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Ardex tile adhesives


ARDEX D11 (Abafix/Flexible Multipurpose) is a white, ready mixed, thin bed, interior wall tile adhes

By  Last updated: 4th September 2010

ARDEX D11 (Abafix/Flexible Multipurpose) is a white, ready mixed, thin bed, interior wall tile adhesive

Section 1 – CHEMICAL PRODUCT AND COMPANY IDENTIFICATION
PRODUCT NAME
ARDEX D11
SYNONYMS
abafix, “flexible multipurpose”
PRODUCT USE
Premixed wall tile adhesive used to fix ceramic tile in interior situations.
SUPPLIER
Company: Ardex Australia Pty Ltd
Address:
20 Powers Road
Seven Hills
NSW, 2147
AUS
Telephone: 1800 224 070
Fax: +61 2 9838 7817
CHEMWATCH HAZARD RATINGS
Flammability
Toxicity
Body Contact
Reactivity
Chronic
SCALE: Min/Nil=0 Low=1 Moderate=2 High=3 Extreme=4
Section 2 – HAZARDS IDENTIFICATION
STATEMENT OF HAZARDOUS NATURE
NON-HAZARDOUS SUBSTANCE. NON-DANGEROUS GOODS. According to the Criteria of
NOHSC, and the ADG Code.
POISONS SCHEDULE
None
RISK SAFETY
None under normal operating conditions. Avoid contact with skin.
Section 3 – COMPOSITION / INFORMATION ON INGREDIENTS
NAME CAS RN %
acrylic emulsion 10-60
fillers 10-60
cellulosic thickener 1-10
bacteriacide 0-1
ethylene glycol 107-21-1 <0.5

Section 3 – COMPOSITION / INFORMATION ON INGREDIENTS
water 7732-18-5 30-60
Section 4 – FIRST AID MEASURES
SWALLOWED
• 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.
EYE
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.
• If pain persists or recurs seek medical attention.
• Removal of contact lenses after an eye injury should only be undertaken by skilled
personnel.
SKIN
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.
INHALED
• If fumes or combustion products are inhaled remove from contaminated area.
• Other measures are usually unnecessary.
NOTES TO PHYSICIAN
Treat symptomatically.
Section 5 – FIRE FIGHTING MEASURES
EXTINGUISHING MEDIA
• There is no restriction on the type of extinguisher which may be used.
• Use extinguishing media suitable for surrounding area.
FIRE FIGHTING
• Alert Fire Brigade and tell them location and nature of hazard.
• Wear breathing apparatus plus protective gloves for fire only.
• Prevent, by any means available, spillage from entering drains or water courses.
• Use fire fighting procedures suitable for surrounding area.
• DO NOT approach containers suspected to be hot.
• Cool fire exposed containers with water spray from a protected location.
• If safe to do so, remove containers from path of fire.
• Equipment should be thoroughly decontaminated after use.

Section 5 – FIRE FIGHTING MEASURES
FIRE/EXPLOSION HAZARD
• The material is not readily combustible under normal conditions.
• However, it will break down under fire conditions and the organic component may burn.
• Not considered to be a significant fire risk.
• Heat may cause expansion or decomposition with violent rupture of containers.
• Decomposes on heating and may produce toxic fumes of carbon monoxide (CO).
• May emit acrid smoke.
FIRE INCOMPATIBILITY
• Avoid reaction with oxidising agents.
HAZCHEM: None
Section 6 – ACCIDENTAL RELEASE MEASURES
EMERGENCY PROCEDURES
MINOR SPILLS
• Clean up all spills immediately.
• Avoid breathing vapours and contact with skin and eyes.
• Control personal contact 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.
MAJOR SPILLS
Minor hazard.
• Clear area of personnel.
• Alert Fire Brigade and tell them location and nature of hazard.
• Control personal contact by using protective equipment as required.
• Prevent spillage from entering drains or water ways.
• Contain spill with sand, earth or vermiculite.
• Collect recoverable product into labelled containers for recycling.
• Absorb remaining product with sand, earth or vermiculite and place in appropriate
containers for disposal.
• Wash area and prevent runoff into drains or waterways.
• If contamination of drains or waterways occurs, advise emergency services.
Personal Protective Equipment advice is contained in Section 8 of the MSDS.
Section 7 – HANDLING AND STORAGE
PROCEDURE FOR HANDLING
• Limit all unnecessary personal contact.
• Wear protective clothing when risk of exposure occurs.
• Use in a well-ventilated area.
• Avoid contact with incompatible materials.
• When handling, DO NOT eat, drink or smoke.
• Keep containers securely sealed when not in use.
• Avoid physical damage to containers.
• Always wash hands with soap and water after handling.
• Work clothes should be laundered separately.
• Use good occupational work practice.
• Observe manufacturer’s storing and handling recommendations.

Section 7 – HANDLING AND STORAGE
• Atmosphere should be regularly checked against established exposure standards to ensure
safe working conditions are maintained.
SUITABLE CONTAINER
• Lined metal can, lined metal pail/ can.
• Plastic pail.
• Polyliner drum.
• Packing as recommended by manufacturer.
• Check all containers are clearly labelled and free from leaks.
STORAGE INCOMPATIBILITY
Avoid storage with oxidisers.
STORAGE REQUIREMENTS
• Store in original containers.
• Keep containers securely sealed.
• Store in a cool, dry, well-ventilated area.
• Store away from incompatible materials and foodstuff containers.
• Protect containers against physical damage and check regularly for leaks.
• Observe manufacturer’s storing and handling recommendations.
Section 8 – EXPOSURE CONTROLS / PERSONAL PROTECTION
EXPOSURE CONTROLS
Source Material TWA ppm TWA mg/m³ STEL ppm STEL mg/m³
Australia Exposure ethylene glycol 20 52 40 104
Standards (Ethylene glycol
(vapour))
Australia Exposure ethylene glycol 10
Standards (Ethylene glycol
(particulate))
The following materials had no OELs on our records
• water: CAS:7732- 18- 5
MATERIAL DATA
None assigned for mixture or identified for ingredient(s).
INGREDIENT DATA
WATER:
No exposure limits set by NOHSC or ACGIH.
PERSONAL PROTECTION
EYE
• Safety glasses with side shields; or as required,
• 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 lens or
restrictions on use, should be created for each workplace or task. This should include a
review of lens absorption and adsorption for the class of chemicals in use and an account
of injury experience. Medical and first-aid personnel should be trained in their removal
and suitable equipment should be readily available. In the event of chemical exposure,
begin eye irrigation immediately and remove contact lens as soon as practicable. Lens

Section 8 – EXPOSURE CONTROLS / PERSONAL PROTECTION
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].
HANDS/FEET
Wear chemical protective gloves, eg. PVC.
Wear safety footwear.
OTHER
• Overalls.
• Eyewash unit.
RESPIRATOR
Selection of the Class and Type of respirator will depend upon the level of breathing
zone contaminant and the chemical nature of the contaminant. Protection Factors (defined
as the ratio of contaminant outside and inside the mask) may also be important.
Breathing Zone Level Maximum Protection Half- face Respirator Full- Face Respirator
ppm (volume) Factor
1000 10 A- AUS P –
1000 50 – A- AUS P
5000 50 Airline * –
5000 100 – A- 2 P
10000 100 – A- 3 P
100+ Airline**
* – Continuous Flow ** – Continuous-flow or positive pressure demand.
The local concentration of material, quantity and conditions of use determine the type of
personal protective equipment required.
For further information consult site specific
CHEMWATCH data (if available), or your
Occupational Health and Safety Advisor.
ENGINEERING CONTROLS
General exhaust is adequate under normal operating conditions. If risk of overexposure
exists, wear SAA approved respirator. Correct fit is essential to obtain adequate
protection. Provide adequate ventilation in warehouse or closed storage areas.
Refer also to protective measures for the other component used with the product. Read
both MSDS before using; store and attach MSDS together.
Section 9 – PHYSICAL AND CHEMICAL PROPERTIES
APPEARANCE
Thick white paste with a slight odour; partly mixes with water.
PHYSICAL PROPERTIES
Liquid.
Does not mix with water.
Sinks in water.
Molecular Weight: Not applicable Boiling Range (°C): 100
Melting Range (°C): Not available Specific Gravity (water= 1): 1.6 (approx.)
Solubility in water (g/L): Partly miscible pH (as supplied): 8.7- 9.2
pH (1% solution): Not available Vapour Pressure (kPa): Not available
Volatile Component (%vol): Not available Evaporation Rate: Not available
Relative Vapour Density (air=1): Not Flash Point (°C): Not a pplicable

Section 9 – PHYSICAL AND CHEMICAL PROPERTIES
available
Lower Explosive Limit (%): Not applicable Upper Explosive Limit (%): Not applicable
Autoignition Temp (°C): Not applicable Decomposition Temp (°C): Not available
State: Non slump paste Viscosity: Not available
Section 10 – CHEMICAL STABILITY AND REACTIVITY INFORMATION
CONDITIONS CONTRIBUTING TO INSTABILITY
• Presence of incompatible materials.
• Product is considered stable.
• Hazardous polymerisation will not occur.
Section 11 – TOXICOLOGICAL INFORMATION
POTENTIAL HEALTH EFFECTS
ACUTE HEALTH EFFECTS
SWALLOWED
The liquid is. discomforting to the gastro-intestinal tract.
Ingestion may result in nausea, abdominal irritation, pain and vomiting.
Considered an unlikely route of entry in commercial/industrial environments.
EYE
The liquid is discomforting to the eyes and is capable of causing a mild, temporary
redness of the conjunctiva (similar to wind-burn), temporary impairment of vision and/ or
other transient eye damage/ ulceration.
SKIN
The material may be. discomforting to the skin if exposure is prolonged and is capable of
causing skin reactions which may lead to dermatitis from repeated exposures over long
periods.
INHALED
Not normally a hazard due to non-volatile nature of product.
The vapour/mist is. discomforting to the upper respiratory tract.
CHRONIC HEALTH EFFECTS
Principal routes of exposure are usually by skin contact/eye contact.
Prolonged or repeated skin contact may cause drying with cracking, irritation and
possible dermatitis following.
As with any chemical product, contact with unprotected bare skin; inhalation of vapour,
mist or dust in work place atmosphere; or ingestion in any form, should be avoided by
observing good occupational work practice.
TOXICITY AND IRRITATION
unless otherwise specified data extracted from RTECS – Register of Toxic Effects of
Chemical Substances.
Not available for mixture or identified for ingredient(s).
ETHYLENE GLYCOL:
unless otherwise specified data extracted from RTECS – Register of Toxic Effects of
Chemical Substances.
TOXICITY IRRITATION
Oral (rat) LD50: 4700 mg/kg Skin (rabbit): 555 mg(open)- Mild

Section 11 – TOXICOLOGICAL INFORMATION
Oral (human) LDLo: 398 mg/kg Eye (rabbit): 100 mg/1h – Mild
Oral (child) TDLo: 5500 mg/kg Eye (rabbit): 1440mg/6h- Moderate
Inhalation (human) TCLo: 10000 mg/m³ Eye (rabbit): 500 mg/24h – Mild
Dermal (rabbit) LD50: 9530 mg/kg Eye (rabbit): 12 mg/m³/3D
Inhalation (rat) LC50: 50100 mg/m³/8 hr
For ethylene glycol:
Ethylene glycol is quickly and extensively absorbed through the gastrointestinal tract.
Limited information suggests that it is also absorbed through the respiratory tract;
dermal absorption is apparently slow. Following absorption, ethylene glycol is
distributed throughout the body according to total body water. In most mammalian species,
including humans, ethylene glycol is initially metabolised by alcohol.
dehydrogenase to form glycolaldehyde, which is rapidly converted to glycolic acid and
glyoxal by aldehyde oxidase and aldehyde dehydrogenase. These metabolites are oxidised to
glyoxylate; glyoxylate may be further metabolised to formic acid, oxalic acid, and
glycine. Breakdown of both glycine and formic acid can generate CO2, which is one of the
major elimination products of ethylene glycol. In addition to exhaled CO2, ethylene
glycol is eliminated in the urine as both the parent compound and glycolic acid.
Elimination of ethylene glycol from the plasma in both humans and laboratory animals is
rapid after oral exposure; elimination half-lives are in the range of 1-4 hours in most
species tested.
Respiratory Effects. Respiratory system involvement occurs 12-24 hours after ingestion of
sufficient amounts of ethylene glycol and is considered to be part of a second stage in
ethylene glycol poisoning. The symptoms include hyperventilation, shallow rapid breathing,
and generalized pulmonary edema with calcium oxalate crystals occasionally present in the
lung parenchyma. Respiratory system involvement appears to be dose-dependent and occurs
concomitantly with cardiovascular changes. Pulmonary infiltrates and other changes
compatible with adult respiratory distress syndrome (ARDS) may characterise the second
stage of ethylene glycol poisoning. Pulmonary oedema can be secondary to cardiac failure,
ARDS, or aspiration of gastric contents. Symptoms related to acidosis such as hyperpnea
and tachypnea are frequently observed; however, major respiratory morbidities such as
pulmonary edema and bronchopneumonia are relatively rare and usually only observed with
extreme poisoning (e.g., in only 5 of 36 severely poisoned cases).
Cardiovascular Effects. Cardiovascular system involvement in humans occurs at the same
time as respiratory system involvement, during the second phase of oral ethylene glycol
poisoning, which is 12- 24 hours after acute exposure. The symptoms of cardiac
involvement include tachycardia, ventricular gallop and cardiac enlargement. Ingestion
of ethylene glycol may also cause hypertension or hypotension, which may progress to
cardiogenic shock. Myocarditis has been observed at autopsy in cases of people who died
following acute ingestion of ethylene glycol . As in the case of respiratory effects,
cardiovascular involvement occurs with ingestion of relatively high doses of ethylene
glycol.
Nevertheless, circulatory disturbances are a rare occurrence, having been reported in
only 8 of 36 severely poisoned cases .Therefore, it appears that acute exposure to high
levels of ethylene glycol can cause serious cardiovascular effects in humans. The effects
of a long-term, low-dose exposure are unknown.
Gastrointestinal Effects. Nausea, vomiting with or without blood, pyrosis, and abdominal
cramping and pain are common early effects of acute ethylene glycol ingestion. Acute
effects of ethylene glycol ingestion in one patient included intermittent diarrhea and
abdominal pain, which were attributed to mild colonic ischaemia; severe abdominal pain
secondary to colonic stricture and perforation developed 3 months after ingestion, and
histology of the resected colon showed birefringent crystals highly suggestive of oxalate
deposition.
Musculoskeletal Effects. Reported musculoskeletal effects in cases of acute ethylene
glycol poisoning have included diffuse muscle tenderness and myalgias associated with
elevated serum creatinine phosphokinase levels, and myoclonic jerks and tetanic
contractions associated with hypocalcaemia.
Hepatic Effects. Central hydropic or fatty degeneration, parenchymal necrosis, and
calcium oxalate crystals in the liver have been observed at autopsy in cases of people
who died following acute ingestion of ethylene glycol.

Section 11 – TOXICOLOGICAL INFORMATION
Renal Effects. Adverse renal effects after ethylene glycol ingestion in humans can be
observed during the third stage of ethylene glycol toxicity 24-72 hours after acute
exposure. The hallmark of renal toxicity is the presence of birefringent calcium oxalate
monohydrate crystals deposited in renal tubules and their presence in urine after
ingestion of relatively high amounts of ethylene glycol. Other signs of nephrotoxicity
can include tubular cell degeneration and necrosis and tubular interstitial inflammation.
If untreated, the degree of renal damage caused by high doses of ethylene glycol
progresses and leads to haematuria, proteinuria, decreased renal function, oliguria,
anuria , and ultimately renal failure. These changes in the kidney are linked to acute
tubular necrosis but normal or near normal renal function can return with adequate
supportive therapy.
Metabolic Effects. One of the major adverse effects following acute oral exposure of
humans to ethylene glycol involves metabolic changes. These changes occur as early as 12
hours after ethylene glycol exposure. Ethylene glycol intoxication is accompanied by
metabolic acidosis which is manifested by decreased pH and bicarbonate content of serum
and other bodily fluids caused by accumulation of excess glycolic acid. Other
characteristic metabolic effects of ethylene glycol poisoning are increased serum anion
gap, increased osmolal gap, and hypocalcaemia. Serum anion gap is calculated from
concentrations of sodium, chloride, and bicarbonate, is normally 12-16 mM, and is
typically elevated after ethylene glycol ingestion due to increases in unmeasured
metabolite anions (mainly glycolate).
Neurological Effects: Adverse neurological reactions are among the first symptoms to
appear in humans after ethylene glycol ingestion. These early neurotoxic effects are also
the only symptoms attributed to unmetabolised ethylene glycol. Together with metabolic
changes, they occur during the period of 30 minutes to 12 hours after exposure and are
considered to be part of the first stage in ethylene glycol intoxication. In cases of
acute intoxication, in which a large amount of ethylene glycol is ingested over a very
short time period, there is a progression of neurological manifestations which, if not
treated, may lead to generalized seizures and coma. Ataxia, slurred speech, confusion,
and somnolence are common during the initial phase of ethylene glycol intoxication as are
irritation, restlessness, and disorientation. Cerebral edema and crystalline deposits of
calcium oxalate in the walls of small blood vessels in the brain were found at autopsy in
people who died after acute ethylene glycol ingestion.
Effects on cranial nerves appear late (generally 5-20 days post-ingestion), are
relatively rare, and according to some investigators constitute a fourth, late cerebral
phase in ethylene glycol intoxication. Clinical manifestations of the cranial neuropathy
commonly involve lower motor neurons of the facial and bulbar nerves and are reversible
over many months.
Reproductive Effects: Reproductive function after intermediate-duration oral exposure to
ethylene glycol has been tested in three multi-generation studies (one in rats and two in
mice) and several shorter studies (15-20 days in rats and mice). In these studies,
effects on fertility, foetal viability, and male reproductive organs were observed in
mice, while the only effect in rats was an increase in gestational duration.
Developmental Effects: The developmental toxicity of ethylene glycol has been assessed in
several acute-duration studies using mice, rats, and rabbits. Available studies indicate
that malformations, especially skeletal malformations occur in both mice and rats exposed
during gestation; mice are apparently more sensitive to the developmental effects of
ethylene glycol. Other evidence of embyrotoxicity in laboratory animals exposed to
ethylene glycol exposure includes reduction in foetal body weight.
Cancer: No studies were located regarding cancer effects in humans or animals after
dermal exposure to ethylene glycol.
Genotoxic Effects: Studies in humans have not addressed the genotoxic effects of ethylene
glycol. However, available in vivo and in vitro laboratory studies provide consistently
negative genotoxicity results for ethylene glycol.
[Estimated Lethal Dose (human) 100 ml; RTECS quoted by Orica]
Substance is reproductive effector in rats (birth defects).
Mutagenic to rat cells.

Section 11 – TOXICOLOGICAL INFORMATION
unless otherwise specified data extracted from RTECS – Register of Toxic Effects of
Chemical Substances.
No significant acute toxicological data identified in literature search.
Section 12 – ECOLOGICAL INFORMATION
No data for Ardex D11.
Refer to data for ingredients, which follows:
ETHYLENE GLYCOL:
Hazardous Air Pollutant: Yes
Fish LC50 (96hr.) (mg/l): 18500- 4100
Algae IC50 (72hr.) (mg/l): 180000
log Kow (Prager 1995): – 1.36
log Kow (Sangster 1997): – 1.36
log Pow (Verschueren 1983): – 1.93
BOD5: 35%
COD: 94%
ThOD: 1.26
Half- life Soil – High (hours): 288
Half- life Soil – Low (hours): 48
Half- life Air – High (hours): 83
Half- life Air – Low (hours): 8.3
Half- life Surface water – High (hours): 288
Half- life Surface water – Low (hours): 48
Half- life Ground water – High (hours): 576
Half- life Ground water – Low (hours): 96
Aqueous biodegradation – Aerobic – High (hours): 288
Aqueous biodegradation – Aerobic – Low (hours): 48
Aqueous biodegradation – Anaerobic – High (hours): 1152
Aqueous biodegradation – Anaerobic – Low (hours): 192
Aqueous biodegradation – Removal secondary treatment – High (hours): 100%
Aqueous biodegradation – Removal secondary treatment – Low (hours): 80%
Photooxidation half- life water – High (hours): 566000
Photooxidation half- life water – Low (hours): 6400
Photooxidation half- life air – High (hours): 83
Photooxidation half- life air – Low (hours): 8.3
for ethylene glycol:
log Kow : -1.93- -1.36
Half-life (hr) air : 24
Henry’s atm m3 /mol: 6.00E-08
BOD 5 : 0.15-0.81,12%
COD : 1.21-1.29
ThOD : 1.26
BCF : 10-190
In the atmosphere ethylene glycol exists mainly in the vapour phase. It is degraded in
the atmosphere by reaction with photochemically produced hydroxy radicals (estimated halflife
24-50 hours).
Ethylene glycol does not concentrate in the food chain.
Environmental fate:
Ethylene glycol has a low vapour pressure (7.9 Pa at 20 C); it is expected to exist
almost entirely in the vapour phase if released to the atmosphere. The Henry’s law
constant for ethylene glycol is 1.41 × 10-3 or 6.08 × 10-3 Pa.m3/mol, depending on method
of calculation, indicating a low capacity for volatilisation from water bodies or soil
surfaces.
Ethylene glycol adsorbed onto silica gel and irradiated with light (wavelength >290 nm)

Section 12 – ECOLOGICAL INFORMATION
degraded by 12.1% over 17 h . Photodegradation is not expected, as the molecule should
not absorb at these wavelengths; the mechanism of this breakdown is, therefore, unknown.
Estimated half-life in the atmosphere for reaction with hydroxyl radicals from various
reports is 2.1 days , 8-84 h or 1 day.
Ethylene glycol released to the atmosphere will be degraded by reaction with hydroxyl
radicals; the half-life for the compound in this reaction has been estimated at between
0.3 and 3.5 days. No hydrolysis of ethylene glycol is expected in surface waters.
The compound has little or no capacity to bind to particulates and will be mobile in
soil. Soil partition coefficients (log Koc) of 0-0.62 were determined. Migration rates in
five soil types were measured at between 4 and 27 cm per 12 h
The low octanol/water partition coefficient (log Kow -1.93 to -1.36)and measured
bioconcentration factors in a few organisms indicate low capacity for bioaccumulation.
Bioconcentration factors of 190 for the green algae (Chlorella fusca) , up to 0.27 in
specific tissues of the crayfish ( Procambarus sp.) , and 10 for the golden orfe
(Leuciscus idus melanotus) confirm low bioaccumulation.
Ethylene glycol is readily biodegradable in standard tests using sewage sludge. Many
studies show biodegradation under both aerobic and anaerobic conditions. Some studies
suggest a lag phase before degradation, but many do not. Degradation occurs in both
adapted and unadapted sludges. Rapid degradation has been reported in surface waters
(less in salt water than in fresh water), groundwater, and soil inocula. Several strains
of microorganisms capable of utilising ethylene glycol as a carbon source have been
identified.
Ethylene glycol has been identified as a metabolite of the growth regulator ethylene in a
number of higher plants and as naturally occurring in the edible fungus Tricholoma
matsutake
Ecotoxicity:
Fish LC50 (96 h):118-550 mg/L
Ethylene glycol has generally low toxicity to aquatic organisms. Toxic thresholds for
microorganisms are above 1000 mg/litre. EC50s for growth in microalgae are 6500 mg/litre
or higher. Acute toxicity tests with aquatic invertebrates where a value could be
determined show LC50s above 20 000 mg/litre, and those with fish show LC50s above 17 800
mg/litre. An amphibian test showed an LC50 for tadpoles at 17 000 mg/litre. A no-observedeffect
concentration (NOEC) for chronic tests on daphnids of 8590 mg/litre (for
reproductive end-points) has been reported. A NOEC following short-term exposure of fish
has been reported at 15 380 mg/litre for growth. Tests using deicer containing ethylene
glycol showed greater toxicity to aquatic organisms than observed with the pure compound,
indicating other toxic components of the formulations. Laboratory tests exposing aquatic
organisms to stream water receiving runoff from airports have demonstrated toxic effects
and death. Field studies in the vicinity of an airport have reported toxic signs
consistent with ethylene glycol poisoning, fish kills, and reduced biodiversity. These
effects cannot definitively be ascribed to ethylene glycol. Terrestrial organisms are
much less likely to be exposed to ethylene glycol and generally show low sensitivity to
the compound. Concentrations above 100 000 mg/litre were needed to produce toxic effects
on yeasts and fungi from soil. Very high concentrations and soaking of seeds produced
inhibition of germination in some experiments; these are not considered of environmental
significance. A no-observed-effect level (NOEL) for orally dosed ducks at 1221 mg/kg body
weight and reported lethal doses for poultry at around 8000 mg/kg body weight indicate
low toxicity to birds.
DO NOT discharge into sewer or waterways.
Section 13 – DISPOSAL CONSIDERATIONS
• Consult manufacturer for recycling options and recycle where possible.
• Consult State Land Waste Management Authority for disposal.
• Break the emulsion and separate components.
• Bury or incinerate residue at an approved site.
• Recycle containers where possible, or dispose of in an authorised landfill.
continued…
ARDEX D11
Chemwatch Material Safety Data Sheet
Issue Date: 18-Aug-2008 CHEMWATCH 7516-94
NC317ECP Version No:4
CD 2008/2 Page 11 of 12
Section 14 – TRANSPORTATION INFORMATION
HAZCHEM: None
NOT REGULATED FOR TRANSPORT OF DANGEROUS GOODS:UN, IATA,
IMDG
Section 15 – REGULATORY INFORMATION
POISONS SCHEDULE: None
REGULATIONS
Ardex D11 (CAS: None):
No regulations applicable
ethylene glycol (CAS: 107-21-1) is found on the following regulatory lists;
Australia – Victoria Occupational Health and Safety Regulations – Schedule 9: Materials at Major Hazard Facilities (And Their Threshold Quantity) Table 2
Australia Exposure Standards
Australia Hazardous Substances
Australia High Volume Industrial Chemical List (HVICL)
Australia Inventory of Chemical Substances (AICS)
Australia National Pollutant Inventory
Australia Standard for the Uniform Scheduling of Drugs and Poisons (SUSDP) – Appendix E (Part 2)
Australia Standard for the Uniform Scheduling of Drugs and Poisons (SUSDP) – Schedule 5
Australia Standard for the Uniform Scheduling of Drugs and Poisons (SUSDP) – Schedule 6
GESAMP/EHS Composite List of Hazard Profiles – Hazard evaluation of substances transported by ships
IMO IBC Code Chapter 17: Summary of minimum requirements
IMO MARPOL 73/78 (Annex II) – List of Noxious Liquid Substances Carried in Bulk
IMO MARPOL 73/78 (Annex II) – List of Other Liquid Substances
IMO Provisional Categorization of Liquid Substances – List 1: Pure or technically pure products
IMO Provisional Categorization of Liquid Substances – List 2: Pollutant only mixtures containing at least 99% by weight of components already assessed by IMO
International Council of Chemical Associations (ICCA) – High Production Volume List
OECD Representative List of High Production Volume (HPV) Chemicals
water (CAS: 7732-18-5) is found on the following regulatory lists;
Australia Inventory of Chemical Substances (AICS)
GESAMP/EHS Composite List of Hazard Profiles – Hazard evaluation of substances transported by ships
IMO IBC Code Chapter 18: List of products to which the Code does not apply
OECD Representative List of High Production Volume (HPV) Chemicals
Section 16 – OTHER INFORMATION
REPRODUCTIVE HEALTH GUIDELINES
Ingredient ORG UF Endpoi CR Adeq
nt TLV
ethylene glycol 26 mg/m3 100 R NA –
These exposure guidelines have been derived from a screening level of risk assessment and
should not be construed as unequivocally safe limits. ORGS represent an 8-hour timeweighted
average unless specified otherwise.
CR = Cancer Risk/10000; UF = Uncertainty factor:
TLV believed to be adequate to protect reproductive health:
LOD: Limit of detection
Toxic endpoints have also been identified as:
D = Developmental; R = Reproductive; TC = Transplacental carcinogen
Jankovic J., Drake F.: A Screening Method for Occupational Reproductive
American Industrial Hygiene Association Journal 57: 641-649 (1996).
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/references.
continued…
ARDEX D11
Chemwatch Material Safety Data Sheet
Issue Date: 18-Aug-2008 CHEMWATCH 7516-94
NC317ECP Version No:4
CD 2008/2 Page 12 of 12
Section 16 – OTHER INFORMATION
The (M)SDS is a Hazard Communication tool and should be used to assist in the Risk
Assessment. Many factors determine whether the reported Hazards are Risks in the
workplace or 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.
 source: ARDEX

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