) and intracellular oedema of the epidermis. Prolonged contact is unlikely, to hours of a documented exposure to the irritant. A reversible airflow pattern, on spirometry, with the presence of moderate to severe bronchial hyperreactivity given the severity of response, but repeated exposures may produce severe ulceration. on methacholine challenge testing and the lack of minimal lymphocytic inflammation, without eosinophilia, have also been included in the criteria for diagnosis For alkyl polyamines: of RADS. RADS (or asthma) following an irritating inhalation is an infrequent disorder with rates related to the concentration of and duration of exposure to the The alkyl polyamines cluster consists of organic compounds containing two terminal primary amine groups and at least one secondary amine group.Typically irritating substance. Industrial bronchitis, on the other hand, is a disorder that occurs as result of exposure due to high concentrations of irritating substance these substances are derivatives of ethylenediamine, propylenediamine or hexanediamine. The molecular weight range for the entire cluster is relatively narrow, (often particulate in nature) and is completely reversible after exposure ceases. The disorder is characterised by dyspnea, cough and mucus production. ranging from 103 to 232 Triethylenetetramine (TETA) is a severe irritant to skin and eyesand induces skin sensitisation. Acute toxicity of the alkyl polyamines cluster is low to moderate via oral exposure and a moderate to high via dermal exposure. Cluster members have been TETA is of moderate acute toxicity: LD50(oral, rat) > 2000mg/kg bw, LD50(dermal, rabbit) = 550 - 805 mg/kg bw. Acute exposure tosaturated vapour via shown to be eye irritants, skin irritants, and skin sensitisers in experimental animals. Repeated exposure in rats via the oral route indicates a range of toxicity from low to high hazard. Most cluster members gave positive results in tests for potential genotoxicity. Limited carcinogenicity studies on several members of the cluster showed no evidence of carcinogenicity. Unlike aromatic amines, aliphatic amines areContinued... not expected to be potential carcinogens because they are not expected to undergo metabolic activation, nor would activated intermediates be stable enough to reach target macromolecules. Polyamines potentiate NMDA induced whole-cell currents in cultured striatal neurons

Continued... Version No: 1.2 Page 13 of 22 Issue Date: 01/04/2016 Print Date: 01/04/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part B)

As a group PGEs exhibits low acute toxicity by the oral, dermal,and inhalation routes. Rat oral LD50s range from >3,000 mg/kg (PnB) to>5,000 mg/kg (DPMA). Dermal LD50s are all > 2,000 mg/kg (PnB, & DPnB;where no deaths occurred), and ranging up to >15,000 mg/kg (TPM). InhalationLC50 values were higher than 5,000 mg/m3 for DPMA (4-hour exposure), and TPM(1-hour exposure). For DPnB the 4-hour LC50 is >2,040 mg/m3. For PnB, the4-hour LC50 was >651 ppm (>3,412 mg/m3), representing the highestpractically attainable vapor level. No deaths occurred at these concentrations.PnB and TPM are moderately irritating to eyes while the remaining categorymembers are only slightly irritating to nonirritating. PnB is moderatelyirritating to skin while the remaining category members are slightly tonon-irritating None are skin sensitisers. In repeated dose studies ranging in duration from 2 to 13 weeks,few adverse effects were found even at high exposure levels and effects thatdid occur were mild in nature. By the oral route of administration, NOAELs of350 mg/kg-d (PnB – 13 wk) and 450 mg/kg-d (DPnB – 13 wk) were observed forliver and kidney weight increases (without accompanying histopathology). LOAELsfor these two chemicals were 1000 mg/kg-d (highest dose tested). Dermal repeated-dose toxicity tests have been performed for manyPGEs. For PnB, no effects were seen in a 13-wk study at doses as high as 1,000mg/kg-d. A dose of 273 mg/kg-d constituted a LOAEL (increased organ weightswithout histopathology) in a 13-week dermal study for DPnB. For TPM, increasedkidney weights (no histopathology) and transiently decreased body weights werefound at a dose of 2,895 mg/kg-d in a 90-day study in rabbits. By inhalation,no effects were observed in 2-week studies in rats at the highest testedconcentrations of 3244 mg/m3 (600 ppm) for PnB and 2,010 mg/m3 (260 ppm) forDPnB. TPM caused increased liver weights without histopathology by inhalationin a 2-week study at a LOAEL of 360 mg/m3 (43 ppm). In this study, the highesttested TPM concentration, 1010 mg/m3 (120 ppm), also caused increased liverweights without accompanying histopathology. Although no repeated-dose studiesare available for the oral route for TPM, or for any route for DPMA, it isanticipated that these chemicals would behave similarly to other categorymembers. One and two-generation reproductive toxicity testing has beenconducted in mice, rats, and rabbits via the oral or inhalation routes ofexposure on PM and PMA. In an inhalation rat study using PM, the NOAEL forparental toxicity is 300 ppm (1106 mg/m3) with decreases in body and organweights occurring at the LOAEL of 1000 ppm (3686 mg/m3). For offspring toxicitythe NOAEL is 1000 ppm (3686 mg/m3), with decreased body weights occurring at3000 ppm (11058 mg/m3). For PMA, the NOAEL for parental and offspring toxicityis 1000 mg/kg/d. in a two generation gavage study in rats. No adverse effectswere found on reproductive organs, fertility rates, or other indices commonlymonitored in such studies. In addition, there is no evidence fromhistopathological data from repeated-dose studies for the category members thatwould indicate that these chemicals would pose a reproductive hazard to humanhealth. In developmental toxicity studies many PGEs have been tested byvarious routes of exposure and in various species at significant exposurelevels and show no frank developmental effects. Due to the rapid hydrolysis ofDPMA to DPM, DPMA would not be expected to show teratogenic effects. At highdoses where maternal toxicity occurs (e.g., significant body weight loss), anincreased incidence of some anomalies such as delayed skeletal ossification orincreased 13th ribs, have been reported. Commercially available PGEs showed noteratogenicity. The weight of the evidence indicates that propylene glycol ethersare not likely to be genotoxic. In vitro, negative results havebeen seen in a number of assays for PnB, DPnB, DPMA and TPM. Positive resultswere only seen in 3 out of 5 chromosome aberration assays in mammalian cellswith DPnB. However, negative results were seen in a mouse micronucleus assaywith DPnB and PM. Thus, there is no evidence to suggest these PGEs would begenotoxic in vivo. In a 2-year bioassay on PM, there were nostatistically significant increases in tumors in rats and mice. A BASF report (in ECETOC ) showed that inhalation exposure to 545 ppm PGMEA (beta isomer) was associated with a teratogenic response in rabbits; but exposure to 145 ppm and 36 ppm had no adverse effects. The beta isomer of PGMEA comprises only 10% of the commercial material, the remaining 90% is alpha isomer. Hazard appears low but emphasizes the need for care in handling this chemical. [I.C.I]

A BASF report (in ECETOC ) showed that inhalation exposure to 545 ppm PGMEA (beta isomer) was associated with a teratogenic response in rabbits; but exposure to 145 ppm and 36 ppm had no adverse effects. The beta isomer of PGMEA comprises only 10% of the commercial material, the remaining 90% is alpha isomer. Hazard appears low but emphasizes the need for care in handling this chemical. [I.C.I] *Shin-Etsu SDS 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. Handling ethyleneamine products is complicated by their tendency to react with other chemicals, such as carbon dioxide in the air, which results in the formation of solid carbamates. Because of their ability to produce chemical burns, skin rashes, and asthma-like symptoms, ethyleneamines also require substantial care Safety Datain handling. Higher molecularSheet weight ethyleneamines are often handled at elevated temperatures further increasing the possibility of vapor exposure to these compounds. Because of the fragility of eye tissue, almost any eye contact with any ethyleneamine may cause irreparable damage, even blindness. A single, short exposure to ethyleneamines, may cause severe skin burns, while a single, prolonged exposure may result in the material being absorbed through the skin in harmful amounts. Exposures have caused allergic skin reactions in some individuals. Single dose oral toxicity of ethyleneamines is low. The oral LD50 for rats is in the range of 1000 to 4500 mg/kg for the ethyleneamines. In general, the low-molecular weight polyamines have been positive in the Ames assay, increase sister chromatid exchange in Chinese hamster ovary (CHO) cells, and are positive for unscheduled DNA synthesis although they are negative in the mouse micronucleus assay. It is believed that the positive results are based on its ability to chelate copper

The material may produce severe irritation to the eye causing pronounced inflammation. Repeated or prolonged exposure to irritants may produce conjunctivitis. The material may produce severe 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) thickening of the epidermis. TRIETHYLENETETRAMINE Histologically there may be intercellular oedema of the spongy layer (spongiosis) and intracellular oedema of the epidermis. Prolonged contact is unlikely, given the severity of response, but repeated exposures may produce severe ulceration. For alkyl polyamines: The alkyl polyamines cluster consists of organic compounds containing two terminal primary amine groups and at least one secondary amine group.Typically these substances are derivatives of ethylenediamine, propylenediamine or hexanediamine. The molecular weight range for the entire cluster is relatively narrow, ranging from 103 to 232 Acute toxicity of the alkyl polyamines cluster is low to moderate via oral exposure and a moderate to high via dermal exposure. Cluster members have been shown to be eye irritants, skin irritants, and skin sensitisers in experimental animals. Repeated exposure in rats via the oral route indicates a range of toxicity from low to high hazard. Most cluster members gave positive results in tests for potential genotoxicity. Limited carcinogenicity studies on several members of the cluster showed no evidence of carcinogenicity. Unlike aromatic amines, aliphatic amines are not expected to be potential carcinogens because they are not expected to undergo metabolic activation, nor would activated intermediates be stable enough to reach target macromolecules. Polyamines potentiate NMDA induced whole-cell currents in cultured striatal neurons

Asthma-like symptoms may continue for months or even years after exposure to the material ceases. This may be due to a non-allergenic condition known as reactive airways dysfunction syndrome (RADS) which can occur following exposure to high levels of highly irritating compound. Key criteria for the diagnosis of RADS include the absence of preceding respiratory disease, in a non-atopic individual, with abrupt onset of persistent asthma-like symptoms within minutes to hours of a documented exposure to the irritant. A reversible airflow pattern, on spirometry, with the presence of moderate to severe bronchial hyperreactivity Version No: 1.2 on methacholine challenge testing and the lack ofPage minimal 14 lymphocyticof 22 inflammation, without eosinophilia, have also been included in the criteriaIssue for Date: diagnosis 01/04/2016 of RADS. RADS (or asthma) following an irritating inhalation is an infrequent disorder with rates related to the concentration of and duration of exposure to the Print Date: 01/04/2016 irritating8329TFS substance. Slow Industrial Cure, bronchitis, Thermally on the other Conductive hand, is a disorder Adhesive, that occurs Flowableas result of exposure (Part due B) to high concentrations of irritating substance (often particulate in nature) and is completely reversible after exposure ceases. The disorder is characterised by dyspnea, cough and mucus production. Triethylenetetramine (TETA) is a severe irritant to skin and eyesand induces skin sensitisation. TETA is of moderate acute toxicity: LD50(oral, rat) > 2000mg/kg bw, LD50(dermal, rabbit) = 550 - 805 mg/kg bw. Acute exposure tosaturated vapour via inhalation was tolerated without impairment. Exposure to to aerosol leads to reversible irritations of the mucous membranes inthe respiratory tract. Following repeated oral dosing via drinking water only in mice butnot in rats at concentration of 3000 ppm there were signs of impairment. TheNOAEL is 600 Continued... ppm [92 mg/kg bw (oral, 90 days)]. Lifelong dermal application tomice (1.2 mg/mouse) did not result in tumour formation. There are differing results of the genetic toxicity for TETA. Thepositive results of the in vitro tests may be the result of a direct geneticaction as well as a result of an interference with essential metal ions. Due tothis uncertainty of the in vitro tests, the genetic toxicity of TETA has to beassessed on the basis of in vivo tests. The in vivo micronucleus tests (i.p. and oral) and the SLRL testshowed negative results. There are no human data on reproductive toxicity (fertilityassessment). The analogue diethylenetriamine had no effects on reproduction.TETA shows developmental toxicity in animal studies if the chelating propertyof the substance is effective. The NOEL is 830 mg/kg bw (oral). Experience with female patients suffering from Wilson´s diseasedemonstrated that no miscarriages and no foetal abnormalities occur duringtreatment with TETA.. In rats, there are several studies concerning developmentaltoxicity. The oral treatment of rats with 75, 375 and 750 mg/kg resulted in noeffects on dams and fetuses, except slight increased fetal body weight After oral treatment of rats with 830 or 1670 mg/kg bw only in thehighest dose group increased foetal abnormalities in 27/44 fetus (69,2 %) wererecorded, when simultaneously the copper content of the feed was reduced. Coppersupplementation in the feed reduced significant the fetal abnormalities of thehighest dose group to 3/51 (6,5 % foetus. These findings suggest that thedevelopmental toxicity is produced as a secondary consequence of the chelatingproperties of TETA. Exposure to the material for prolonged periods may cause physical defects in the developing embryo (teratogenesis). No significant acute toxicological data identified in literature search.

CARBON BLACK WARNING: This substance has been classified by the IARC as Group 2B: Possibly Carcinogenic to Humans. Inhalation (rat) TCLo: 50 mg/m3/6h/90D-I Nil reported

Legend: – Data available but does not fill the criteria for classification – Data required to make classification available – Data Not Available to make classification

SECTION 12 ECOLOGICAL INFORMATION

12.1. Toxicity

Ingredient Endpoint Test Duration (hr) Species Value Source aluminium oxide LC50 96 Fish 0.0029mg/L 2 aluminium oxide EC50 168 Crustacea 0.0076mg/L 2 www.element14.com aluminium oxide EC50 48 Crustacea 0.7364mg/L 2 www.farnell.comaluminium oxide EC50 96 Algae or other aquatic plants 0.0054mg/L 2 www.newark.comaluminium oxide NOEC 72 Algae or other aquatic plants >=0.004mg/L 2 zinc oxide BCF 336 Fish 4376.673mg/L 4 zinc oxide EC20 72 Page Algae<39> or other aquatic plants 0.023mg/L 28/10/184 V1.0 zinc oxide EC50 72 Algae or other aquatic plants 0.042mg/L 4 zinc oxide LC50 96 Fish 0.112mg/L 2 zinc oxide EC50 48 Crustacea 0.105mg/L 2 zinc oxide NOEC 72 Algae or other aquatic plants 0.0000013mg/L 2 tall oil/ triethylenetetramine LC50 96 Fish 7.07mg/L 2 polyamides tall oil/ triethylenetetramine EC50 24 Crustacea 9.72mg/L 2 polyamides tall oil/ triethylenetetramine EC50 48 Crustacea 7.07mg/L 2 polyamides tall oil/ triethylenetetramine EC50 72 Algae or other aquatic plants 4.34mg/L 2 polyamides tall oil/ triethylenetetramine NOEC 72 Algae or other aquatic plants 0.5mg/L 2 polyamides diethylene glycol, EC50 96 Algae or other aquatic plants 268.339mg/L 3 di(3-aminopropyl) ether diethylene glycol, LC50 96 Fish >215- <464mg/L 2 di(3-aminopropyl) ether diethylene glycol, EC50 48 Crustacea 218.16mg/L 2 di(3-aminopropyl) ether diethylene glycol, NOEC Not Applicable Crustacea >1mg/L 2 di(3-aminopropyl) ether diethylene glycol, EC50 72 Algae or other aquatic plants >500mg/L 2 di(3-aminopropyl) ether propylene glycol monomethyl ether acetate, EC50 96 Algae or other aquatic plants 9.337mg/L 3 alpha-isomer

Continued... Version No: 1.2 Page 14 of 22 Issue Date: 01/04/2016 Print Date: 01/04/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part B)

inhalation was tolerated without impairment. Exposure to to aerosol leads to reversible irritations of the mucous membranes inthe respiratory tract. Following repeated oral dosing via drinking water only in mice butnot in rats at concentration of 3000 ppm there were signs of impairment. TheNOAEL is 600 ppm [92 mg/kg bw (oral, 90 days)]. Lifelong dermal application tomice (1.2 mg/mouse) did not result in tumour formation. There are differing results of the genetic toxicity for TETA. Thepositive results of the in vitro tests may be the result of a direct geneticaction as well as a result of an interference with essential metal ions. Due tothis uncertainty of the in vitro tests, the genetic toxicity of TETA has to beassessed on the basis of in vivo tests. The in vivo micronucleus tests (i.p. and oral) and the SLRL testshowed negative results. There are no human data on reproductive toxicity (fertilityassessment). The analogue diethylenetriamine had no effects on reproduction.TETA shows developmental toxicity in animal studies if the chelating propertyof the substance is effective. The NOEL is 830 mg/kg bw (oral). Experience with female patients suffering from Wilson´s diseasedemonstrated that no miscarriages and no foetal abnormalities occur duringtreatment with TETA.. In rats, there are several studies concerning developmentaltoxicity. The oral treatment of rats with 75, 375 and 750 mg/kg resulted in noeffects on dams and fetuses, except slight increased fetal body weight After oral treatment of rats with 830 or 1670 mg/kg bw only in thehighest dose group increased foetal abnormalities in 27/44 fetus (69,2 %) wererecorded, when simultaneously the copper content of the feed was reduced. Coppersupplementation in the feed reduced significant the fetal abnormalities of thehighest dose group to 3/51 (6,5 % foetus. These findings suggest that thedevelopmental toxicity is produced as a secondary consequence of the chelatingproperties of TETA. Exposure to the material for prolonged periods may cause physical defects in the developing embryo (teratogenesis). No significant acute toxicological data identified in literature search.

CARBON BLACK WARNING: This substance has been classified by the IARC as Group 2B: Possibly Carcinogenic to Humans. Inhalation (rat) TCLo: 50 mg/m3/6h/90D-I Nil reported

Acute Toxicity Carcinogenicity Skin Irritation/Corrosion Reproductivity Serious Eye STOT - Single Exposure Damage/Irritation Respiratory or Skin STOT - Repeated Exposure sensitisation SafetyMutagenicity Data Sheet Aspiration Hazard Legend: – Data available but does not fill the criteria for classification – Data required to make classification available – Data Not Available to make classification

SECTION 12 ECOLOGICAL INFORMATION

12.1. Toxicity

Ingredient Endpoint Test Duration (hr) Species Value Source aluminium oxide LC50 96 Fish 0.0029mg/L 2 aluminium oxide EC50 168 Crustacea 0.0076mg/L 2 aluminium oxide EC50 48 Crustacea 0.7364mg/L 2 aluminium oxide EC50 96 Algae or other aquatic plants 0.0054mg/L 2 aluminium oxide NOEC 72 Algae or other aquatic plants >=0.004mg/L 2 zinc oxide BCF 336 Fish 4376.673mg/L 4 zinc oxide EC20 72 Algae or other aquatic plants 0.023mg/L 4 zinc oxide EC50 72 Algae or other aquatic plants 0.042mg/L 4 zinc oxide LC50 96 Fish 0.112mg/L 2 zinc oxide EC50 48 Crustacea 0.105mg/L 2 zinc oxide NOEC 72 Algae or other aquatic plants 0.0000013mg/L 2 tall oil/ triethylenetetramine LC50 96 Fish 7.07mg/L 2 polyamides tall oil/ triethylenetetramine EC50 24 Crustacea 9.72mg/L 2 polyamides tall oil/ triethylenetetramine EC50 48 Crustacea 7.07mg/L 2 polyamides tall oil/ triethylenetetramine EC50 72 Algae or other aquatic plants 4.34mg/L 2 polyamides tall oil/ triethylenetetramine NOEC 72 Algae or other aquatic plants 0.5mg/L 2 polyamides diethylene glycol, EC50 96 Algae or other aquatic plants 268.339mg/L 3 di(3-aminopropyl) ether diethylene glycol, LC50 96 Fish >215- <464mg/L 2 di(3-aminopropyl) ether diethylene glycol, EC50 48 Crustacea 218.16mg/L 2 di(3-aminopropyl) ether diethylene glycol, NOEC Not Applicable Crustacea >1mg/L 2 di(3-aminopropyl) ether Versiondiethylene No: 1.2 glycol, Page 15 of 22 Issue Date: 01/04/2016 EC50 72 Algae or other aquatic plants >500mg/L 2 di(3-aminopropyl) ether Print Date: 01/04/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part B) propylene glycol monomethyl ether acetate, EC50 96 Algae or other aquatic plants 9.337mg/L 3 alpha-isomer propylene glycol monomethyl ether acetate, LC50 96 Fish 100mg/L 1 alpha-isomer Continued... propylene glycol monomethyl ether acetate, NOEC 336 Fish 47.5mg/L 2 alpha-isomer propylene glycol monomethyl ether acetate, EC50 48 Crustacea 373mg/L 2 alpha-isomer propylene glycol monomethyl ether acetate, EC50 504 Crustacea >100mg/L 2 alpha-isomer triethylenetetramine EC50 48 Crustacea 31.1mg/L 1 triethylenetetramine EC10 72 Algae or other aquatic plants 0.67mg/L 1 triethylenetetramine EC50 72 Algae or other aquatic plants 2.5mg/L 1 triethylenetetramine NOEC 72 Algae or other aquatic plants <2.5mg/L 1 triethylenetetramine LC50 96 Fish 180mg/L 1 carbon black LC50 96 Fish >100mg/L 2 carbon black NOEC 720 Fish 17mg/L 2 carbon black EC50 48 Crustacea >100mg/L 2 carbon black EC50 384 Crustacea 4.9mg/L 2 www.element14.com carbon black EC50 96 Algae or other aquatic plants 95mg/L 2 www.farnell.com Extracted from 1. IUCLID Toxicity Data 2. Europe ECHA Registered Substances - Ecotoxicological Information - Aquatic Toxicity 3. EPIWIN Suite V3.12 - www.newark.comLegend: Aquatic Toxicity Data (Estimated) 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 aquatic organisms, may cause long-term adverse effects in the aquatic environment.Page <40> 28/10/18 V1.0 Do NOT allow product to come in contact with surface waters or to intertidal areas below the mean high water mark. Do not contaminate water when cleaning equipment or disposing of equipment wash-waters. Wastes resulting from use of the product must be disposed of on site or at approved waste sites. Foraluminium and its compounds and salts: Despiteits prevalence in the environment, no known form of life uses aluminium saltsmetabolically. In keeping with its pervasiveness, aluminium is well toleratedby plants and animals.Owing to their prevalence, potential beneficial (orotherwise) biological roles of aluminium compounds are of continuing interest. Environmentalfate: Aluminiumoccurs in the environment in the form of silicates, oxides and hydroxides,combined with other elements such as sodium, fluorine and arsenic complexeswith organic matter. Acidificationof soils releases aluminium as a transportable solution. Mobilisation ofaluminium by acid rain results in aluminium becoming available for plantuptake. As anelement, aluminum cannot be degraded in the environment, but may undergovarious precipitation or ligand exchange reactions. Aluminum in compounds hasonly one oxidation state (+3), and would not undergo oxidation-reductionreactions under environmental conditions. Aluminum can be complexed by variousligands present in the environment (e.g., fulvic and humic acids). Thesolubility of aluminum in the environment will depend on the ligands presentand the pH. Thetrivalent aluminum ion is surrounded by six water molecules in solution. Thehydrated aluminum ion, [Al(H2O)6]3+, undergoes hydrolysis, in which a stepwisedeprotonation of the coordinated water ligands forms bound hydroxide ligands(e.g., [Al(H2O)5(OH)]2+, [Al(H2O)4(OH)2]+). The speciation of aluminum in wateris pH dependent. The hydrated trivalent aluminum ion is the predominant form atpH levels below 4. Between pH 5 and 6, the predominant hydrolysis products areAl(OH)2+ and Al(OH)2+, while the solid Al(OH)3 is most prevalent between pH 5.2and 8.8. The soluble species Al(OH)4- is the predominant species above pH 9,and is the only species present above pH 10. Polymeric aluminum hydroxidesappear between pH 4.7 and 10.5, and increase in size until they are transformedinto colloidal particles of amorphous Al(OH)3, which crystallise to gibbsite inacid waters. Polymerisation is affected by the presence of dissolved silica;when enough silica is present, aluminum is precipitated as poorly crystallisedclay mineral species. Hydroxyaluminumcompounds are considered amphoteric (e.g., they can act as both acids and basesin solution). Because of this property, aluminum hydroxides can act as buffersand resist pH changes within the narrow pH range of 4-5. Monomericaluminum compounds, typified by aluminum fluoride, chloride, and sulfate, areconsidered reactive or labile compounds, whereas polymeric aluminum speciesreact much more slowly in the environment. Aluminum has a stronger attractionfor fluoride in an acidic environment compared to other inorganic ligand. Theadsorption of aluminum onto clay surfaces can be a significant factor incontrolling aluminum mobility in the environment, and these adsorptionreactions, measured in one study at pH 3.0-4.1, have been observed to be veryrapid. However, clays may act either as a sink or a source for soluble aluminumdepending on the degree of aluminum saturation on the clay surface. Withinthe pH range of 5-6, aluminum complexes with phosphate and is removed fromsolution. Because phosphate is a necessary nutrient in ecological systems, thisimmobilization of both aluminum and phosphate may result in depleted nutrientstates in surface water. Plantspecies and cultivars of the same species differ considerably in their abilityto take up and translocate aluminum to above-ground parts. Tea leaves maycontain very high concentrations of aluminum, >5,000 mg/kg in old leaves.Other plants that may contain high levels of aluminum include Lycopodium(Lycopodiaceae), a few ferns, Symplocos (Symplocaceae), and Orites(Proteaceae). Aluminum is often taken up and concentrated in root tissue. Insub-alpine ecosystems, the large root biomass of the Douglas fir, Abiesamabilis, takes up aluminum and immobilizes it, preventing largeaccumulation in above-ground tissue. It is unclear to what extent aluminum istaken up into root food crops and leafy vegetables. An uptake factor(concentration of aluminum in the plant/concentration of aluminum in soil) of0.004 for leafy vegetables and 0.00065 for fruits and tubers has been reported,but the pH and plant species from which these uptake factors were derived areunclear. Based upon these values, however, it is clear that aluminum is nottaken up in plants from soil, but is instead biodiluted. Aluminumconcentrations in rainbow trout from an alum-treated lake, an untreated lake,and a hatchery were highest in gill tissue and lowest in muscle. Aluminumresidue analyses in brook trout have shown that whole-body aluminum contentdecreases as the fish advance from larvae to juveniles. These results implythat the aging larvae begin to decrease their rate of aluminum uptake, toeliminate aluminum at a rate that exceeds uptake, or to maintain approximatelythe same amount of aluminum while the body mass increases. The decline inwhole-body aluminum residues in juvenile brook trout may be related to growthand dilution by edible muscle tissue that accumulated less aluminum than didthe other tissues. Thegreatest fraction of the gill-associated aluminum was not sorbed to the gilltissue, but to the gill mucus. It is thought that mucus appears to retardaluminum transport from solution to the membrane surface, thus delaying theacute biological response of the fish. It has been reported that concentrationsof aluminum in whole-body tissue of the Atlantic salmon exposed to highconcentrations of aluminum ranging from 3 ug/g (for fish exposed to 33 ug/L) to96 ug/g (for fish exposed to 264 ug/L) at pH 5.5. After 60 days of exposure,BCFs ranged from 76 to 190 and were directly related to the aluminum exposureconcentration. In acidic waters (pH 4.6-5.3) with low concentrations of calcium(0.5-1.5 mg Ca/L), labile aluminum between 25 and 75 ug/L is toxic. Becausealuminum is toxic to many aquatic species, it is not bioaccumulated to asignificant degree (BCF <300) in most fish and shellfish; therefore,consumption of contaminated fish does not appear to be a significant source ofaluminum exposure in humans. Bioconcentrationof aluminum has also been reported for several aquatic invertebrate species.BCF values ranging from 0.13 to 0.5 in the whole-body were reported for thesnail. Bioconcentration of aluminum has also been reported for aquatic insects. Ecotoxicity: Freshwaterspecies pH >6.5 Fish:Acute LC50 (48-96 h) 5 spp: 0.6 (Salmo salar) - 106 mg/L; Chronic NOEC(8-28 d): 7 spp,NOEC, 0.034-7.1 mg/L. The lowest measured chronic figure was an8-d LC50 of 0.17 mg/L for Micropterus sp. Amphibian:Acute LC50 (4 d): Bufo americanus, 0.86-1.66 mg/L; Chronic LC50 (8-d)2.28 mg/L CrustaceansLC50 (48 h): 1 sp 2.3-36 9 mg/L; Chronic NOEC (7-28 d) 3 spp, 0.136-1.72 mg/L AlgaeEC50 (96 h): population growth, 0.46-0.57 mg/L; 2 spp, chronic NOEC, 0.8-2.0mg/L Freshwaterspecies pH <6.5 (all between pH 4.5 and 6.0) Fish LC50(24-96 h): 4 spp, 0.015 (S. trutta) - 4.2 mg/L; chronic data on Salmotrutta, LC50 (21-42 d) 0.015- 0.105 mg/L AmphibiansLC50 (4-5 d): 2 spp, 0.540-2.670 m/L (absolute range 0.40-5.2 mg/L)

Continued... Version No: 1.2 Page 15 of 22 Issue Date: 01/04/2016 Print Date: 01/04/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part B)

propylene glycol monomethyl ether acetate, LC50 96 Fish 100mg/L 1 alpha-isomer propylene glycol monomethyl ether acetate, NOEC 336 Fish 47.5mg/L 2 alpha-isomer propylene glycol monomethyl ether acetate, EC50 48 Crustacea 373mg/L 2 alpha-isomer propylene glycol monomethyl ether acetate, EC50 504 Crustacea >100mg/L 2 alpha-isomer triethylenetetramine EC50 48 Crustacea 31.1mg/L 1 triethylenetetramine EC10 72 Algae or other aquatic plants 0.67mg/L 1 triethylenetetramine EC50 72 Algae or other aquatic plants 2.5mg/L 1 Safetytriethylenetetramine DataNOEC Sheet72 Algae or other aquatic plants <2.5mg/L 1 triethylenetetramine LC50 96 Fish 180mg/L 1 carbon black LC50 96 Fish >100mg/L 2 carbon black NOEC 720 Fish 17mg/L 2 carbon black EC50 48 Crustacea >100mg/L 2 carbon black EC50 384 Crustacea 4.9mg/L 2 carbon black EC50 96 Algae or other aquatic plants 95mg/L 2 Extracted from 1. IUCLID Toxicity Data 2. Europe ECHA Registered Substances - Ecotoxicological Information - Aquatic Toxicity 3. EPIWIN Suite V3.12 - Legend: Aquatic Toxicity Data (Estimated) 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 aquatic organisms, may cause long-term adverse effects in the aquatic environment. Do NOT allow product to come in contact with surface waters or to intertidal areas below the mean high water mark. Do not contaminate water when cleaning equipment or disposing of equipment wash-waters. Wastes resulting from use of the product must be disposed of on site or at approved waste sites. Foraluminium and its compounds and salts: Despiteits prevalence in the environment, no known form of life uses aluminium saltsmetabolically. In keeping with its pervasiveness, aluminium is well toleratedby plants and animals.Owing to their prevalence, potential beneficial (orotherwise) biological roles of aluminium compounds are of continuing interest. Environmentalfate: Aluminiumoccurs in the environment in the form of silicates, oxides and hydroxides,combined with other elements such as sodium, fluorine and arsenic complexeswith organic matter. Acidificationof soils releases aluminium as a transportable solution. Mobilisation ofaluminium by acid rain results in aluminium becoming available for plantuptake. As anelement, aluminum cannot be degraded in the environment, but may undergovarious precipitation or ligand exchange reactions. Aluminum in compounds hasonly one oxidation state (+3), and would not undergo oxidation-reductionreactions under environmental conditions. Aluminum can be complexed by variousligands present in the environment (e.g., fulvic and humic acids). Thesolubility of aluminum in the environment will depend on the ligands presentand the pH. Thetrivalent aluminum ion is surrounded by six water molecules in solution. Thehydrated aluminum ion, [Al(H2O)6]3+, undergoes hydrolysis, in which a stepwisedeprotonation of the coordinated water ligands forms bound hydroxide ligands(e.g., [Al(H2O)5(OH)]2+, [Al(H2O)4(OH)2]+). The speciation of aluminum in wateris pH dependent. The hydrated trivalent aluminum ion is the predominant form atpH levels below 4. Between pH 5 and 6, the predominant hydrolysis products areAl(OH)2+ and Al(OH)2+, while the solid Al(OH)3 is most prevalent between pH 5.2and 8.8. The soluble species Al(OH)4- is the predominant species above pH 9,and is the only species present above pH 10. Polymeric aluminum hydroxidesappear between pH 4.7 and 10.5, and increase in size until they are transformedinto colloidal particles of amorphous Al(OH)3, which crystallise to gibbsite inacid waters. Polymerisation is affected by the presence of dissolved silica;when enough silica is present, aluminum is precipitated as poorly crystallisedclay mineral species. Hydroxyaluminumcompounds are considered amphoteric (e.g., they can act as both acids and basesin solution). Because of this property, aluminum hydroxides can act as buffersand resist pH changes within the narrow pH range of 4-5. Monomericaluminum compounds, typified by aluminum fluoride, chloride, and sulfate, areconsidered reactive or labile compounds, whereas polymeric aluminum speciesreact much more slowly in the environment. Aluminum has a stronger attractionfor fluoride in an acidic environment compared to other inorganic ligand. Theadsorption of aluminum onto clay surfaces can be a significant factor incontrolling aluminum mobility in the environment, and these adsorptionreactions, measured in one study at pH 3.0-4.1, have been observed to be veryrapid. However, clays may act either as a sink or a source for soluble aluminumdepending on the degree of aluminum saturation on the clay surface. Withinthe pH range of 5-6, aluminum complexes with phosphate and is removed fromsolution. Because phosphate is a necessary nutrient in ecological systems, thisimmobilization of both aluminum and phosphate may result in depleted nutrientstates in surface water. Plantspecies and cultivars of the same species differ considerably in their abilityto take up and translocate aluminum to above-ground parts. Tea leaves maycontain very high concentrations of aluminum, >5,000 mg/kg in old leaves.Other plants that may contain high levels of aluminum include Lycopodium(Lycopodiaceae), a few ferns, Symplocos (Symplocaceae), and Orites(Proteaceae). Aluminum is often taken up and concentrated in root tissue. Insub-alpine ecosystems, the large root biomass of the Douglas fir, Abiesamabilis, takes up aluminum and immobilizes it, preventing largeaccumulation in above-ground tissue. It is unclear to what extent aluminum istaken up into root food crops and leafy vegetables. An uptake factor(concentration of aluminum in the plant/concentration of aluminum in soil) of0.004 for leafy vegetables and 0.00065 for fruits and tubers has been reported,but the pH and plant species from which these uptake factors were derived areunclear. Based upon these values, however, it is clear that aluminum is nottaken up in plants from soil, but is instead biodiluted. Aluminumconcentrations in rainbow trout from an alum-treated lake, an untreated lake,and a hatchery were highest in gill tissue and lowest in muscle. Aluminumresidue analyses in brook trout have shown that whole-body aluminum contentdecreases as the fish advance from larvae to juveniles. These results implythat the aging larvae begin to decrease their rate of aluminum uptake, toeliminate aluminum at a rate that exceeds uptake, or to maintain approximatelythe same amount of aluminum while the body mass increases. The decline inwhole-body aluminum residues in juvenile brook trout may be related to growthand dilution by edible muscle tissue that accumulated less aluminum than didthe other tissues. Thegreatest fraction of the gill-associated aluminum was not sorbed to the gilltissue, but to the gill mucus. It is thought that mucus appears to retardaluminum transport from solution to the membrane surface, thus delaying theacute biological response of the fish. It has been reported that concentrationsof aluminum in whole-body tissue of the Atlantic salmon exposed to highconcentrations of aluminum ranging from 3 ug/g (for fish exposed to 33 ug/L) to96 ug/g (for fish exposed to 264 ug/L) at pH 5.5. After 60 days of exposure,BCFs ranged from 76 to 190 and were directly related to the aluminum exposureconcentration. In acidic waters (pH 4.6-5.3) with low concentrations of calcium(0.5-1.5 mg Ca/L), labile aluminum between 25 and 75 ug/L is toxic. Becausealuminum is toxic to many aquatic species, it is not bioaccumulated to asignificant degree (BCF <300) in most fish and shellfish; therefore,consumption of contaminated fish does not appear to be a significant source ofaluminum exposure in humans. Bioconcentrationof aluminum has also been reported for several aquatic invertebrate species.BCF values ranging from 0.13 to 0.5 in the whole-body were reported for thesnail. Bioconcentration of aluminum has also been reported for aquatic insects. Ecotoxicity: Freshwaterspecies pH >6.5 Fish:Acute LC50 (48-96 h) 5 spp: 0.6 (Salmo salar) - 106 mg/L; Chronic NOEC(8-28 d): 7 spp,NOEC, 0.034-7.1 mg/L. The lowest measured chronic figure was an8-d LC50 of 0.17 mg/L for Micropterus sp. Amphibian:Acute LC50 (4 d): Bufo americanus, 0.86-1.66 mg/L; Chronic LC50 (8-d)2.28 mg/L VersionCrustaceansLC50 No: 1.2 (48 h): 1 sp 2.3-36 9 mg/L; Chronic NOEC (7-28 d) 3 spp, 0.136-1.72Page mg/L 16 of 22 Issue Date: 01/04/2016 AlgaeEC50 (96 h): population growth, 0.46-0.57 mg/L; 2 spp, chronic NOEC, 0.8-2.0mg/L Print Date: 01/04/2016 Freshwaterspecies pH <6.5 (all between8329TFS pH 4.5 andSlow 6.0) Cure, Thermally Conductive Adhesive, Flowable (Part B) Fish LC50(24-96 h): 4 spp, 0.015 (S. trutta) - 4.2 mg/L; chronic data on Salmotrutta, LC50 (21-42 d) 0.015- 0.105 mg/L AmphibiansLC50 (4-5 d): 2 spp, 0.540-2.670 m/L (absolute range 0.40-5.2 mg/L) Alga: 1sp NOEC growth 2.0 mg/L Amongfreshwater aquatic plants, single-celled plants are generally the mostsensitive to aluminium. Fish are generally more sensitive to aluminium thanaquatic invertebrates. AluminiumContinued... is a gill toxicant to fish, causing bothionoregulatory and respiratory effects. Thebioavailability and toxicity of aluminium is generally greatest in acidsolutions. Aluminium in acid habitats has been observed to be toxic to fish andphytoplankton. Aluminium is generally more toxic over the pH range 4.4.5.4,with a maximum toxicity occurring around pH 5.0.5.2. The inorganic single unitaluminium species (Al(OH)2 +) is thought to be the most toxic. Under very acidconditions, the toxic effects of the high H+ concentration appear to be moreimportant than the effects of low concentrations of aluminium; at approximatelyneutral pH values, the toxicity of aluminium is greatly reduced. The solubilityof aluminium is also enhanced under alkaline conditions, due to its amphotericcharacter, and some researchers found that the acute toxicity of aluminiumincreased from pH 7 to pH 9. However, the opposite relationship was found inother studies. The uptake and toxicity of aluminium in freshwater organismsgenerally decreases with increasing water hardness under acidic, neutral andalkaline conditions. Complexing agents such as fluoride, citrate and humicsubstances reduce the availability of aluminium to organisms, resulting inlower toxicity. Silicon can also reduce aluminium toxicity to fish. DrinkingWater Standards: aluminium:200 ug/l (UK max.) 200 ug/l(WHO guideline) chloride:400 mg/l (UK max.) www.element14.com250 mg/l(WHO guideline) www.farnell.comfluoride:1.5 mg/l (UK max.) 1.5 mg/l(WHO guideline) www.newark.comnitrate:50 mg/l (UK max.) 50 mg/l(WHO guideline) sulfate:250 mg/l (UK max.) SoilGuideline: none available. Page <41> 28/10/18 V1.0 AirQuality Standards: none available. For zinc and its compounds: Environmental fate: Zinc is capable of forming complexes with a variety of organic andinorganic groups (ligands). Biological activity can affect the mobility of zincin the aquatic environment, although the biota contains relatively little zinccompared to the sediments. Zinc bioconcentrates moderately in aquaticorganisms; bioconcentration is higher in crustaceans and bivalve species thanin fish. Zinc does not concentrate appreciably in plants, and it does notbiomagnify significantly through terrestrial food chains. However biomagnification may be of concern if concentration ofzinc exceeds 1632 ppm in the top 12 inches of soil. Zinc can persist in water indefinitely and can be toxic to aquaticlife. The threshold concentration for fish is 0.1 ppm. Zinc may be concentratedin the aquatic food chain; it is concentrated over 200,000 times in oysters.Copper is synergistic but calcium is antagonistic to zinc toxicity in fish.Zinc can accumulate in freshwater animals at 5 -1,130 times the concentrationpresent in the water. Furthermore, although zinc actively bioaccumulates inaquatic systems, biota appears to represent a relatively minor sink compared tosediments. Steady-state zinc bioconcentration factors (BCFs) for 12 aquaticspecies range from 4 to 24,000. Crustaceans and fish can accumulate zinc fromboth water and food. A BCF of 1,000 was reported for both aquatic plants andfish, and a value of 10,000 was reported for aquatic invertebrates. The orderof enrichment of zinc in different aquatic organisms was as follows (zincconcentrations in µg/g dry weight appear in parentheses): fish (25), shrimp(50), mussel (60), periphyton (260), zooplankton (330), and oyster (3,300). Thehigh enrichment in oysters may be due to their ingestion of particulate mattercontaining higher concentrations of zinc than ambient water. Otherinvestigators have also indicated that organisms associated with sediments havehigher zinc concentrations than organisms living in the aqueous layer. Withrespect to bioconcentration from soil by terrestrial plants, invertebrates, andmammals, BCFs of 0.4, 8, and 0.6, respectively, have been reported. Theconcentration of zinc in plants depends on the plant species, soil pH, and thecomposition of the soil. Plant species do not concentrate zinc above the levels present insoil. In some fish, it has been observed that the level of zinc found intheir bodies did not directly relate to the exposure concentrations. Bioaccumulationof zinc in fish is inversely related to the aqueous exposure. This evidencesuggests that fish placed in environments with lower zinc concentrations cansequester zinc in their bodies. The concentration of zinc in drinking water may increase as aresult of the distribution system and household plumbing. Common pipingmaterials used in distribution systems often contain zinc, as well as othermetals and alloys. Trace metals may enter the water through corrosion productsor simply by the dissolution of small amounts of metals with which the watercomes in contact. Reactions with materials of the distribution system,particularly in soft low-pH waters, very often have produced concentrations ofzinc in tap water much greater than those in the raw or treated waters at theplant of origin. Zinc gives water a metallic taste at low levels. Overexposuresto zinc also have been associated with toxic effects. Ingestion of zinc orzinc-containing compounds has resulted in a variety of systemic effects in thegastrointestinal and hematological systems and alterations in the blood lipidprofile in humans and animals. In addition, lesions have been observed in theliver, pancreas, and kidneys of animals. Environmental toxicity of zinc in water is dependent upon theconcentration of other minerals and the pH of the solution, which affect theligands that associate with zinc. Zinc occurs in the environment mainly in the +2 oxidation state.Sorption is the dominant reaction, resulting in the enrichment of zinc in suspendedand bed sediments. Zinc in aerobic waters is partitioned into sediments throughsorption onto hydrous iron and manganese oxides, clay minerals, and organicmaterial. The efficiency of these materials in removing zinc from solutionvaries according to their concentrations, pH, redox potential (Eh), salinity,nature and concentrations of complexing ligands, cation exchange capacity, andthe concentration of zinc. Precipitation of soluble zinc compounds appears tobe significant only under reducing conditions in highly polluted water.Generally, at lower pH values, zinc remains as the free ion. The free ion(Zn+2) tends to be adsorbed and transported by suspended solids in unpollutedwaters. Zinc is an essential nutrient that is present in all organisms.Although biota appears to be a minor reservoir of zinc relative to soils andsediments, microbial decomposition of biota in water can produce ligands, suchas humic acids, that can affect the mobility of zinc in the aquatic environmentthrough zinc precipitation and adsorption. The relative mobility of zinc in soil is determined by the samefactors that affect its transport in aquatic systems (i.e., solubility of thecompound, pH, and salinity) The redox status of the soil may shift zinc partitioning. Reductivedissolution of iron and manganese (hydr)oxides under suboxic conditions releasezinc into the aqueous phase; the persistence of suboxic conditions may thenlead to a repartitioning of zinc into sulfide and carbonate solids. Themobility of zinc in soil depends on the solubility of the speciated forms ofthe element and on soil properties such as cation exchange capacity, pH, redoxpotential, and chemical species present in soil; under anaerobic conditions,zinc sulfide is the controlling species. Since zinc sulfide is insoluble, the mobility of zinc in anaerobicsoil is low. In a study of the effect of pH on zinc solubility: When the pH is<7, an inverse relationship exists between the pH and the amount of zinc insolution. As negative charges on soil surfaces increase with increasing pH,additional sites for zinc adsorption are activated and the amount of zinc insolution decreases. The active zinc species in the adsorbed state is the singlycharged zinc hydroxide species (i.e., Zn[OH]+). Other investigators have alsoshown that the mobility of zinc in soil increases at lower soil pH underoxidizing conditions and at a lower cation exchange capacity of soil. On theother hand, the amount of zinc in solution generally increases when the pH is>7 in soils high in organic matter. This is a result of the release oforganically complexed zinc, reduced zinc adsorption at higher pH, or anincrease in the concentration of chelating agents in soil. For calcareoussoils, the relationship between zinc solubility and pH is nonlinear. At a highpH, zinc in solution is precipitated as Zn(OH)2, zinc carbonate (ZnCO3), orcalcium zincate. Clay and metal oxides are capable of sorbing zinc and tend toretard its mobility in soil. Zinc was more mobile at pH 4 than at pH 6.5 as aconsequence of sorption Zinc concentrations in the air are relatively low, except nearindustrial sources such as smelters. No estimate for the atmospheric lifetimeof zinc is available at this time, but the fact that zinc is transported longdistances in air indicates that its lifetime in air is at least on the order ofdays. There are few data regarding the speciation of zinc released to theatmosphere. Zinc is removed from the air by dry and wet deposition, but zincparticles with small diameters and low densities suspended in the atmospheretravel long distances from emission sources. DO NOT discharge into sewer or waterways.

12.2. Persistence and degradability

Ingredient Persistence: Water/Soil Persistence: Air diethylene glycol, HIGH HIGH di(3-aminopropyl) ether propylene glycol monomethyl LOW LOW ether acetate, alpha-isomer triethylenetetramine LOW LOW

12.3. Bioaccumulative potential

Ingredient Bioaccumulation zinc oxide LOW (BCF = 217) diethylene glycol, LOW (LogKOW = -1.4594) di(3-aminopropyl) ether

Continued... Version No: 1.2 Page 16 of 22 Issue Date: 01/04/2016 Print Date: 01/04/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part B)

Alga: 1sp NOEC growth 2.0 mg/L Amongfreshwater aquatic plants, single-celled plants are generally the mostsensitive to aluminium. Fish are generally more sensitive to aluminium thanaquatic invertebrates. Aluminium is a gill toxicant to fish, causing bothionoregulatory and respiratory effects. Thebioavailability and toxicity of aluminium is generally greatest in acidsolutions. Aluminium in acid habitats has been observed to be toxic to fish andphytoplankton. Aluminium is generally more Safetytoxic over the pH range 4.4.5.4,with Data a maximum toxicity occurringSheet around pH 5.0.5.2. The inorganic single unitaluminium species (Al(OH)2 +) is thought to be the most toxic. Under very acidconditions, the toxic effects of the high H+ concentration appear to be moreimportant than the effects of low concentrations of aluminium; at approximatelyneutral pH values, the toxicity of aluminium is greatly reduced. The solubilityof aluminium is also enhanced under alkaline conditions, due to its amphotericcharacter, and some researchers found that the acute toxicity of aluminiumincreased from pH 7 to pH 9. However, the opposite relationship was found inother studies. The uptake and toxicity of aluminium in freshwater organismsgenerally decreases with increasing water hardness under acidic, neutral andalkaline conditions. Complexing agents such as fluoride, citrate and humicsubstances reduce the availability of aluminium to organisms, resulting inlower toxicity. Silicon can also reduce aluminium toxicity to fish. DrinkingWater Standards: aluminium:200 ug/l (UK max.) 200 ug/l(WHO guideline) chloride:400 mg/l (UK max.) 250 mg/l(WHO guideline) fluoride:1.5 mg/l (UK max.) 1.5 mg/l(WHO guideline) nitrate:50 mg/l (UK max.) 50 mg/l(WHO guideline) sulfate:250 mg/l (UK max.) SoilGuideline: none available. AirQuality Standards: none available. For zinc and its compounds: Environmental fate: Zinc is capable of forming complexes with a variety of organic andinorganic groups (ligands). Biological activity can affect the mobility of zincin the aquatic environment, although the biota contains relatively little zinccompared to the sediments. Zinc bioconcentrates moderately in aquaticorganisms; bioconcentration is higher in crustaceans and bivalve species thanin fish. Zinc does not concentrate appreciably in plants, and it does notbiomagnify significantly through terrestrial food chains. However biomagnification may be of concern if concentration ofzinc exceeds 1632 ppm in the top 12 inches of soil. Zinc can persist in water indefinitely and can be toxic to aquaticlife. The threshold concentration for fish is 0.1 ppm. Zinc may be concentratedin the aquatic food chain; it is concentrated over 200,000 times in oysters.Copper is synergistic but calcium is antagonistic to zinc toxicity in fish.Zinc can accumulate in freshwater animals at 5 -1,130 times the concentrationpresent in the water. Furthermore, although zinc actively bioaccumulates inaquatic systems, biota appears to represent a relatively minor sink compared tosediments. Steady-state zinc bioconcentration factors (BCFs) for 12 aquaticspecies range from 4 to 24,000. Crustaceans and fish can accumulate zinc fromboth water and food. A BCF of 1,000 was reported for both aquatic plants andfish, and a value of 10,000 was reported for aquatic invertebrates. The orderof enrichment of zinc in different aquatic organisms was as follows (zincconcentrations in µg/g dry weight appear in parentheses): fish (25), shrimp(50), mussel (60), periphyton (260), zooplankton (330), and oyster (3,300). Thehigh enrichment in oysters may be due to their ingestion of particulate mattercontaining higher concentrations of zinc than ambient water. Otherinvestigators have also indicated that organisms associated with sediments havehigher zinc concentrations than organisms living in the aqueous layer. Withrespect to bioconcentration from soil by terrestrial plants, invertebrates, andmammals, BCFs of 0.4, 8, and 0.6, respectively, have been reported. Theconcentration of zinc in plants depends on the plant species, soil pH, and thecomposition of the soil. Plant species do not concentrate zinc above the levels present insoil. In some fish, it has been observed that the level of zinc found intheir bodies did not directly relate to the exposure concentrations. Bioaccumulationof zinc in fish is inversely related to the aqueous exposure. This evidencesuggests that fish placed in environments with lower zinc concentrations cansequester zinc in their bodies. The concentration of zinc in drinking water may increase as aresult of the distribution system and household plumbing. Common pipingmaterials used in distribution systems often contain zinc, as well as othermetals and alloys. Trace metals may enter the water through corrosion productsor simply by the dissolution of small amounts of metals with which the watercomes in contact. Reactions with materials of the distribution system,particularly in soft low-pH waters, very often have produced concentrations ofzinc in tap water much greater than those in the raw or treated waters at theplant of origin. Zinc gives water a metallic taste at low levels. Overexposuresto zinc also have been associated with toxic effects. Ingestion of zinc orzinc-containing compounds has resulted in a variety of systemic effects in thegastrointestinal and hematological systems and alterations in the blood lipidprofile in humans and animals. In addition, lesions have been observed in theliver, pancreas, and kidneys of animals. Environmental toxicity of zinc in water is dependent upon theconcentration of other minerals and the pH of the solution, which affect theligands that associate with zinc. Zinc occurs in the environment mainly in the +2 oxidation state.Sorption is the dominant reaction, resulting in the enrichment of zinc in suspendedand bed sediments. Zinc in aerobic waters is partitioned into sediments throughsorption onto hydrous iron and manganese oxides, clay minerals, and organicmaterial. The efficiency of these materials in removing zinc from solutionvaries according to their concentrations, pH, redox potential (Eh), salinity,nature and concentrations of complexing ligands, cation exchange capacity, andthe concentration of zinc. Precipitation of soluble zinc compounds appears tobe significant only under reducing conditions in highly polluted water.Generally, at lower pH values, zinc remains as the free ion. The free ion(Zn+2) tends to be adsorbed and transported by suspended solids in unpollutedwaters. Zinc is an essential nutrient that is present in all organisms.Although biota appears to be a minor reservoir of zinc relative to soils andsediments, microbial decomposition of biota in water can produce ligands, suchas humic acids, that can affect the mobility of zinc in the aquatic environmentthrough zinc precipitation and adsorption. The relative mobility of zinc in soil is determined by the samefactors that affect its transport in aquatic systems (i.e., solubility of thecompound, pH, and salinity) The redox status of the soil may shift zinc partitioning. Reductivedissolution of iron and manganese (hydr)oxides under suboxic conditions releasezinc into the aqueous phase; the persistence of suboxic conditions may thenlead to a repartitioning of zinc into sulfide and carbonate solids. Themobility of zinc in soil depends on the solubility of the speciated forms ofthe element and on soil properties such as cation exchange capacity, pH, redoxpotential, and chemical species present in soil; under anaerobic conditions,zinc sulfide is the controlling species. Since zinc sulfide is insoluble, the mobility of zinc in anaerobicsoil is low. In a study of the effect of pH on zinc solubility: When the pH is<7, an inverse relationship exists between the pH and the amount of zinc insolution. As negative charges on soil surfaces increase with increasing pH,additional sites for zinc adsorption are activated and the amount of zinc insolution decreases. The active zinc species in the adsorbed state is the singlycharged zinc hydroxide species (i.e., Zn[OH]+). Other investigators have alsoshown that the mobility of zinc in soil increases at lower soil pH underoxidizing conditions and at a lower cation exchange capacity of soil. On theother hand, the amount of zinc in solution generally increases when the pH is>7 in soils high in organic matter. This is a result of the release oforganically complexed zinc, reduced zinc adsorption at higher pH, or anincrease in the concentration of chelating agents in soil. For calcareoussoils, the relationship between zinc solubility and pH is nonlinear. At a highpH, zinc in solution is precipitated as Zn(OH)2, zinc carbonate (ZnCO3), orcalcium zincate. Clay and metal oxides are capable of sorbing zinc and tend toretard its mobility in soil. Zinc was more mobile at pH 4 than at pH 6.5 as aconsequence of sorption Zinc concentrations in the air are relatively low, except nearindustrial sources such as smelters. No estimate for the atmospheric lifetimeof zinc is available at this time, but the fact that zinc is transported longdistances in air indicates that its lifetime in air is at least on the order ofdays. There are few data regarding the speciation of zinc released to theatmosphere. Zinc is removed from the air by dry and wet deposition, but zincparticles with small diameters and low densities suspended in the atmospheretravel long distances from emission sources. DO NOT discharge into sewer or waterways.

12.2. Persistence and degradability

Ingredient Persistence: Water/Soil Persistence: Air diethylene glycol, HIGH HIGH di(3-aminopropyl) ether propylene glycol monomethyl LOW LOW ether acetate, alpha-isomer triethylenetetramine LOW LOW

12.3. Bioaccumulative potential

Ingredient Bioaccumulation zinc oxide LOW (BCF = 217) diethylene glycol, LOW (LogKOW = -1.4594) di(3-aminopropyl) ether www.element14.com www.farnell.com Continued... www.newark.com

Page <42> 28/10/18 V1.0 Version No: 1.2 Page 16 of 22 Issue Date: 01/04/2016 Print Date: 01/04/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part B)

Alga: 1sp NOEC growth 2.0 mg/L Amongfreshwater aquatic plants, single-celled plants are generally the mostsensitive to aluminium. Fish are generally more sensitive to aluminium thanaquatic invertebrates. Aluminium is a gill toxicant to fish, causing bothionoregulatory and respiratory effects. Thebioavailability and toxicity of aluminium is generally greatest in acidsolutions. Aluminium in acid habitats has been observed to be toxic to fish andphytoplankton. Aluminium is generally more toxic over the pH range 4.4.5.4,with a maximum toxicity occurring around pH 5.0.5.2. The inorganic single unitaluminium species (Al(OH)2 +) is thought to be the most toxic. Under very acidconditions, the toxic effects of the high H+ concentration appear to be moreimportant than the effects of low concentrations of aluminium; at approximatelyneutral pH values, the toxicity of aluminium is greatly reduced. The solubilityof aluminium is also enhanced under alkaline conditions, due to its amphotericcharacter, and some researchers found that the acute toxicity of aluminiumincreased from pH 7 to pH 9. However, the opposite relationship was found inother studies. The uptake and toxicity of aluminium in freshwater organismsgenerally decreases with increasing water hardness under acidic, neutral andalkaline conditions. Complexing agents such as fluoride, citrate and humicsubstances reduce the availability of aluminium to organisms, resulting inlower toxicity. Silicon can also reduce aluminium toxicity to fish. DrinkingWater Standards: aluminium:200 ug/l (UK max.) 200 ug/l(WHO guideline) chloride:400 mg/l (UK max.) 250 mg/l(WHO guideline) fluoride:1.5 mg/l (UK max.) 1.5 mg/l(WHO guideline) nitrate:50 mg/l (UK max.) 50 mg/l(WHO guideline) sulfate:250 mg/l (UK max.) SoilGuideline: none available. AirQuality Standards: none available. For zinc and its compounds: Environmental fate: Zinc is capable of forming complexes with a variety of organic andinorganic groups (ligands). Biological activity can affect the mobility of zincin the aquatic environment, although the biota contains relatively little zinccompared to the sediments. Zinc bioconcentrates moderately in aquaticorganisms; bioconcentration is higher in crustaceans and bivalve species thanin fish. Zinc does not concentrate appreciably in plants, and it does notbiomagnify significantly through terrestrial food chains. However biomagnification may be of concern if concentration ofzinc exceeds 1632 ppm in the top 12 inches of soil. Zinc can persist in water indefinitely and can be toxic to aquaticlife. The threshold concentration for fish is 0.1 ppm. Zinc may be concentratedin the aquatic food chain; it is concentrated over 200,000 times in oysters.Copper is synergistic but calcium is antagonistic to zinc toxicity in fish.Zinc can accumulate in freshwater animals at 5 -1,130 times the concentrationpresent in the water. Furthermore, although zinc actively bioaccumulates inaquatic systems, biota appears to represent a relatively minor sink compared tosediments. Steady-state zinc bioconcentration factors (BCFs) for 12 aquaticspecies range from 4 to 24,000. Crustaceans and fish can accumulate zinc fromboth water and food. A BCF of 1,000 was reported for both aquatic plants andfish, and a value of 10,000 was reported for aquatic invertebrates. The orderof enrichment of zinc in different aquatic organisms was as follows (zincconcentrations in µg/g dry weight appear in parentheses): fish (25), shrimp(50), mussel (60), periphyton (260), zooplankton (330), and oyster (3,300). Thehigh enrichment in oysters may be due to their ingestion of particulate mattercontaining higher concentrations of zinc than ambient water. Otherinvestigators have also indicated that organisms associated with sediments havehigher zinc concentrations than organisms living in the aqueous layer. Withrespect to bioconcentration from soil by terrestrial plants, invertebrates, andmammals, BCFs of 0.4, 8, and 0.6, respectively, have been reported. Theconcentration of zinc in plants depends on the plant species, soil pH, and thecomposition of the soil. Plant species do not concentrate zinc above the levels present insoil. In some fish, it has been observed that the level of zinc found intheir bodies did not directly relate to the exposure concentrations. Bioaccumulationof zinc in fish is inversely related to the aqueous exposure. This evidencesuggests that fish placed in environments with lower zinc concentrations cansequester zinc in their bodies. The concentration of zinc in drinking water may increase as aresult of the distribution system and household plumbing. Common pipingmaterials used in distribution systems often contain zinc, as well as othermetals and alloys. Trace metals may enter the water through corrosion productsor simply by the dissolution of small amounts of metals with which the watercomes in contact. Reactions with materials of the distribution system,particularly in soft low-pH waters, very often have produced concentrations ofzinc in tap water much greater than those in the raw or treated waters at theplant of origin. Zinc gives water a metallic taste at low levels. Overexposuresto zinc also have been associated with toxic effects. Ingestion of zinc orzinc-containing compounds has resulted in a variety of systemic effects in thegastrointestinal and hematological systems and alterations in the blood lipidprofile in humans and animals. In addition, lesions have been observed in theliver, pancreas, and kidneys of animals. Environmental toxicity of zinc in water is dependent upon theconcentration of other minerals and the pH of the solution, which affect theligands that associate with zinc. Zinc occurs in the environment mainly in the +2 oxidation state.Sorption is the dominant reaction, resulting in the enrichment of zinc in suspendedand bed sediments. Zinc in aerobic waters is partitioned into sediments throughsorption onto hydrous iron and manganese oxides, clay minerals, and organicmaterial. The efficiency of these materials in removing zinc from solutionvaries according to their concentrations, pH, redox potential (Eh), salinity,nature and concentrations of complexing ligands, cation exchange capacity, andthe concentration of zinc. Precipitation of soluble zinc compounds appears tobe significant only under reducing conditions in highly polluted water.Generally, at lower pH values, zinc remains as the free ion. The free ion(Zn+2) tends to be adsorbed and transported by suspended solids in unpollutedwaters. Zinc is an essential nutrient that is present in all organisms.Although biota appears to be a minor reservoir of zinc relative to soils andsediments, microbial decomposition of biota in water can produce ligands, suchas humic acids, that can affect the mobility of zinc in the aquatic environmentthrough zinc precipitation and adsorption. The relative mobility of zinc in soil is determined by the samefactors that affect its transport in aquatic systems (i.e., solubility of thecompound, pH, and salinity) The redox status of the soil may shift zinc partitioning. Reductivedissolution of iron and manganese (hydr)oxides under suboxic conditions releasezinc into the aqueous phase; the persistence of suboxic conditions may thenlead to a repartitioning of zinc into sulfide and carbonate solids. Themobility of zinc in soil depends on the solubility of the speciated forms ofthe element and on soil properties such as cation exchange capacity, pH, redoxpotential, and chemical species present in soil; under anaerobic conditions,zinc sulfide is the controlling species. Since zinc sulfide is insoluble, the mobility of zinc in anaerobicsoil is low. In a study of the effect of pH on zinc solubility: When the pH is<7, an inverse relationship exists between the pH and the amount of zinc insolution. As negative charges on soil surfaces increase with increasing pH,additional sites for zinc adsorption are activated and the amount of zinc insolution decreases. The active zinc species in the adsorbed state is the singlycharged zinc hydroxide species (i.e., Zn[OH]+). Other investigators have alsoshown that the mobility of zinc in soil increases at lower soil pH underoxidizing conditions and at a lower cation exchange capacity of soil. On theother hand, the amount of zinc in solution generally increases when the pH is>7 in soils high in organic matter. This is a result of the release oforganically complexed zinc, reduced zinc adsorption at higher pH, or anincrease in the concentration of chelating agents in soil. For calcareoussoils, the relationship between zinc solubility and pH is nonlinear. At a highpH, zinc in solution is precipitated as Zn(OH)2, zinc carbonate (ZnCO3), orcalcium zincate. Clay and metal oxides are capable of sorbing zinc and tend toretard its mobility in soil. Zinc was more mobile at pH 4 than at pH 6.5 as aconsequence of sorption Zinc concentrations in the air are relatively low, except nearindustrial sources such as smelters. No estimate for the atmospheric lifetimeof zinc is available at this time, but the fact that zinc is transported longdistances in air indicates that its lifetime in air is at least on the order ofdays. There are few data regarding the speciation of zinc released to theatmosphere. Zinc is removed from the air by dry and wet deposition, but zincparticles with small diameters and low densities suspended in the atmospheretravel long distances from emission sources. DO NOT discharge into sewer or waterways.

12.2. Persistence and degradability

Ingredient Persistence: Water/Soil Persistence: Air diethylene glycol, HIGH HIGH Safetydi(3-aminopropyl) ether Data Sheet propylene glycol monomethyl LOW LOW ether acetate, alpha-isomer triethylenetetramine LOW LOW

12.3. Bioaccumulative potential Version No: 1.2 Page 17 of 22 Issue Date: 01/04/2016 Ingredient Bioaccumulation Print Date: 01/04/2016 zinc oxide LOW8329TFS (BCF = 217) Slow Cure, Thermally Conductive Adhesive, Flowable (Part B) diethylene glycol, LOW (LogKOW = -1.4594) di(3-aminopropyl) ether propylene glycol monomethyl LOW (LogKOW = 0.56) ether acetate, alpha-isomer Continued... triethylenetetramine LOW (LogKOW = -2.6464)

12.4. Mobility in soil

Ingredient Mobility diethylene glycol, LOW (KOC = 10) di(3-aminopropyl) ether propylene glycol monomethyl HIGH (KOC = 1.838) ether acetate, alpha-isomer triethylenetetramine LOW (KOC = 309.9)

12.5.Results of PBT and vPvB assessment

P B T Relevant available data Not Available Not Available Not Available PBT Criteria fulfilled? Not Available Not Available Not Available

12.6. Other adverse effects No data available

SECTION 13 DISPOSAL CONSIDERATIONS

13.1. Waste treatment methods

Waste treatment options Not Available Sewage disposal options Not Available

SECTION 14 TRANSPORT INFORMATION

Labels Required

For 8329TFS-25ML, 8329TFS-50ML

www.element14.com NOT REGULATED by Ground ADR Special Provision 375 www.farnell.com NOT REGULATED by Air IATA Special Provision A197 NOT REGULATED by Sea IMDG per 2.10.2.7 www.newark.com NOT REGUATED by ADN Special Provision 274 (The provision of 3.1.2.8 apply)

Page <43> 28/10/18 V1.0

Land transport (ADR)

14.1.UN number 3077 14.2.Packing group III 14.3.UN proper shipping ENVIRONMENTALLY HAZARDOUS SUBSTANCE, SOLID, N.O.S. (contains zinc oxide) name

Continued... Version No: 1.2 Page 17 of 22 Issue Date: 01/04/2016 Print Date: 01/04/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part B)

propylene glycol monomethyl LOW (LogKOW = 0.56) ether acetate, alpha-isomer triethylenetetramine LOW (LogKOW = -2.6464)

12.4. Mobility in soil

Ingredient Mobility diethylene glycol, LOW (KOC = 10) di(3-aminopropyl) ether propylene glycol monomethyl HIGH (KOC = 1.838) ether acetate, alpha-isomer triethylenetetramine LOW (KOC = 309.9)

12.5.Results of PBT and vPvB assessment

P B T Relevant available data Not Available Not Available Not Available PBT Criteria fulfilled? Not Available Not Available Not Available

12.6. Other adverse effects No data available

SECTION 13 DISPOSAL CONSIDERATIONS

13.1. Waste treatment methods

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. Legislation addressing waste disposal requirements may differ by country, state and/ or territory. Each user must refer to laws operating in their area. In some areas, certain wastes must be tracked. A Hierarchy of Controls seems to be common - the user should investigate: Reduction Reuse Product / Packaging Recycling disposal Disposal (if all else fails) This material may be recycled if unused, or if it has not been contaminated so as to make it unsuitable for its intended use. If it has been contaminated, it may be possible to reclaim the product by filtration, distillation or some other means. Shelf life considerations should also be applied in making decisions of this type. Note that properties of a material may change in use, and recycling or reuse may not always be appropriate. DO NOT allow wash water from cleaning or process equipment to enter drains. It may be necessary to collect all wash water for treatment before disposal. In all cases disposal to sewer may be subject to local laws and regulations and these should be considered first. Where in doubt contact the responsible authority. Recycle wherever possible or consult manufacturer for recycling options. Consult State Land Waste Authority for disposal. Bury or incinerate residue at an approved site. Safety DataRecycle containers Sheet if possible, or dispose of in an authorised landfill. Waste treatment options Not Available Sewage disposal options Not Available

SECTION 14 TRANSPORT INFORMATION

Labels Required

For 8329TFS-25ML,MC002977 - 25 8329TFS-50ML ML

Land transport (ADR) Version No: 1.2 Page 18 of 22 Issue Date: 01/04/2016 14.1.UN number 3077 Print Date: 01/04/2016 14.2.Packing group III8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part B) 14.3.UN proper shipping ENVIRONMENTALLY HAZARDOUS SUBSTANCE, SOLID, N.O.S. (contains zinc oxide) name 14.4.Environmental hazard Not Applicable Continued... 14.5. Transport hazard Class 9 class(es) Subrisk Not Applicable

Hazard identification (Kemler) 90 Classification code M7 14.6. Special precautions for Hazard Label 9 user Special provisions 274 335 375 601 Limited quantity 5 kg

Air transport (ICAO-IATA / DGR)

14.1. UN number 3077 14.2. Packing group III 14.3. UN proper shipping Environmentally hazardous substance, solid, n.o.s. * (contains zinc oxide) name 14.4. Environmental hazard Not Applicable

ICAO/IATA Class 9 14.5. Transport hazard ICAO / IATA Subrisk Not Applicable class(es) ERG Code 9L

Special provisions A97 A158 A179 A197 Cargo Only Packing Instructions 956 Cargo Only Maximum Qty / Pack 400 kg 14.6. Special precautions for Passenger and Cargo Packing Instructions 956 user Passenger and Cargo Maximum Qty / Pack 400 kg Passenger and Cargo Limited Quantity Packing Instructions Y956 Passenger and Cargo Limited Maximum Qty / Pack 30 kg G

Sea transport (IMDG-Code / GGVSee)

14.1. UN number 3077 14.2. Packing group III 14.3. UN proper shipping ENVIRONMENTALLY HAZARDOUS SUBSTANCE, SOLID, N.O.S. (contains zinc oxide) www.element14.comname www.farnell.com14.4. Environmental hazard Marine Pollutant www.newark.com 14.5. Transport hazard IMDG Class 9 class(es) IMDG Subrisk Not Applicable Page <44> 28/10/18 V1.0

EMS Number F-A, S-F 14.6. Special precautions for Special provisions 274 335 966 967 969 user Limited Quantities 5 kg

Inland waterways transport (ADN)

14.1. UN number 3077 14.2. Packing group III 14.3. UN proper shipping ENVIRONMENTALLY HAZARDOUS SUBSTANCE, SOLID, N.O.S. (contains zinc oxide) name 14.4. Environmental hazard Not Applicable

14.5. Transport hazard 9 Not Applicable class(es)

Classification code M7 Special provisions 274; 335; 375; 601 14.6. Special precautions for user Limited quantity 5 kg Equipment required PP, A*** Fire cones number 0

Continued... Version No: 1.2 Page 18 of 22 Issue Date: 01/04/2016 Print Date: 01/04/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part B)

14.4.Environmental hazard Not Applicable

14.5. Transport hazard Class 9 class(es) Subrisk Not Applicable

Hazard identification (Kemler) 90 Classification code M7 14.6. Special precautions for Hazard Label 9 user Special provisions 274 335 375 601 Limited quantity 5 kg

Air transport (ICAO-IATA / DGR)

14.1. UN number 3077 14.2. Packing group III 14.3. UN proper shipping Environmentally hazardous substance, solid, n.o.s. * (contains zinc oxide) name 14.4. Environmental hazard Not Applicable

ICAO/IATA Class 9 14.5. Transport hazard ICAO / IATA Subrisk Not Applicable class(es) ERG Code 9L

Special provisions A97 A158 A179 A197 Cargo Only Packing Instructions 956 Cargo Only Maximum Qty / Pack 400 kg 14.6. Special precautions for Passenger and Cargo Packing Instructions 956 user Safety DataPassenger and Cargo Sheet Maximum Qty / Pack 400 kg Passenger and Cargo Limited Quantity Packing Instructions Y956 Passenger and Cargo Limited Maximum Qty / Pack 30 kg G

Sea transport (IMDG-Code / GGVSee)

14.1. UN number 3077 14.2. Packing group III 14.3. UN proper shipping ENVIRONMENTALLY HAZARDOUS SUBSTANCE, SOLID, N.O.S. (contains zinc oxide) name 14.4. Environmental hazard Marine Pollutant

14.5. Transport hazard IMDG Class 9 class(es) IMDG Subrisk Not Applicable

EMS Number F-A, S-F 14.6. Special precautions for Special provisions 274 335 966 967 969 user Limited Quantities 5 kg

Inland waterways transport (ADN)

14.1. UN number 3077 14.2. Packing group III 14.3. UN proper shipping ENVIRONMENTALLY HAZARDOUS SUBSTANCE, SOLID, N.O.S. (contains zinc oxide) name 14.4. Environmental hazard Not Applicable

14.5. Transport hazard 9 Not Applicable class(es)

Classification code M7 Special provisions 274; 335; 375; 601 Version14.6. No: Special 1.2 precautions for Page 19 of 22 Issue Date: 01/04/2016 Limited quantity 5 kg user Print Date: 01/04/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part B) Equipment required PP, A*** Fire cones number 0

Transport in bulk according to Annex II of MARPOL and the IBC code Continued... Not Applicable

SECTION 15 REGULATORY INFORMATION

15.1. Safety, health and environmental regulations / legislation specific for the substance or mixture

ZINC OXIDE(1314-13-2) IS FOUND ON THE FOLLOWING REGULATORY LISTS EU European Chemicals Agency (ECHA) Community Rolling Action Plan (CoRAP) List of European Union - European Inventory of Existing Commercial Chemical Substances (EINECS) Substances (English) EU REACH Regulation (EC) No 1907/2006 - Annex XVII - Restrictions on the manufacture, European Union (EU) Annex I to Directive 67/548/EEC on Classification and Labelling of placing on the market and use of certain dangerous substances, mixtures and articles Dangerous Substances - updated by ATP: 31 European Customs Inventory of Chemical Substances ECICS (English) European Union (EU) Regulation (EC) No 1272/2008 on Classification, Labelling and European Trade Union Confederation (ETUC) Priority List for REACH Authorisation Packaging of Substances and Mixtures - Annex VI International Agency for Research on Cancer (IARC) - Agents Classified by the IARC Monographs

LINOLEIC ACID/4,7,10-TRIOXA-1,13-TRIDECANEDIAMINE POLYAMID(68541-13-9) IS FOUND ON THE FOLLOWING REGULATORY LISTS Not Applicable

TALL OIL/ TRIETHYLENETETRAMINE POLYAMIDES(68082-29-1) IS FOUND ON THE FOLLOWING REGULATORY LISTS European Union (EU) No-Longer Polymers List (NLP) (67/548/EEC)

DIETHYLENE GLYCOL, DI(3-AMINOPROPYL) ETHER(4246-51-9) IS FOUND ON THE FOLLOWING REGULATORY LISTS www.element14.comEuropean Customs Inventory of Chemical Substances ECICS (English) European Union - European Inventory of Existing Commercial Chemical Substances (EINECS) www.farnell.com (English)

www.newark.comPROPYLENE GLYCOL MONOMETHYL ETHER ACETATE, ALPHA-ISOMER(108-65-6) IS FOUND ON THE FOLLOWING REGULATORY LISTS EU Consolidated List of Indicative Occupational Exposure Limit Values (IOELVs) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) EU REACH Regulation (EC) No 1907/2006 - Annex XVII - Restrictions on the manufacture,Page <45>(Hungarian) 28/10/18 V1.0 placing on the market and use of certain dangerous substances, mixtures and articles European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) European Customs Inventory of Chemical Substances ECICS (English) (Italian) European Union - European Inventory of Existing Commercial Chemical Substances (EINECS) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) (English) (Latvian) European Union (EU) Annex I to Directive 67/548/EEC on Classification and Labelling of European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) Dangerous Substances - updated by ATP: 31 (Lithuanian) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) (Bulgarian) (Maltese) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) (Czech) (Polish) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) (Danish) (Portuguese) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) (Dutch) (Romanian) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) (English) (Slovak) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) (Estonian) (Slovenian) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) (Finnish) (Spanish) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) (French) (Swedish) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) European Union (EU) Regulation (EC) No 1272/2008 on Classification, Labelling and (German) Packaging of Substances and Mixtures - Annex VI European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) UK Workplace Exposure Limits (WELs) (Greek)

TRIETHYLENETETRAMINE(112-24-3) IS FOUND ON THE FOLLOWING REGULATORY LISTS EU REACH Regulation (EC) No 1907/2006 - Annex XVII - Restrictions on the manufacture, European Union - European Inventory of Existing Commercial Chemical Substances (EINECS) placing on the market and use of certain dangerous substances, mixtures and articles (English) European Customs Inventory of Chemical Substances ECICS (English) European Union (EU) Annex I to Directive 67/548/EEC on Classification and Labelling of European Trade Union Confederation (ETUC) Priority List for REACH Authorisation Dangerous Substances - updated by ATP: 31 European Union (EU) Regulation (EC) No 1272/2008 on Classification, Labelling and Packaging of Substances and Mixtures - Annex VI

CARBON BLACK(1333-86-4) IS FOUND ON THE FOLLOWING REGULATORY LISTS EU REACH Regulation (EC) No 1907/2006 - Annex XVII - Restrictions on the manufacture, European Union - European Inventory of Existing Commercial Chemical Substances (EINECS) placing on the market and use of certain dangerous substances, mixtures and articles (English) European Customs Inventory of Chemical Substances ECICS (English) International Agency for Research on Cancer (IARC) - Agents Classified by the IARC European List of Notified Chemical Substances (ELINCS) Monographs European Trade Union Confederation (ETUC) Priority List for REACH Authorisation UK Workplace Exposure Limits (WELs)

This safety data sheet is in compliance with the following EU legislation and its adaptations - as far as applicable - : 67/548/EEC, 1999/45/EC, 98/24/EC, 92/85/EC, 94/33/EC, 91/689/EEC,

Continued... Version No: 1.2 Page 19 of 22 Issue Date: 01/04/2016 Print Date: 01/04/2016 8329TFS Slow Cure, Thermally Conductive Adhesive, Flowable (Part B)

Transport in bulk according to Annex II of MARPOL and the IBC code Not Applicable

SECTION 15 REGULATORY INFORMATION

15.1. Safety, health and environmental regulations / legislation specific for the substance or mixture

ZINC OXIDE(1314-13-2) IS FOUND ON THE FOLLOWING REGULATORY LISTS EU European Chemicals Agency (ECHA) Community Rolling Action Plan (CoRAP) List of European Union - European Inventory of Existing Commercial Chemical Substances (EINECS) Substances (English) EU REACH Regulation (EC) No 1907/2006 - Annex XVII - Restrictions on the manufacture, European Union (EU) Annex I to Directive 67/548/EEC on Classification and Labelling of placing on the market and use of certain dangerous substances, mixtures and articles Dangerous Substances - updated by ATP: 31 European Customs Inventory of Chemical Substances ECICS (English) European Union (EU) Regulation (EC) No 1272/2008 on Classification, Labelling and European Trade Union Confederation (ETUC) Priority List for REACH Authorisation Packaging of Substances and Mixtures - Annex VI Safety Data Sheet International Agency for Research on Cancer (IARC) - Agents Classified by the IARC Monographs

LINOLEIC ACID/4,7,10-TRIOXA-1,13-TRIDECANEDIAMINE POLYAMID(68541-13-9) IS FOUND ON THE FOLLOWING REGULATORY LISTS Not Applicable

TALL OIL/ TRIETHYLENETETRAMINE POLYAMIDES(68082-29-1) IS FOUND ON THE FOLLOWING REGULATORY LISTS European Union (EU) No-Longer Polymers List (NLP) (67/548/EEC)

DIETHYLENE GLYCOL, DI(3-AMINOPROPYL) ETHER(4246-51-9) IS FOUND ON THE FOLLOWING REGULATORY LISTS European Customs Inventory of Chemical Substances ECICS (English) European Union - European Inventory of Existing Commercial Chemical Substances (EINECS) (English)

PROPYLENE GLYCOL MONOMETHYL ETHER ACETATE, ALPHA-ISOMER(108-65-6) IS FOUND ON THE FOLLOWING REGULATORY LISTS EU Consolidated List of Indicative Occupational Exposure Limit Values (IOELVs) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) EU REACH Regulation (EC) No 1907/2006 - Annex XVII - Restrictions on the manufacture, (Hungarian) placing on the market and use of certain dangerous substances, mixtures and articles European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) European Customs Inventory of Chemical Substances ECICS (English) (Italian) European Union - European Inventory of Existing Commercial Chemical Substances (EINECS) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) (English) (Latvian) European Union (EU) Annex I to Directive 67/548/EEC on Classification and Labelling of European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) Dangerous Substances - updated by ATP: 31 (Lithuanian) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) (Bulgarian) (Maltese) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) (Czech) (Polish) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) (Danish) (Portuguese) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) (Dutch) (Romanian) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) (English) (Slovak) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) (Estonian) (Slovenian) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) (Finnish) (Spanish) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) (French) (Swedish) European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) European Union (EU) Regulation (EC) No 1272/2008 on Classification, Labelling and (German) Packaging of Substances and Mixtures - Annex VI European Union (EU) First List of Indicative Occupational Exposure Limit Values (IOELVs) UK Workplace Exposure Limits (WELs) (Greek)

CARBON BLACK(1333-86-4) IS FOUND ON THE FOLLOWING REGULATORY LISTS EU REACH Regulation (EC) No 1907/2006 - Annex XVII - Restrictions on the manufacture, European Union - European Inventory of Existing Commercial Chemical Substances (EINECS) placing on the market and use of certain dangerous substances, mixtures and articles (English) Version No: 1.2 Page 20 of 22 Issue Date: 01/04/2016 European Customs Inventory of Chemical Substances ECICS (English) International Agency for Research on Cancer (IARC) - Agents Classified by the IARC Print Date: 01/04/2016 European List of Notified Chemical Substances8329TFS (ELINCS) Slow Cure, Thermally ConductiveMonographs Adhesive, Flowable (Part B) European Trade Union Confederation (ETUC) Priority List for REACH Authorisation UK Workplace Exposure Limits (WELs)

This safety data sheet is in compliance with the following EU legislation and its adaptations - as far as applicable - : 67/548/EEC, 1999/45/EC, 98/24/EC, 92/85/EC, 94/33/EC, 91/689/EEC, 1999/13/EC, Commission Regulation (EU) 2015/830, Regulation (EC) No 1272/2008 and their amendments as well as the following British legislation: - The Control of Substances Hazardous to Health Regulations (COSHH) 2002 - COSHH Essentials - The Management of Health and Safety at Work Regulations 1999 Continued...

15.2. Chemical safety assessment For further information please look at the Chemical Safety Assessment and Exposure Scenarios prepared by your Supply Chain if available.

ECHA SUMMARY

Ingredient CAS number Index No ECHA Dossier aluminium oxide 1344-28-1. Not Available 01-2119817795-27-XXXX, 01-2119529248-35-XXXX

Harmonisation (C&L Pictograms Signal Hazard Class and Category Code(s) Hazard Statement Code(s) Inventory) Word Code(s) H370, H332, H335, H372, H341, H317, GHS08, Dgr, Wng, 1 Not Classified H350, H361, H220, H315, H319, H302, GHS09, GHS02 H225 Not Classified, STOT SE 3, Acute Tox. 4, STOT RE 1, Muta. 2, Skin Sens. 1, Carc. H370, H332, H335, H372, H341, H317, GHS08, Dgr, Wng, 2 1B, Repr. 2, Aquatic Chronic 3, Skin Irrit. 2, Eye Irrit. 2, STOT RE 2, Flam. Liq. 2, H350, H361, H220, H315, H319, H302, GHS09, GHS02 www.element14.com Aquatic Chronic 4 H225 www.farnell.comHarmonisation Code 1 = The most prevalent classification. Harmonisation Code 2 = The most severe classification. www.newark.com Ingredient CAS number Index No ECHA Dossier zinc oxide 1314-13-2 030-013-00-7Page <46> 01-2119463881-32-XXXX 28/10/18 V1.0 Harmonisation (C&L Pictograms Signal Hazard Class and Category Code(s) Hazard Statement Code(s) Inventory) Word Code(s) H360, H335, H370, H372, H314, 1 Aquatic Acute 1 GHS09, Wng H318, H350, H300, H330, H317, H341 Aquatic Acute 1, Aquatic Chronic 1, Acute Tox. 4, Repr. 1A, STOT RE 2, Skin Irrit. 2, Eye H360, H335, H370, H372, H314, GHS09, Wng, GHS08, 2 Irrit. 2, STOT SE 3, STOT SE 1, Not Classified, STOT RE 1, Skin Corr. 1B, Eye Dam. 1, H318, H350, H300, H330, H317, Dgr, GHS05, GHS06 Carc. 1A, Acute Tox. 2, Skin Sens. 1, Muta. 2 H341 H360, H335, H370, H372, H314, 1 Aquatic Acute 1, Aquatic Chronic 1 GHS09, Wng H318, H350, H300, H330, H317, H341 H360, H335, H370, H372, H314, 2 Aquatic Acute 1, Aquatic Chronic 1 GHS09, Wng H318, H350, H300, H330, H317, H341 Harmonisation Code 1 = The most prevalent classification. Harmonisation Code 2 = The most severe classification.

Ingredient CAS number Index No ECHA Dossier linoleic acid/4,7,10-trioxa- 1,13-tridecanediamine 68541-13-9 Not Available Not Available polyamid

Harmonisation (C&L Hazard Class and Category Code(s) Pictograms Signal Word Code(s) Hazard Statement Code(s) Inventory) 1 Eye Irrit. 2 GHS07, Wng H319 2 Not Classified, Eye Irrit. 2, Skin Irrit. 2, Skin Sens. 1, Eye Dam. 1 Wng, GHS05, Dgr H315, H317, H318 Harmonisation Code 1 = The most prevalent classification. Harmonisation Code 2 = The most severe classification.

Ingredient CAS number Index No ECHA Dossier tall oil/ triethylenetetramine 68082-29-1 Not Available Not Available polyamides

Harmonisation (C&L Pictograms Signal Hazard Statement Hazard Class and Category Code(s) Inventory) Word Code(s) Code(s) Skin Irrit. 2, Skin Sens. 1A, Eye Dam. 1, Aquatic Chronic 2, Skin Sens. 1, Aquatic Chronic 3, Eye Irrit. GHS09, GHS05, Dgr, H317, H318, H334, 2 2, Acute Tox. 4, Resp. Sens. 1, Not Classified, Met. Corr. 1, Aquatic Chronic 4, Skin Corr. 1B, Wng, GHS08, GHS06 H312, H290, H314 Aquatic Acute 1, Aquatic Chronic 1 Harmonisation Code 1 = The most prevalent classification. Harmonisation Code 2 = The most severe classification.

Ingredient CAS number Index No ECHA Dossier diethylene glycol, 4246-51-9 Not Available Not Available di(3-aminopropyl) ether

Harmonisation (C&L Pictograms Signal Word Hazard Statement Hazard Class and Category Code(s) Inventory) Code(s) Code(s) 1 Skin Corr. 1B GHS05, Dgr H314 Skin Corr. 1B, Skin Sens. 1, Eye Dam. 1, Skin Corr. 1C, Aquatic Chronic 3, Met. Corr. 1, 2 GHS05, Dgr, Wng H314, H317, H318, H290 Not Classified, Eye Irrit. 2 1 Skin Corr. 1B, Aquatic Chronic 4 GHS05, Dgr H314 2 Skin Corr. 1B, Aquatic Chronic 4 GHS05, Dgr H314 Harmonisation Code 1 = The most prevalent classification. Harmonisation Code 2 = The most severe classification.

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1999/13/EC, Commission Regulation (EU) 2015/830, Regulation (EC) No 1272/2008 and their amendments as well as the following British legislation: - The Control of Substances Hazardous to Health Regulations (COSHH) 2002 - COSHH Essentials - The Management of Health and Safety at Work Regulations 1999

15.2. Chemical safety assessment For further information please look at the Chemical Safety Assessment and Exposure Scenarios prepared by your Supply Chain if available.

SafetyECHA SUMMARY Data Sheet Ingredient CAS number Index No ECHA Dossier aluminium oxide 1344-28-1. Not Available 01-2119817795-27-XXXX, 01-2119529248-35-XXXX

Ingredient CAS number Index No ECHA Dossier zinc oxide 1314-13-2 030-013-00-7 01-2119463881-32-XXXX

Ingredient CAS number Index No ECHA Dossier linoleic acid/4,7,10-trioxa- 1,13-tridecanediamine 68541-13-9 Not Available Not Available polyamid

Ingredient CAS number Index No ECHA Dossier tall oil/ triethylenetetramine 68082-29-1 Not Available Not Available polyamides

Ingredient CAS number Index No ECHA Dossier diethylene glycol, 4246-51-9 Not Available Not Available di(3-aminopropyl) ether

Continued... www.element14.com www.farnell.com www.newark.com

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Ingredient CAS number Index No ECHA Dossier propylene glycol monomethyl 108-65-6 607-195-00-7 01-2119475791-29-XXXX ether acetate, alpha-isomer

Harmonisation (C&L Hazard Class and Category Code(s) Pictograms Signal Word Code(s) Hazard Statement Code(s) Inventory) 2 Flam. Liq. 3, Eye Irrit. 2, Eye Dam. 1, Not Classified, STOT SE 3 GHS02, Wng, GHS03, GHS05, Dgr H226, H319, H335, H336 Harmonisation Code 1 = The most prevalent classification. Harmonisation Code 2 = The most severe classification.

Ingredient CAS number Index No ECHA Dossier triethylenetetramine 112-24-3 612-059-00-5 Not Available

Harmonisation (C&L Pictograms Signal Word Hazard Class and Category Code(s) Hazard Statement Code(s) Inventory) Code(s) 1 Acute Tox. 4, Skin Corr. 1B, Skin Sens. 1, Aquatic Chronic 3 GHS07, GHS05, Dgr H312, H314, H317 Acute Tox. 4, Skin Corr. 1B, Skin Sens. 1, Aquatic Chronic 3, Eye Dam. 1, Acute Tox. 3, GHS05, Dgr, GHS06, H314, H317, H318, H302, 2 Resp. Sens. 1, STOT SE 3, Aquatic Chronic 2, Not Classified GHS08, GHS09 H311, H334, H335 Harmonisation Code 1 = The most prevalent classification. Harmonisation Code 2 = The most severe classification.

Ingredient CAS number Index No ECHA Dossier carbon black 1333-86-4 Not Available 01-2119384822-32-XXXX, 01-2119489801-30-XXXX, 01-2119475601-40-XXXX

National Inventory Status Australia - AICS Y Canada - DSL Y N (propylene glycol monomethyl ether acetate, alpha-isomer; tall oil/ triethylenetetramine polyamides; linoleic acid/4,7,10-trioxa-1,13-tridecanediamine Canada - NDSL polyamid; aluminium oxide; carbon black; triethylenetetramine) China - IECSC Y Europe - EINEC / ELINCS / N (linoleic acid/4,7,10-trioxa-1,13-tridecanediamine polyamid) NLP Japan - ENCS N (tall oil/ triethylenetetramine polyamides; linoleic acid/4,7,10-trioxa-1,13-tridecanediamine polyamid) Korea - KECI Y New Zealand - NZIoC Y Philippines - PICCS Y USA - TSCA Y Y = All ingredients are on the inventory Legend: N = Not determined or one or more ingredients are not on the inventory and are not exempt from listing(see specific ingredients in brackets)

SECTION 16 OTHER INFORMATION

Full text Risk and Hazard codes

H220 Extremely flammable gas. H225 Highly flammable liquid and vapour. H226 Flammable liquid and vapour. H228 Flammable solid. H251 Self-heating: may catch fire. H290 May be corrosive to metals. Fatal if swallowed. www.element14.comH300 Harmful if swallowed. www.farnell.comH302 H311 Toxic in contact with skin. www.newark.com H312 Harmful in contact with skin. H314 Causes severe skin burns and eye damage. Page <48> 28/10/18 V1.0 H318 Causes serious eye damage. H330 Fatal if inhaled. H332 Harmful if inhaled.

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Ingredient CAS number Index No ECHA Dossier propylene glycol monomethyl 108-65-6 607-195-00-7 01-2119475791-29-XXXX ether acetate, alpha-isomer

Ingredient CAS number Index No ECHA Dossier triethylenetetramine 112-24-3 612-059-00-5 Not Available

Ingredient CAS number Index No ECHA Dossier carbon black 1333-86-4 Not Available 01-2119384822-32-XXXX, 01-2119489801-30-XXXX, 01-2119475601-40-XXXX

SECTION 16 OTHER INFORMATION

Full text Risk and Hazard codes

H220 Extremely flammable gas. SafetyH225 DataHighly flammable liquid Sheet and vapour. H226 Flammable liquid and vapour. H228 Flammable solid. H251 Self-heating: may catch fire. H290 May be corrosive to metals. H300 Fatal if swallowed. H302 Harmful if swallowed. H311 Toxic in contact with skin. H312 Harmful in contact with skin.

Version No: 1.2 H314 Causes severe skin burns and eye damage. Page 22 of 22 Issue Date: 01/04/2016 Print Date: 01/04/2016 H318 Causes8329TFS serious Sloweye damage. Cure, Thermally Conductive Adhesive, Flowable (Part B) H330 Fatal if inhaled. H332 Harmful if inhaled. H334 May cause allergy or asthma symptoms or breathing difficulties if inhaled. Continued... H335 May cause respiratory irritation. H336 May cause drowsiness or dizziness. H341 Suspected of causing genetic defects. H350 May cause cancer. H351 Suspected of causing cancer. H360 May damage fertility or the unborn child. H361 Suspected of damaging fertility or the unborn child. H370 Causes damage to organs. H372 Causes damage to organs. H412 Harmful to aquatic life with long lasting effects.

Other information

Ingredients with multiple cas numbers

Name CAS No zinc oxide 1314-13-2, 175449-32-8 diethylene glycol, 25265-19-4, 4246-51-9 di(3-aminopropyl) ether propylene glycol monomethyl 108-65-6, 142300-82-1, 84540-57-8 ether acetate, alpha-isomer

Classification of the preparation and its individual components has drawn on official and authoritative sources as well as independent review by the Chemwatch Classification committee using available literature references. A list of reference resources used to assist the committee may be found at: www.chemwatch.net

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end of SDS Safety Data Sheet

Part Number MC002977

Important Notice : This data sheet and its contents (the “Information”) belong to the members of the Premier Farnell group of companies (the “Group”) or are licensed to it. No licence is granted for the use of it other than for information purposes in connection with the products to which it relates. No licence of any intellectual property rights is granted. The Information is subject to change without notice and replaces all data sheets previously supplied. The Information supplied is believed to be accurate but the Group assumes no responsibility for its accuracy or completeness, any error in or omission from it or for any use made of it. Users of this data sheet should check for themselves the Information and the suitability of the products for their purpose and not make any assumptions based on information included or omitted. Liability for loss or damage resulting from any reliance on the Information or use of it (including liability resulting from negligence or where the Group was aware of the possibility of such loss or damage arising) is excluded. This will not operate to limit or restrict the Group’s liability for death or personal injury resulting from its negligence. Multicomp is the registered trademark of the Group. © Premier Farnell Limited 2016.

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