Chemwatch Independent Material Safety Data Sheet

Issue Date: 29-Jul-2005



Version No:3





■ Used according to manufacturer's directions.


Company: Benji Distributors Pty Ltd
17 Grandview Pde
VIC, 3221
Telephone: +61 3 5248 1469
Fax: +61 3 5248 6696





Flammability 0
Toxicity 2
Body Contact 2
Reactivity 2
Chronic 3
SCALE: Min/Nil=0 Low=1 Moderate=2 High=3 Extreme=4


■ May form explosive peroxides. • Keep locked up.
■ May cause CANCER. • Do not breathe gas/ fumes/ vapour/ spray.
■ Possible risk of irreversible effects. • Avoid contact with skin.
■ Inhalation, skin contact and/or ingestion may produce health damage*. • Wear suitable protective clothing.
■ Cumulative effects may result following exposure*. • In case of insufficient ventilation, wear suitable respiratory equipment.
■ Possible respiratory and skin sensitiser*. • Wear suitable gloves.
■ May be harmful to the foetus/embryo*. • Wear eye/ face protection.
■ May possibly affect fertility*. • Handle and open container with care.
■ Repeated exposure potentially causes skin dryness and cracking*. • Use only in well ventilated areas.
■ Vapours potentially cause drowsiness and dizziness*. • Keep container in a well ventilated place.
* (limited evidence). • Avoid exposure - obtain special instructions before use.
• To clean the floor and all objects contaminated by this material, use water.
• Keep container tightly closed.
• This material and its container must be disposed of in a safe way.
• Keep away from food, drink and animal feeding stuffs.
• In case of accident by inhalation: remove casualty to fresh air and keep at rest.



sodium tripolyphosphate 7758-29-4 <5
sodium lauryl ether sulfate 9004-82-4 <5
ethylene glycol monobutyl ether 111-76-2 1-9
trichloroethylene 79-01-6 <5



· For advice, contact a Poisons Information Centre or a doctor.
· Urgent hospital treatment is likely to be needed.
· In the mean time, qualified first-aid personnel should treat the patient following observation and employing supportive measures as indicated by the patient's condition.
· If the services of a medical officer or medical doctor are readily available, the patient should be placed in his/her care and a copy of the MSDS should be provided. Further action will be the responsibility of the medical specialist.
· If medical attention is not available on the worksite or surroundings send the patient to a hospital together with a copy of the MSDS.

Where medical attention is not immediately available or where the patient is more than 15 minutes from a hospital or unless instructed otherwise:
· INDUCE vomiting with fingers down the back of the throat, ONLY IF CONSCIOUS. Lean patient forward or place on left side (head-down position, if possible) to maintain open airway and prevent aspiration.
NOTE: Wear a protective glove when inducing vomiting by mechanical means.


■ 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 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 fumes or combustion products are inhaled remove from contaminated area.
· Lay patient down. Keep warm and rested.
· Prostheses such as false teeth, which may block airway, should be removed, where possible, prior to initiating first aid procedures.
· Apply artificial respiration if not breathing, preferably with a demand valve resuscitator, bag-valve mask device, or pocket mask as trained. Perform CPR if necessary.
· Transport to hospital, or doctor.


■ For acute or short term repeated exposures to ethylene glycol:
· Early treatment of ingestion is important. Ensure emesis is satisfactory.
· Test and correct for metabolic acidosis and hypocalcaemia.
· Apply sustained diuresis when possible with hypertonic mannitol.
· Evaluate renal status and begin haemodialysis if indicated. [I.L.O]
· Rapid absorption is an indication that emesis or lavage is effective only in the first few hours. Cathartics and charcoal are generally not effective.
· Correct acidosis, fluid/electrolyte balance and respiratory depression in the usual manner. Systemic acidosis (below 7.2) can be treated with intravenous sodium
bicarbonate solution.
· Ethanol therapy prolongs the half- life of ethylene glycol and reduces the formation of toxic metabolites.
· Pyridoxine and thiamine are cofactors for ethylene glycol metabolism and should be given (50 to 100 mg respectively) intramuscularly, four times per day for 2
· Magnesium is also a cofactor and should be replenished. The status of 4- methylpyrazole, in the treatment regime, is still uncertain. For clearance of the material
and its metabolites, haemodialysis is much superior to peritoneal dialysis. [Ellenhorn and Barceloux: Medical Toxicology]
It has been suggested that there is a need for establishing a new biological exposure limit before a workshift that is clearly below 100 mmol ethoxy- acetic acids
per mole creatinine in morning urine of people occupationally exposed to ethylene glycol ethers. This arises from the finding that an increase in urinary stones may
be associated with such exposures.
Laitinen J., et al: Occupational & Environmental Medicine 1996; 53, 595- 600.



· There is no restriction on the type of extinguisher which may be used.
· Use extinguishing media suitable for surrounding area.


· 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.


· Non combustible.
· Not considered a significant fire risk, however containers may burn.
May emit poisonous fumes.
May emit corrosive fumes.


■ None known.



Personal Protective Equipment

Breathing apparatus.
Gas tight chemical resistant suit.
Limit exposure duration to 1 BA set 30 mins.



· 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.


■ 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.
· Stop leak if safe to do so.
· Contain spill with sand, earth or vermiculite.
· Collect recoverable product into labelled containers for recycling.
· Neutralise/decontaminate residue (see Section 13 for specific agent).
· Collect solid residues and seal in labelled drums for disposal.
· Wash area and prevent runoff into drains.
· After clean up operations, decontaminate and launder all protective clothing and equipment before storing
and re- using.
· If contamination of drains or waterways occurs, advise emergency services.


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



· Avoid all personal contact, including inhalation.
· Wear protective clothing when risk of exposure occurs.
· Use in a well-ventilated area.
· Avoid contact with moisture.
· Avoid contact with incompatible materials.
· When handling, DO NOT eat, drink or smoke.
· Keep containers securely sealed when not in use.
· Avoid physical damage to containers.
· Always wash hands with soap and water after handling.
· Work clothes should be laundered separately. Launder contaminated clothing before re-use.
· Use good occupational work practice.
· Observe manufacturer's storing and handling recommendations.
· Atmosphere should be regularly checked against established exposure standards to ensure safe working conditions are maintained.
· DO NOT allow clothing wet with material to stay in contact with skin.


· Polyethylene or polypropylene container.
· Packing as recommended by manufacturer.
· Check all containers are clearly labelled and free from leaks.


■ None known.


· 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.




+: May be stored together
O: May be stored together with specific preventions
X: Must not be stored together




SourceMaterialTWA ppmTWA mg/m³STEL ppmSTEL mg/m³Notes
Australia Exposure Standardsethylene glycol monobutyl ether (2-Butoxyethanol)2096.950242Sk
Australia Exposure Standardstrichloroethylene (Trichloroethylene)105440216Sk
The following materials had no OELs on our records
• sodium tripolyphosphate: CAS:7758-29-4 CAS:15091-98-2
• sodium lauryl ether sulfate: CAS:9004-82-4



Material Revised IDLH Value (mg/m³) Revised IDLH Value (ppm)
ethylene glycol monobutyl ether 151 700 [Unch]
trichloroethylene 240 1,000 [Unch]
Material Revised IDLH Value (mg/m³) Revised IDLH Value (ppm)
ethylene glycol monobutyl ether 151 700 [Unch]
trichloroethylene 240 1,000 [Unch]



■ Exposed individuals are NOT reasonably expected to be warned, by smell, that the Exposure Standard is being exceeded.
Odour Safety Factor (OSF) is determined to fall into either Class C, D or E.
The Odour Safety Factor (OSF) is defined as:
OSF= Exposure Standard (TWA) ppm/ Odour Threshold Value (OTV) ppm
Classification into classes follows:
Class OSF Description
A 550 Over 90% of exposed individuals are aware by smell that the Exposure Standard (TLV-TWA for example) is being reached, even when distracted by working activities
B 26-550 As "A" for 50-90% of persons being distracted
C 1-26 As "A" for less than 50% of persons being distracted
D 0.18-1 10-50% of persons aware of being tested perceive by smell that the Exposure Standard is being reached
E <0.18 As "D" for less than 10% of persons aware of being tested


■ Sensory irritants are chemicals that produce temporary and undesirable side- effects on the eyes, nose or throat. Historically occupational exposure standards for
these irritants have been based on observation of workers' responses to various airborne concentrations. Present day expectations require that nearly every
individual should be protected against even minor sensory irritation and exposure standards are established using uncertainty factors or safety factors of 5 to 10 or
more. On occasion animal no- observable- effect- levels (NOEL) are used to determine these limits where human results are unavailable. An additional approach,
typically used by the TLV committee (USA) in determining respiratory standards for this group of chemicals, has been to assign ceiling values (TLV C) to rapidly
acting irritants and to assign short- term exposure limits (TLV STELs) when the weight of evidence from irritation, bioaccumulation and other endpoints combine to
warrant such a limit. In contrast the MAK Commission (Germany) uses a five- category system based on intensive odour, local irritation, and elimination half- life.
However this system is being replaced to be consistent with the European Union (EU) Scientific Committee for Occupational Exposure Limits (SCOEL); this is more
closely allied to that of the USA.
OSHA (USA) concluded that exposure to sensory irritants can:
· cause inflammation
· cause increased susceptibility to other irritants and infectious agents
· lead to permanent injury or dysfunction
· permit greater absorption of hazardous substances and
· acclimate the worker to the irritant warning properties of these substances thus increasing the risk of overexposure.
Not available
■ It is the goal of the ACGIH (and other Agencies) to recommend TLVs (or their equivalent) for all substances for which there is evidence of health effects at
airborne concentrations encountered in the workplace.
At this time no TLV has been established, even though this material may produce adverse health effects (as evidenced in animal experiments or clinical experience).
Airborne concentrations must be maintained as low as is practically possible and occupational exposure must be kept to a minimum.
NOTE: The ACGIH occupational exposure standard for Particles Not Otherwise Specified (P.N.O.S) does NOT apply.
■ For ethylene glycol monobutyl ether (2- butoxyethanol)
Odour Threshold Value: 0.10 ppm (detection), 0.35 ppm (recognition)
Although rats appear to be more susceptible than other animals anaemia is not uncommon amongst humans following exposure. The TLV reflects the need to maintain
exposures below levels found to cause blood changes in experimental animals. It is concluded that this limit will reduce the significant risk of irritation,
haematologic effects and other systemic effects observed in humans and animals exposed to higher vapour concentrations. The toxic effects typical of some other
glycol ethers (pancytopenia, testis atrophy and teratogenic effects) are not found with this substance.
Odour Safety Factor (OSF)
Exposed individuals are reasonably expected to be warned, by smell, that the Exposure Standard is being exceeded.
Odour Safety Factor (OSF) is determined to fall into either Class A or B.
The Odour Safety Factor (OSF) is defined as:
OSF= Exposure Standard (TWA) ppm/ Odour Threshold Value (OTV) ppm
Classification into classes follows:
Class OSF Description
A 550 Over 90% of exposed individuals are aware by smell that the Exposure Standard (TLV-TWA for example) is being reached, even when distracted by working activities
B 26-550 As "A" for 50-90% of persons being distracted
C 1-26 As "A" for less than 50% of persons being distracted
D 0.18-1 10-50% of persons aware of being tested perceive by smell that the Exposure Standard is being reached
E <0.18 As "D" for less than 10% of persons aware of being tested
. TRICHLOROETHYLENE: ■ for trichloroethylene: Odour Threshold Value: 82 ppm (detection), 108 ppm (recognition) NOTE: Detector tubes for trichloroethylene, measuring in excess of 10 ppm, are commercially available. Long- term measurements (4 hrs) may be conducted to detect concentrations exceeding 2.5 ppm. Organs systems reported to be affected by excessive exposures of humans and animals to TCE are the central nervous system (CNS) (nausea, ataxia, headache, euphoria, analgesia, anaesthesia); liver (degeneration, hepatocellular carcinomas, mice only); kidney (degeneration); lung (oedema, tachypnea); heart (arrhythmias); skin (irritation, vesication) and paralysis of the fingers following immersion. Exposure at or below the recommended TLV- TWA is thought to minimise the potential for headache, fatigue and irritability. A STEL has been advised to protect against incoordination and other anaesthetic effects. Control of concentrations to these limits should also provide a substantial margin of safety in the prevention of liver and other systemic damage. The lower limit (REL- TWA) recommended by NIOSH is based on acute central nervous system (CNS) effects, headache and fatigue observed in health hazard evaluations at levels of 25 ppm to 50 ppm and upon the potential for cancer in humans (hepatocellular carcinomas in mice exposed by chronic gastric lavage is cited). - Notes on Trichloroethylene Toxicity: - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - Concentration Clinical Effects - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - 100 ppm Odour Threshold barely perceptible to the unacclimated 200 ppm Odour apparent, not unpleasant; slight eye irritation 400 ppm (3 hours) Odour very definite, not unpleasant; slight eye irritation and minimal light- headedness 1000- 1200 ppm (6 min) Very strong odour, unpleasant; definite eye and nasal irritation with light- headedness and dizziness 2000 ppm (5 min) Odour very strong, not tolerable; marked eye and respiratory irritation with drowsiness, dizziness and nausea. Odour Safety Factor(OSF) OSF=1.8 (TRICHLOROETHYLENE.




· 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 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 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].


· Wear chemical protective gloves, eg. PVC.
· Wear safety footwear or safety gumboots, eg. Rubber.
· 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.


· Overalls.
· P.V.C. apron.
· Barrier cream.
· Skin cleansing cream.
· Eye wash unit.
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 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 special circumstances. If risk of overexposure exists,
wear approved respirator. Supplied- air type respirator may be required in special circumstances. Correct fit is essential to ensure adequate protection. Provide
adequate ventilation in warehouses and enclosed storage areas. Air contaminants generated in the workplace possess varying " escape" velocities which, in turn,
determine the " capture velocities" of fresh circulating air required to effectively remove the contaminant.
Type of Contaminant: Air Speed:
solvent, vapours, degreasing etc., evaporating from tank (in still air). 0.25-0.5 m/s (50-100 f/min)
aerosols, fumes from pouring operations, intermittent container filling, low speed conveyer transfers, welding, spray drift, plating acid fumes, pickling (released at low velocity into zone of active generation) 0.5-1 m/s (100-200 f/min.)
direct spray, spray painting in shallow booths, drum filling, conveyer loading, crusher dusts, gas discharge (active generation into zone of rapid air motion) 1-2.5 m/s (200-500 f/min.)
grinding, abrasive blasting, tumbling, high speed wheel generated dusts (released at high initial velocity into zone of very high rapid air motion) 2.5-10 m/s (500-2000 f/min.)
Within each range the appropriate value depends on:
Lower end of the range Upper end of the range
1: Room air currents minimal or favourable to capture 1: Disturbing room air currents
2: Contaminants of low toxicity or of nuisance value only. 2: Contaminants of high toxicity
3: Intermittent, low production. 3: High production, heavy use
4: Large hood or large air mass in motion 4: Small hood-local control only
Simple theory shows that air velocity falls rapidly with distance away from the opening of a simple extraction pipe. Velocity generally decreases with the square of distance from the extraction point (in simple cases). Therefore the air speed at the extraction point should be adjusted, accordingly, after reference to distance from the contaminating source. The air velocity at the extraction fan, for example, should be a minimum of 1- 2 m/s (200- 400 f/min) for extraction of solvents generated in a tank 2 meters distant from the extraction point. Other mechanical considerations, producing performance deficits within the extraction apparatus, make it essential that theoretical air velocities are multiplied by factors of 10 or more when extraction systems are installed or used.



Green liquid with a characteristic odour; mixes with water.


Mixes with water.


StateLiquidMolecular WeightNot Available
Melting Range (ºC)Not AvailableViscosityNot Available
Boiling Range (ºC)Not AvailableSolubility in water (g/L)Miscible
Flash Point (ºC)Not ApplicablepH (1% solution)Not Available
Decomposition Temp (ºC)Not AvailablepH (as supplied)9.4
Autoignition Temp (ºC)Not AvailableVapour Pressure (kPa)Not Available
Upper Explosive Limit (%)Not AvailableSpecific Gravity (water=1)1.02
Lower Explosive Limit (%)Not AvailableRelative Vapour Density (air=1)Not Available
Volatile Component (%vol)Not AvailableEvaporation RateNot Available


ethylene glycol monobutyl ether
log Kow (Prager 1995): 0.83
log Kow (Sangster 1997): 0.8
log Kow (Sangster 1997): 2.42



· Presence of incompatible materials.
· Product is considered stable.
· Hazardous polymerisation will not occur.

For incompatible materials - refer to Section 7 - Handling and Storage.





■ Accidental ingestion of the material may be harmful; animal experiments indicate that ingestion of less than 150 gram may be fatal or may produce serious damage to
the health of the individual.
Strong evidence exists that this substance may cause irreversible mutations (though not lethal) even following a single exposure.
As absorption of phosphates from the bowel is poor, poisoning this way is less likely. Effects can include vomiting, tiredness, fever, diarrhoea, low blood pressure,
slow pulse, cyanosis, spasms of the wrist, coma and severe body spasms.
Ingestion of anionic surfactants may produce diarrhoea, bloated stomach, and occasional vomiting.


■ Although the liquid is not thought to be an irritant (as classified by EC Directives), direct contact with the eye may produce transient discomfort characterised
by tearing or conjunctival redness (as with windburn).


■ Skin contact with the material may be harmful; systemic effects may result following absorption.
The material is not thought to be a skin irritant (as classified by EC Directives using animal models). Temporary discomfort, however, may result from prolonged
dermal exposures. Good hygiene practice requires that exposure be kept to a minimum and that suitable gloves be used in an occupational setting.
Entry into the blood- stream, through, for example, cuts, abrasions or lesions, may produce systemic injury with harmful effects. Examine the skin prior to the use
of the material and ensure that any external damage is suitably protected.


■ Inhalation of vapours or aerosols (mists, fumes), generated by the material during the course of normal handling, may be harmful.
The material is not thought to produce respiratory irritation (as classified by EC Directives using animal models). Nevertheless inhalation of vapours, fumes or
aerosols, especially for prolonged periods, may produce respiratory discomfort and occasionally, distress.
If exposure to highly concentrated solvent atmosphere is prolonged this may lead to narcosis, unconsciousness, even coma and possible death.
Anaesthetics and narcotic effects (with dulling of senses and odour fatigue) are a consequence of exposure to chlorinated solvents.
Individual response varies widely; odour may not be considered objectionable at levels which quickly induce central nervous system effects. High vapour
concentrations may give a feeling of euphoria. This may result in reduced responses, followed by rapid onset of unconsciousness, possible respiratory arrest and


■ Substance accumulation, in the human body, may occur and may cause some concern following repeated or long- term occupational exposure.
There is some evidence that inhaling this product is more likely to cause a sensitisation reaction in some persons compared to the general population.
There is limited evidence that, skin contact with this product is more likely to cause a sensitisation reaction in some persons compared to the general population.
There is ample evidence that this material can be regarded as being able to cause cancer in humans based on experiments and other information.
There is some evidence from animal testing that exposure to this material may result in toxic effects to the unborn baby.
Laboratory (in vitro) and animal studies show, exposure to the material may result in a possible risk of irreversible effects, with the possibility of producing
Sodium phosphate dibasic can cause stones in the kidney, loss of mineral from the bones and loss of thyroid gland function.
Exposure to sulfonates can cause an imbalance in cellular salts and therefore cellular function. Airborne sulfonates may be responsible for respiratory allergies
and, in some instances, minor dermal allergies.
Ethylene glycol esters and their ethers cause wasting of the testicles, reproductive changes, infertility and changes to kidney function. Shorter chain compounds are
more dangerous. They are also associated with the formation of stones in the urine.


■ unless otherwise specified data extracted from RTECS - Register of Toxic Effects of Chemical Substances.
■ The material may produce moderate eye irritation leading to inflammation. Repeated or prolonged exposure to irritants may produce conjunctivitis.
■ Not available. Refer to individual constituents.
Oral (Rat) LD50: 5190 mg/kg Nil Reported
Dermal (Rabbit) LD50: >3160 mg/kg *
■ Asthma- like symptoms may continue for months or even years after exposure to the material ceases. This may be due to a non- allergenic condition known as reactive airways dysfunction syndrome (RADS) which can occur following exposure to high levels of highly irritating compound. Key criteria for the diagnosis of RADS include the absence of preceding respiratory disease, in a non- atopic individual, with abrupt onset of persistent asthma- like symptoms within minutes to hours of a documented exposure to the irritant. A reversible airflow pattern, on spirometry, with the presence of moderate to severe bronchial hyperreactivity on methacholine challenge testing and the lack of minimal lymphocytic inflammation, without eosinophilia, have also been included in the criteria for diagnosis of RADS. RADS (or asthma) following an irritating inhalation is an infrequent disorder with rates related to the concentration of and duration of exposure to the irritating substance. Industrial bronchitis, on the other hand, is a disorder that occurs as result of exposure due to high concentrations of irritating substance (often particulate in nature) and is completely reversible after exposure ceases. The disorder is characterised by dyspnea, cough and mucus production. SODIUM LAURYL ETHER SULFATE:
Oral (rat) LD50: 1600 mg/kg Skin (rabbit):25 mg/24 hr Moderate
Oral (Rat) LD50: >2000 mg/kg *
■ Alcohol ethoxysulfates (AES) are of low acute toxicity. Neat AES are irritant to the skin and eyes. The irritation potential of solutions containing AES depends on concentration. AES is not a contact sensitiser, and contact with the skin at levels seen in laundry or hand dishwashing preparations are not considered to be of concern. AES are not considered to cause mutations, genetic damage, or cancer, and are not reproductive or developmental toxins. * [CESIO] ETHYLENE GLYCOL MONOBUTYL ETHER:
Oral (rat) LD50: 470 mg/kg Skin (rabbit): 500 mg, open; Mild
Dermal (rabbit) LD50: 220 mg/kg Eye (rabbit): 100 mg/24h-Moderate
Inhalation (human) TCLo: 100 ppm Eye (rabbit): 100 mg SEVERE
Inhalation (human) TCLo: 195 ppm/8h * [Union Carbide]
Inhalation (Rat) LC50: 450 ppm *
■ The material may produce severe irritation to the eye causing pronounced inflammation. Repeated or prolonged exposure to irritants may produce conjunctivitis. The material may cause skin irritation after prolonged or repeated exposure and may produce on contact skin redness, swelling, the production of vesicles, scaling and thickening of the skin. 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. 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. For ethylene glycol monoalkyl ethers and their acetates (EGMAEs): Typical members of this category are ethylene glycol propylene ether (EGPE), ethylene glycol butyl ether (EGBE) and ethylene glycol hexyl ether (EGHE) and their acetates. EGMAEs are substrates for alcohol dehydrogenase isozyme ADH- 3, which catalyzes the conversion of their terminal alcohols to aldehydes (which are transient metabolites). Further, rapid conversion of the aldehydes by aldehyde dehydrogenase produces alkoxyacetic acids, which are the predominant urinary metabolites of mono substituted glycol ethers. Acute Toxicity: Oral LD50 values in rats for all category members range from 739 (EGHE) to 3089 mg/kg bw (EGPE), with values increasing with decreasing molecular weight. Four to six hour acute inhalation toxicity studies were conducted for these chemicals in rats at the highest vapour concentrations practically achievable. Values range from LC0 > 85 ppm (508 mg/m3) for EGHE, LC50 > 400ppm (2620 mg/m3) for EGBEA to LC50 > 2132 ppm (9061 mg/m3) for EGPE. No lethality was observed for any of these materials under these conditions. Dermal LD50 values in rabbits range from 435 mg/kg bw (EGBE) to 1500 mg/kg bw (EGBEA). Overall these category members can be considered to be of low to moderate acute toxicity. All category members cause reversible irritation to skin and eyes, with EGBEA less irritating and EGHE more irritating than the other category members. EGPE and EGBE are not sensitisers in experimental animals or humans. Signs of acute toxicity in rats, mice and rabbits are consistent with haemolysis (with the exception of EGHE) and non- specific CNS depression typical of organic solvents in general. Alkoxyacetic acid metabolites, propoxyacetic acid (PAA) and butoxyacetic acid (BAA), are responsible for the red blood cell hemolysis. Signs of toxicity in humans deliberately ingesting cleaning fluids containing 9- 22% EGBE are similar to those of rats, with the exception of haemolysis. Although decreased blood haemoglobin and/or haemoglobinuria were observed in some of the human cases, it is not clear if this was due to haemolysis or haemodilution as a result of administration of large volumes of fluid. Red blood cells of humans are many- fold more resistant to toxicity from EGPE and EGBE in vitro than those of rats. Repeat dose toxicity: The fact that the NOAEL for repeated dose toxicity of EGBE is less than that of EGPE is consistent with red blood cells being more sensitive to EGBE than EGPE. Blood from mice, rats, hamsters, rabbits and baboons were sensitive to the effects of BAA in vitro and displayed similar responses, which included erythrocyte swelling (increased haematocrit and mean corpuscular hemoglobin), followed by hemolysis. Blood from humans, pigs, dogs, cats, and guinea pigs was less sensitive to haemolysis by BAA in vitro. Mutagenicity: In the absence and presence of metabolic activation, EGBE tested negative for mutagenicity in Ames tests conducted in S. typhimurium strains TA97, TA98, TA100, TA1535 and TA1537 and EGHE tested negative in strains TA98, TA100, TA1535, TA1537 and TA1538. In vitro cytogenicity and sister chromatid exchange assays with EGBE and EGHE in Chinese Hamster Ovary Cells with and without metabolic activation and in vivo micronucleus tests with EGBE in rats and mice were negative, indicating that these glycol ethers are not genotoxic. Carcinogenicity: In a 2- year inhalation chronic toxicity and carcinogenicity study with EGBE in rats and mice a significant increase in the incidence of liver haemangiosarcomas was seen in male mice and forestomach tumours in female mice. It was decided that based on the mode of action data available, there was no significant hazard for human carcinogenicity Reproductive and developmental toxicity. The results of reproductive and developmental toxicity studies indicate that the glycol ethers in this category are not selectively toxic to the reproductive system or developing fetus, developmental toxicity is secondary to maternal toxicity. The repeated dose toxicity studies in which reproductive organs were examined indicate that the members of this category are not associated with toxicity to reproductive organs (including the testes). Results of the developmental toxicity studies conducted via inhalation exposures during gestation periods on EGPE (rabbits - 125, 250, 500 ppm or 531, 1062, or 2125 mg/m3 and rats - 100, 200, 300, 400 ppm or 425, 850, 1275, or 1700 mg/m3), EGBE (rat and rabbit - 25, 50, 100, 200 ppm or 121, 241, 483, or 966 mg/m3), and EGHE (rat and rabbit - 20.8, 41.4, 79.2 ppm or 124, 248, or 474 mg/m3) indicate that the members of the category are not teratogenic. The NOAELs for developmental toxicity are greater than 500 ppm or 2125 mg/m3 (rabbit- EGPE), 100 ppm or 425 mg/m3 (rat- EGPE), 50 ppm or 241 mg/m3 (rat EGBE) and 100 ppm or 483 mg/m3 (rabbit EGBE) and greater than 79.2 ppm or 474 mg/m3 (rat and rabbit- EGHE). Exposure of pregnant rats to ethylene glycol monobutyl ether (2- butoxyethanol) at 100 ppm or rabbits at 200 ppm during organogenesis resulted in maternal toxicity and embryotoxicity including a decreased number of viable implantations per litter. Slight foetoxicity in the form of poorly ossified or unossified skeletal elements was also apparent in rats. Teratogenic effects were not observed in other species. At least one researcher has stated that the reproductive effects were less than that of other monoalkyl ethers of ethylene glycol. Chronic exposure may cause anaemia, macrocytosis, abnormally large red cells and abnormal red cell fragility. Exposure of male and female rats and mice for 14 weeks to 2 years produced a regenerative haemolytic anaemia and subsequent effects on the haemopoietic system in rats and mice. In addition, 2- butoxyethanol exposures caused increases in the incidence of neoplasms and nonneoplastic lesions (1). The occurrence of the anaemia was concentration- dependent and more pronounced in rats and females. In this study it was proposed that 2- butoxyethanol at concentrations of 500 ppm and greater produced an acute disseminated thrombosis and bone infarction in male and female rats as a result of severe acute haemolysis and reduced deformability of erythrocytes or through anoxic damage to endothelial cells that compromise blood flow. In two- year studies, 2- butoxyethanol continued to affect circulating erythroid mass, inducing a responsive anaemia. Rats showed a marginal increase in the incidence of benign or malignant pheochromocytomas (combined) of the adrenal gland. In mice, 2- butoxyethanol exposure resulted in a concentration dependent increase in the incidence of squamous cell papilloma or carcinoma of the forestomach. It was hypothesised that exposure- induced irritation produced inflammatory and hyperplastic effects in the forestomach and that the neoplasia were associated with a continuation of the injury/ degeneration process. Exposure also produced a concentration - dependent increase in the incidence of haemangiosarcoma of the liver of male mice and hepatocellular carcinoma. 1: NTP Toxicology Program Technical report Series 484, March 2000. NOTE: Changes in kidney, liver, spleen and lungs are observed in animals exposed to high concentrations of this substance by all routes. TRICHLOROETHYLENE:
Oral (human) LDLo: 7000 mg/kg Skin(rabbit): 500 mg/24h - SEVERE
Oral (man) TDLo: 2143 mg/kg Eye(rabbit): 20 mg/24h - SEVERE
Oral (rat) LD50: 5650 mg/kg
Inhalation (man) LCLo: 2900 ppm
Inhalation (human) TDLo: 812 mg/kg
Inhalation (human) TCLo: 6900 mg/m³/10 m
Inhalation (man) TCLo: 2900 ppm
Inhalation (man) TCLo: 110 ppm/8h
Inhalation (man) TCLo: 160 ppm/83 m
■ The material may cause severe skin irritation after prolonged or repeated exposure and may produce on contact skin redness, swelling, the production of vesicles, scaling and thickening of the skin. Repeated exposures may produce severe ulceration. Overexposure to trichloroethylene fumes causes liver damage, irregular heartbeat, brain depression and death. Deaths due to this substances have been reported in the workplace, often in degreasing operations, and have been attributed mostly to irregularities in heart rhythm or depression of the central nervous system. Repeated oral intake produces appetite loss, nausea and vomiting. A rare disease of the small intestine, seen in Japanese lens cleaners and polishers were attributed to exposure in the workplace. There is some evidence that trichloroethylene may be toxic to the liver. Damage to animal kidney had been noted but there has been no identifiable effect on the human kidney so far. Stevens- Johnson syndrome reported on five people exposed was attributed to trichloroethylene hypersensitivity. Trichloroethylene can also cause damage to the nervous system, affecting the face. Prolonged exposure is reported to cause cancer. So far evidence is inconclusive as to whether trichloroethylene alone is responsible for an increased rate of miscarriages in women exposed to it.



2-ButoxyethanolInternational Agency for Research on Cancer (IARC) - Agents Reviewed by the IARC MonographsGroup3
TrichloroethyleneInternational Agency for Research on Cancer (IARC) - Agents Reviewed by the IARC MonographsGroup2A


trichloroethyleneILO Chemicals in the electronics industry that have toxic effects on reproductionReduced fertility or sterilityH si


ethylene glycol monobutyl etherAustralia Exposure Standards - SkinNotesSk
trichloroethyleneAustralia Exposure Standards - SkinNotesSk



■ 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.
■ DO NOT discharge into sewer or waterways.
■ May cause long- term adverse effects in the aquatic environment. May cause long- term adverse effects in the aquatic environment. The principal problems of phosphate contamination of the environment relates to eutrophication processes in lakes and ponds. Phosphorus is an essential plant nutrient and is usually the limiting nutrient for blue- green algae. A lake undergoing eutrophication shows a rapid growth of algae in surface waters. Planktonic algae cause turbidity and flotation films. Shore algae cause ugly muddying, films and damage to reeds. Decay of these algae causes oxygen depletion in the deep water and shallow water near the shore. The process is self- perpetuating because anoxic conditions at the sediment/water interface causes the release of more adsorbed phosphates from the sediment. The growth of algae produces undesirable effects on the treatment of water for drinking purposes, on fisheries, and on the use of lakes for recreational purposes. SODIUM LAURYL ETHER SULFATE:
■ For surfactants: Environmental fate: Octanol/water partition coefficients cannot easily be determined for surfactants because one part of the molecule is hydrophilic and the other part is hydrophobic. Consequently they tend to accumulate at the interface and are not extracted into one or other of the liquid phases. As a result surfactants are expected to transfer slowly, for example, from water into the flesh of fish. During this process, readily biodegradable surfactants are expected to be metabolised rapidly during the process of bioaccumulation. This was emphasised by the OECD Expert Group stating that chemicals are not to be considered to show bioaccumulation potential if they are readily biodegradable. Several anionic and nonionic surfactants have been investigated to evaluate their potential to bioconcentrate in fish. BCF values (BCF - bioconcentration factor) ranging from 1 to 350 were found. These are absolute maximum values, resulting from the radiolabelling technique used. In all these studies, substantial oxidative metabolism was found resulting in the highest radioactivity in the gall bladder. This indicates liver transformation of the parent compound and biliary excretion of the metabolised compounds, so that " real" bioconcentration is overstated. After correction it can be expected that " real" parent BCF values are one order of magnitude less than those indicated above, i.e. " real" BCF is <100. Therefore the usual data used for classification by EU directives to determine whether a substance is " Dangerous to the " Environment" has little bearing on whether the use of the surfactant is environmentally acceptable. Ecotoxicity: Surfactant should be considered to be toxic (EC50 and LC50 values of < 10 mg/L) to aquatic species under conditions that allow contact of the chemicals with the organisms. The water solubility of the chemicals does not impact the toxicity except as it relates to the ability to conduct tests appropriately to obtain exposure of the test species. The acute aquatic toxicity generally is considered to be related to the effects of the surfactant properties on the organism and not to direct chemical toxicity. for alkyl ether sulfates (alkyl or alcohol ethoxysulfates): Environmental fate: A large environmental data set is available for alcohol ethoxysulfates (AES). On the environmental fate side, this includes standard biodegradation studies, advanced simulation studies of removal in treatment systems, and field monitoring data. On the environmental effects side, acute as well as chronic single- species data are available, as well as advanced studies in micro- and mesocosm systems. By means of these higher tier exposure and effects data, it could be shown that the use of AES in household detergents and cleaning products results in risk characterization ratios less than one, indicating no concern, for all environmental compartments. The most frequent initial step in the biodegradation of AES is the cleavage of an ether bond.. The cleavage may take place at any ether bond producing a fatty alcohol or an alcohol ethoxylate and ethylene glycol sulfates of various lengths.. The length of the alkyl chain and the number of EO units apparently do not affect the degree of aerobic biodegradation, but branching of the alkyl chain may hinder the primary biodegradation of AES. AES are degraded readily and completely under aerobic conditions. E.g., for C12- 14 AE3S, a rapid primary degradation of 90- 100% is reported to take place within a period of 1 to 5 days. In activated sludge simulation tests 67- 99% DOC was removed by degradation of C12- 14 AE2S and C12- 15 AE3S. The ultimate biodegradation of AES has been confirmed in OECD 301 tests for ready biodegradability. Based on at least one study, AES are not considered to bioconcentrate in aquatic organisms. Ecotoxicity: The chemical structure of AES highly influences the effect on aquatic organisms. The relations between alkyl chain length, number of EO groups and toxicity are complex and not yet resolved, but in general, changes in EO numbers affects toxicity more than changes in the alkyl chain length. In AES with alkyl chains of less than C16, the toxicity tended to decrease with increasing numbers of EO, but this was reversed for alkyl chain lengths above C16. The toxicity of AES thus seems to peak at alkyl chain lengths of C16. In a study of the acute toxicity of various AES (C8 to C19.6 and 1- 3 EO) to bluegill sunfish (Lepomis macrochirus), the LC50 fell from > 250 mg/l for C8 and 375 mg/l for C10 to 24 mg/l for C13, 4- 7 mg/l for C14, 2 mg/l for C15 and 0.3 mg/l for C16, and then increased to 10.8 mg/l for C17.9 and 17 mg/l for C19.6. Reported ranges for EC50 for the acute toxicity of AES to daphnids between 1 and 50 mg/l. However, an EC50 of 0.37 mg/l was observed in a 21- day reproduction test with Daphnia magna. The LC50 values for fish are in the range between 0.39 to 450 mg/l. A LOEC value of 0.22 mg/l has been reported for a chronic life cycle test with a duration of 1 year. The toxicity of AES towards fish seems to increase with increasing alkyl chain length for AES with up to 16 carbons. Environmental and Health Assessment of Substances in Household Detergents and Cosmetic Detergent Products, Environment Project, 615, 2001. Torben Madsen et al: Miljoministeriet (Danish Environmental Protection Agency). ETHYLENE GLYCOL MONOBUTYL ETHER:
Fish LC50 (96hr.) (mg/l):&nbsp;
log Kow (Prager 1995):&nbsp;
log Kow (Sangster 1997):&nbsp;
Half-life Soil - High (hours):&nbsp;
Half-life Soil - Low (hours):&nbsp;
Half-life Air - High (hours):&nbsp;
Half-life Air - Low (hours):&nbsp;
Half-life Surface water - High (hours):&nbsp;
Half-life Surface water - Low (hours):&nbsp;
Half-life Ground water - High (hours):&nbsp;
Half-life Ground water - Low (hours):&nbsp;
Aqueous biodegradation - Aerobic - High (hours):&nbsp;
Aqueous biodegradation - Aerobic - Low (hours):&nbsp;
Aqueous biodegradation - Anaerobic - High (hours):&nbsp;
Aqueous biodegradation - Anaerobic - Low (hours):&nbsp;
Photooxidation half-life air - High (hours):&nbsp;
Photooxidation half-life air - Low (hours):&nbsp;
Fish LC50 (96hr.) (mg/l):&nbsp;
Daphnia magna EC50 (48hr.) (mg/l):&nbsp;
■ For ethylene glycol monoalkyl ethers and their acetates: Members of this category include ethylene glycol propyl ether (EGPE), ethylene glycol butyl ether (EGBE) and ethylene glycol hexyl ether (EGHE) Environmental fate: The ethers, like other simple glycol ethers possess no functional groups that are readily subject to hydrolysis in the presence of waters. The acetates possess an ester group that hydrolyses in neutral ambient water under abiotic conditions. Level III fugacity modeling indicates that category members, when released to air and water, will partition predominately to water and, to a lesser extent, to air and soil. Estimates of soil and sediment partition coefficients (Kocs ranging from 1- 10) suggest that category members would exhibit high soil mobility. Estimated bioconcentration factors (log BCF) range from 0.463 to 0.732. Biodegradation studies indicate that all category members are readily biodegradable. The physical chemistry and environmental fate properties indicate that category members will not persist or bioconcentrate in the environment. Ecotoxicity: Glycol ether acetates do not hydrolyse rapidly into their corresponding glycol ethers in water under environmental conditions. The LC50 or EC50 values for EGHE are lower than those for EGPE and EGBE (which have shorter chain lengths and lower log Kow values). Overall, the LC50 values for the glycol ethers in aquatic species range from 94 to > 5000 mg/L. For EGHE, the 96- hour LC50 for Brachydanio rerio (zebra fish) is between 94 and mg/L, the 48- hour EC50 for Daphnia magna was 145 mg/L and the 72- hour EC50 values for biomass and growth rate of algae (Scenedesmus subspicatus) were 98 and 198 mg/L, respectively. LC50/EC50 values for EGPE and EGBE in aquatic species are 835 mg/l or greater. Aquatic toxicity data for EGBEA show a 96- hour LC50 of 28.3 mg/L for rainbow trout (Oncorhynchus mykiss), a 48- hour LC50 of 37- 143 mg/L for Daphnia magna, a 72- hour EC50 of greater than 500 mg/L for biomass or growth rate of algae (Scenedesmus subspicatus and Pseudokirchneriella subcapitata, respectively), and a 7- day EC10 of 30.4 mg/L and a NOEC of 16.4 mg/L for reproduction in Ceriodaphnia dubia. For glycol ethers: Environmental fate: Ether groups are generally stable to hydrolysis in water under neutral conditions and ambient temperatures. OECD guideline studies indicate ready biodegradability for several glycol ethers although higher molecular weight species seem to biodegrade at a slower rate. No glycol ethers that have been tested demonstrate marked resistance to biodegradative processes. Upon release to the atmosphere by evaporation, high boiling glycol ethers are estimated to undergo photodegradation (atmospheric half lives = 2.4- 2.5 hr). When released to water, glycol ethers undergo biodegradation (typically 47- 92% after 8- 21 days) and have a low potential for bioaccumulation (log Kow ranges from - 1.73 to +0.51). Ecotoxicity: Aquatic toxicity data indicate that the tri- and tetra ethylene glycol ethers are " practically non- toxic" to aquatic species. No major differences are observed in the order of toxicity going from the methyl- to the butyl ethers. Glycols exert a high oxygen demand for decomposition and once released to the environments cause the death of aquatic organisms if dissolved oxygen is depleted. log Kow: 0.76- 0.83 Koc: 67 Half- life (hr) air: 17 Henry' s atm m³ /mol: 2.08E- 08 BOD 5 if unstated: 0.71 COD: 2.2 Log BCF: 0.4 Fish LC50 (24 h): 983- 1650 mg/L Fish LC50 (96 h): fathead minnow 1700 mg/L ** Invertebrate toxicity: cell mult. inhib.91- 900mg/L (Daphnia) 48h LC50: >1000 mg/L ** Bioaccumulation: not sig Effects on algae and plankton: cell mult. inhib.35- 900mg/L Degradation Biological: rapid processes Abiotic: no hydrol&photol, RxnOH* ** [Union Carbide] TRICHLOROETHYLENE:
Hazardous Air Pollutant:&nbsp;
Fish LC50 (96hr.) (mg/l):&nbsp;
Algae IC50 (72hr.) (mg/l):&nbsp;
log Kow (Sangster 1997):&nbsp;
Half-life Soil - High (hours):&nbsp;
Half-life Soil - Low (hours):&nbsp;
Half-life Air - High (hours):&nbsp;
Half-life Air - Low (hours):&nbsp;
Half-life Surface water - High (hours):&nbsp;
Half-life Surface water - Low (hours):&nbsp;
Half-life Ground water - High (hours):&nbsp;
Half-life Ground water - Low (hours):&nbsp;
Aqueous biodegradation - Aerobic - High (hours):&nbsp;
Aqueous biodegradation - Aerobic - Low (hours):&nbsp;
Aqueous biodegradation - Anaerobic - High (hours):&nbsp;
Aqueous biodegradation - Anaerobic - Low (hours):&nbsp;
Photooxidation half-life air - High (hours):&nbsp;
Photooxidation half-life air - Low (hours):&nbsp;
First order hydrolysis half-life (hours):&nbsp;
■ Harmful to aquatic organisms, may cause long- term adverse effects in the aquatic environment. for trichloroethylene: log Kow : 2.2- 3.3 log Koc : 2 Koc : 87- 150 Henry' s atm m3 /mol: 0.0103 BCF : 17- 1160 Drinking Water Standards: trichloroethylene: 30 mg/l (UK max.) 70 mg/l (WHO provisional guideline) hydrocarbon total: 10 ug/l (UK max.) Soil Guidelines: Dutch Criteria: 0.001 mg/kg (target) 60 mg/kg (intervention) Air Quality Standards: 1 mg/m3 averaging time 24 hours (WHO Guideline Trichloroethylene quickly reacts in air, especially under smog conditions; atmospheric residence time is up to 5 days. Phosgene, dichloroacetylchloride, and formyl chloride may form. Photo- oxidative degradation may occur (half- life 7 days). The relatively short predicted half- life of trichloroethylene in the atmosphere indicates that long- range global transport is unlikely. However, its constant release, as well as its role as an intermediate in tetrachloroethylene degradation, may account for its persistence and the fact that trichloroethylene is often present in remote areas. The Henry’s law constant value of 2.0x10- 2 atm- m3 /mol at 20 C suggests that trichloroethylene partitions rapidly to the atmosphere from surface water. The major route of removal of trichloroethylene from water is volatilisation. Although volatilisation is rapid, actual volatilization rates are dependent upon temperature, water movement and depth, associated air movement, and other factors. Soil: The majority of trichloroethylene present on soil surfaces will volatilise to the atmosphere or leach into the subsurface. Once trichloroethylene leaches into the soil, it appears not to become chemically transformed or undergo covalent bonding with soil components Because trichloroethylene is a dense nonaqueous phase liquid, it can move through the unsaturated zone into the saturated zone where it can displace soil pore water Volatilisation of trichloroethylene from soil is slower than it is from water but more rapid than that of many other volatile organic compounds. One study found that an average of 37% of the applied trichloroethylene was volatilized 168 hours after treatment at 12 C and 45% was volatilised at 21 C. Sorption of organic compounds to soil has been found to be most reliably predicted when related to the organic carbon content of the soil. The components of soil organic matter had widely varying affinities for trichloroethylene, with the fats- waxes- resins fraction (Koc = 460) being responsible for stronger adsorption of trichloroethylene. The calculated Koc values are indicative of medium- to- high mobility in soil. Others have also shown that trichloroethylene is highly mobile in sandy soil. Another study comparing predicted and observed sorption on clay and organic soils suggested that sorption/desorption to inorganic mineral surfaces may also play a role, and the reactions generally follow reversible pseudo first- order kinetics. Sorption of trichloroethylene to the surfaces of soil particles, which may decrease its transport and bioavailability, is dependent on soil moisture content, since polar water molecules will compete aggressively with nonpolar vapor phase trichloroethylene for polar sorption sites. This has been experimentally confirmed with real soil samples, in which it was found that the solid/vapor partition coefficient decreased dramatically with increased moisture content. Accurate prediction of trichloroethylene transport in groundwater is complicated by the sorption effect of organic and inorganic solids. It has been shown that the biodegradation of trichloroethylene in soil increases with the organic content of the soil There is evidence that trichloroethylene may inhibit total soil biomass and fungi, possibly resulting in the inhibition of microbial transformation processes. However, the same authors observed an increase in anaerobic and specialised aerobic bacteria, which might indicate an opportunistic response to a suitable substrate by these microorganisms. Degradation of trichloroethylene by anaerobes via reductive dehalogenation can be problematic because a common product is vinyl chloride, a known carcinogen. microbial activity is greater in vegetated soils and that trichloroethylene degradation occurs faster in the vegetated than in the non vegetated soils. An anaerobic bacterium that dechlorinates tetrachloroethylene and trichloroethylene to ethylene using hydrogen as the electron donor has been isolated. The isolated strain did not appear to belong to any presently known genus or species Methane- utilizing bacteria were shown to aerobically degrade trichloroethylene to carbon dioxide in soil columns perfused with natural gas within 2 weeks A possible reason for the persistence of trichloroethylene in the environment despite these natural decomposition processes lies in the sensitive balance which must be maintained between enough co- substrate to induce the degrading enzymes and too much co- substrate, which could outcompete the trichloroethylene and inhibit its decomposition .Such balance may rarely be achieved in nature. Bioaccumulation: Experimentally measured bioconcentration factors (BCFs), which provide an indication of the tendency of a chemical to partition to the fatty tissue of organisms, have been found to range between 10 and 100 for trichloroethylene in fish. Somewhat lower BCFs were determined for blue mussel (4.52) and killifish (2.71). These numbers are suggestive of a low tendency to bioaccumulate. Trichloroethylene has also been detected in small amounts in fruits and vegetables, suggesting a potential for bioconcentration in plants. Laboratory studies with carrot and radish plants and radioactively labelled trichloroethylene revealed that uptake occurred mainly through the foliage as opposed to the roots in these plants, although subsequent translocation resulted in substantial distribution throughout the plants. The study authors determined fairly moderate BCFs of between 4.4 and 63.9. Air: The dominant transformation process for trichloroethylene in the atmosphere is reaction with photochemically produced hydroxyl radicals. Using the recommended rate constant for this reaction at 25 C (2.36x10+12 cm3 /molecule- second) and a typical atmospheric hydroxyl radical concentration (5x10+5 molecules/cm3), the half- life can be estimated to be 6.8 days. It should be noted that the half- lives determined by assuming first- order kinetics represent the calculated time for loss of the first 50% of trichloroethylene; the time required for the loss of the remaining 50% may be substantially longer. The reaction of volatile chlorinated hydrocarbons with hydroxyl radicals is temperature dependent and thus varies with the seasons, although such variation in the atmospheric concentration of trichloroethylene may be minimal because of its brief residence time . The degradation products of this reaction include phosgene, dichloroacetyl chloride, and formyl chloride. Reaction of trichloroethylene with ozone in the atmosphere is too slow to be an effective agent in trichloroethylene removal. Water: Oxidation of trichloroethylene in the aquatic environment does not appear to be a significant fate process, probably because of its having already been oxidised by the chlorine atoms. The rate of hydrolysis is also too slow to be an important transformation process. One study indicated that the rate of volatilisation of trichloroethylene proceeds more rapidly than photooxidation or hydrolysis. Chemical hydrolysis appeared to occur only at elevated temperature in a high pH environment and, even then, at a very slow rate. Studies of the degradation of trichloroethylene in water during ultraviolet irradiation indicated that degradation decreased with increases in the total organic content of the water. Biotransformation was also strongly indicated as a factor in the degradation of trichloroethylene in a case of soil and groundwater pollution. Since neither biodegradation nor hydrolysis occurs at a rapid rate, most trichloroethylene present in surface waters can be expected to volatilize into the atmosphere. However, because trichloroethylene is denser than and only moderately soluble in water, that which is not immediately volatilized may be expected to submerge and thus be removed from contact with the surface.


IngredientPersistence: Water/SoilPersistence: AirBioaccumulationMobility
TrafficNo Data AvailableNo Data Available
sodium tripolyphosphateNo Data AvailableNo Data Available
sodium lauryl ether sulfateNo Data AvailableNo Data Available
ethylene glycol monobutyl etherLOWLOWLOWHIGH



· Recycle wherever possible.
· Consult manufacturer for recycling options or consult local or regional waste management authority for disposal if no suitable treatment or disposal facility can be identified.
· Dispose of by: burial in a land-fill specifically licenced to accept chemical and / or pharmaceutical wastes or incineration in a licenced apparatus (after admixture with suitable combustible material).
· Decontaminate empty containers. Observe all label safeguards until containers are cleaned and destroyed.
· Containers may still present a chemical hazard/ danger when empty.
· Return to supplier for reuse/ recycling if possible.
· If container can not be cleaned sufficiently well to ensure that residuals do not remain or if the container cannot be used to store the same product, then puncture containers, to prevent re-use, and bury at an authorised landfill.
· Where possible retain label warnings and MSDS and observe all notices pertaining to the product.



None (ADG7)




Regulations for ingredients

sodium tripolyphosphate (CAS: 7758-29-4,15091-98-2) is found on the following regulatory lists;

"Australia High Volume Industrial Chemical List (HVICL)","Australia Inventory of Chemical Substances (AICS)"

sodium lauryl ether sulfate (CAS: 9004-82-4) is found on the following regulatory lists;

"Australia High Volume Industrial Chemical List (HVICL)","Australia Inventory of Chemical Substances (AICS)","International Fragrance Association (IFRA) Survey: Transparency List"

ethylene glycol monobutyl ether (CAS: 111-76-2) is found on the following regulatory lists;

"Australia Exposure Standards","Australia Hazardous Substances","Australia High Volume Industrial Chemical List (HVICL)","Australia Inventory of Chemical Substances (AICS)","IMO MARPOL 73/78 (Annex II) - List of Other Liquid Substances","International Agency for Research on Cancer (IARC) - Agents Reviewed by the IARC Monographs","International Fragrance Association (IFRA) Survey: Transparency List"

trichloroethylene (CAS: 79-01-6) is found on the following regulatory lists;

"Australia - Australian Capital Territory - Environment Protection Regulation: Pollutants entering waterways taken to cause environmental harm (Aquatic habitat)","Australia Exposure Standards","Australia Hazardous Substances","Australia High Volume Industrial Chemical List (HVICL)","Australia Inventory of Chemical Substances (AICS)","Australia National Pollutant Inventory","Australia New Zealand Food Standards Code - Maximum Residue Limits (Australia only) - Schedule 1","Australia New Zealand Food Standards Code - Maximum Residue Limits (Australia only) - Schedule 3 - Chemical Groups","Australia Standard for the Uniform Scheduling of Medicines and Poisons (SUSMP) - Appendix E (Part 2)","Australia Standard for the Uniform Scheduling of Medicines and Poisons (SUSMP) - Appendix F (Part 3)","GESAMP/EHS Composite List - GESAMP Hazard Profiles","IMO IBC Code Chapter 17: Summary of minimum requirements","IMO MARPOL 73/78 (Annex II) - List of Noxious Liquid Substances Carried in Bulk","International Agency for Research on Cancer (IARC) - Agents Reviewed by the IARC Monographs","International Chemical Secretariat (ChemSec) SIN List (*Substitute It Now!)","WHO Guidelines for Drinking-water Quality - Guideline values for chemicals that are of health significance in drinking-water"

No data for Traffic (CW: 5131-14)


Denmark Advisory list for selfclassification of dangerous substances

Substance CAS Suggested codes
sodium lauryl ether sulfate 9004- 82- 4 Carc3; R40
Mut3; R68 Rep3;



Ingredient Name CAS
sodium tripolyphosphate 7758-29-4, 15091-98-2



■ Established occupational exposure limits frequently do not take into consideration reproductive end points 
that are clearly below the thresholds for other toxic effects. Occupational reproductive guidelines (ORGs) 
have been suggested as an additional standard. These have been established after a literature search for 
reproductive no-observed-adverse effect-level (NOAEL) and the lowest-observed-adverse-effect-level (LOAEL). 
In addition the US EPA's procedures for risk assessment for hazard identification and dose-response 
assessment as applied by NIOSH were used in the creation of such limits. Uncertainty factors (UFs) have also 
been incorporated.
Ingredient ORG UF Endpoint CR Adeq TLV
ethylene glycol monobutyl ether 3.6 mg/m3 100 D NA -
trichloroethylene 5.5 mg/m3 100 D 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 time-weighted 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).



Paul Milward-Bason
17 Grandview Parade
Moolap 3221
Victoria Australia


■ 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:


■ 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.



This document is copyright. Apart from any fair dealing for the purposes of private study, research, review or
criticism, as permitted under the Copyright Act, no part may be reproduced by any process without written
permission from CHEMWATCH. TEL (+61 3) 9572 4700.


Issue Date: 29-Jul-2005

Print Date: 17-Feb-2012



This is the end of the MSDS.