Schuelke.co.in
MICROSHIELD T TRICLOSAN CLEANSERChemwatch Hazard Alert Code: 1
Issue Date: 06/10/2015
Version No: 2.1.1.1
Print Date: 13/10/2015
Safety Data Sheet according to WHS and ADG requirements Initial Date: Not Available
SECTION 1 IDENTIFICATION OF THE SUBSTANCE / MIXTURE AND OF THE COMPANY / UNDERTAKING
Product name
MICROSHIELD T TRICLOSAN CLEANSER Other means of
Relevant identified uses of the substance or mixture and uses advised against
SDS are intended for use in the workplace. For domestic-use products, refer to consumer labels.
Hand and skin antiseptic for external use.
Details of the supplier of the safety data sheet
Schulke Australia Suite 3, Level 2, 2-4 Lyon Park Road Macquarie Park 2113 NSW Australia Emergency telephone number
SECTION 2 HAZARDS IDENTIFICATION
Classification of the substance or mixture
NON-HAZARDOUS CHEMICAL. NON-DANGEROUS GOODS. According to the Model WHS Regulations and the ADG Code.
CHEMWATCH HAZARD RATINGS
2 = Moderate3 = High GHS Classification [1]
Chronic Aquatic Hazard Category 3 1. Classified by Chemwatch; 2. Classification drawn from HSIS ; 3. Classification drawn from EC Directive 1272/2008 - Annex GHS label elements
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SIGNAL WORD
Harmful to aquatic life with long lasting effects Precautionary statement(s) Prevention
Avoid release to the environment.
Precautionary statement(s) Response
Precautionary statement(s) Storage
Precautionary statement(s) Disposal
Dispose of contents/container in accordance with local regulations.
SECTION 3 COMPOSITION / INFORMATION ON INGREDIENTS
See section below for composition of Mixtures citric acid, ethanolamine salt sodium cumenesulfonate sodium lauryl ether sulfate lanolin, ethoxylated The specific chemical identity and/or exact percentage (concentration) of composition has been withheld as a trade secret.
SECTION 4 FIRST AID MEASURES
Description of first aid measures
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 Eye Contact
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. No adverse effects anticipated from normal use. If skin or hair contact occurs: Skin Contact
Flush skin and hair with running water (and soap if available). Seek medical attention in event of irritation. If fumes, aerosols or combustion products are inhaled remove from contaminated area. Other measures are usually unnecessary. For advice, contact a Poisons Information Centre or a doctor.
If swallowed do NOT induce vomiting.
If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain open airway and prevent aspiration. Observe the patient carefully. Never give liquid to a person showing signs of being sleepy or with reduced awareness; i.e. becoming unconscious Give water to rinse out mouth, then provide liquid slowly and as much as casualty can comfortably drink. Seek medical advice. Indication of any immediate medical attention and special treatment needed
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Emesis is contraindicated as the product may foam. Gastric lavage may be considered.
SECTION 5 FIREFIGHTING MEASURES
There is no restriction on the type of extinguisher which may be used. Use extinguishing media suitable for surrounding area. Special hazards arising from the substrate or mixture
Advice for firefighters
Alert Fire Brigade and tell them location and nature of hazard. Wear breathing apparatus plus protective gloves in the event of a fire. 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 to be a significant fire risk. Expansion or decomposition on heating may lead to violent rupture of containers. Decomposes on heating and may produce toxic fumes of carbon monoxide (CO). May emit acrid smoke. Decomposes on heating and produces toxic fumes of:, carbon dioxide (CO2) SECTION 6 ACCIDENTAL RELEASE MEASURES
Personal precautions, protective equipment and emergency procedures
Slippery when spilt.
Clean up all spills immediately.
Minor Spills
Place in clean drum then flush area with water.
Slippery when spilt.
Minor hazard.
Clear area of personnel. Alert Fire Brigade and tell them location and nature of hazard. Control personal contact with the substance, by using protective equipment as required. Major Spills
Prevent spillage from entering drains or water ways. Contain spill with sand, earth or vermiculite. Collect recoverable product into labelled containers for recycling. Absorb remaining product with sand, earth or vermiculite and place in appropriate containers for disposal. Wash area and prevent runoff into drains or waterways. If contamination of drains or waterways occurs, advise emergency services. Personal Protective Equipment advice is contained in Section 8 of the SDS.
SECTION 7 HANDLING AND STORAGE
Precautions for safe handling
Limit all unnecessary personal contact. Wear protective clothing when risk of exposure occurs. Use in a well-ventilated area. When handling DO NOT eat, drink or smoke.
Always wash hands with soap and water after handling. Avoid physical damage to containers. Use good occupational work practice. Observe manufacturer's storage and handling recommendations contained within this SDS.
Keep cool. Store below 25 deg.C Store in original containers. Keep containers securely sealed. Page 4 of 16
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Store in a cool, dry, well-ventilated area. Store away from incompatible materials and foodstuff containers. Protect containers against physical damage and check regularly for leaks. Observe manufacturer's storage and handling recommendations contained within this SDS.
Conditions for safe storage, including any incompatibilities
Plastic container SECTION 8 EXPOSURE CONTROLS / PERSONAL PROTECTION
OCCUPATIONAL EXPOSURE LIMITS (OEL)
Propane-1,2-diol total: (vapour & Australia Exposure particulates) / Propane-1,2-diol: particulates only Propylene glycol; (1,2-Propanediol) Revised IDLH
citric acid, ethanolamine sodium lauryl ether lanolin, ethoxylated None assigned. Refer to individual constituents. None under normal operating conditions.
Provide adequate ventilation in warehouse or closed storage areas.
No special equipment for minor exposure i.e. when handling small quantities.
Safety glasses with side shields.
Contact lenses may pose a special hazard; soft contact lenses may absorb and concentrate irritants. A written policy Eye and face
document, describing the wearing of lenses or restrictions on use, should be created for each workplace or task. This should include a review of lens absorption and adsorption for the class of chemicals in use and an account of injury experience.
Medical and first-aid personnel should be trained in their removal and suitable equipment should be readily available. In the event of chemical exposure, begin eye irrigation immediately and remove contact lens as soon as practicable. Lens should be removed at the first signs of eye redness or irritation - lens should be removed in a clean environment only after Page 5 of 16
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workers have washed hands thoroughly. [CDC NIOSH Current Intelligence Bulletin 59], [AS/NZS 1336 or national See Hand protection below Wear general protective gloves, eg. light weight rubber gloves.
See Other protection below No special equipment needed when handling small quantities.
GLOVE SELECTION INDEX
Type A-P Filter of sufficient capacity. (AS/NZS 1716 & 1715, EN 143:2000 Glove selection is based on a modified presentation of the: & 149:2001, ANSI Z88 or national equivalent) "Forsberg Clothing Performance Index".
Where the concentration of gas/particulates in the breathing zone, The effect(s) of the following substance(s) are taken into account in the approaches or exceeds the "Exposure Standard" (or ES), respiratory computer-generated selection:
protection is required.
MICROSHIELD T TRICLOSAN CLEANSER Degree of protection varies with both face-piece and Class of filter; the nature of protection varies with Type of filter.
Powered Air
* CPI - Chemwatch Performance Index A: Best Selection * - Continuous-flow; ** - Continuous-flow or positive pressure demand B: Satisfactory; may degrade after 4 hours continuous immersion C: Poor to Dangerous Choice for other than short term immersion A(All classes) = Organic vapours, B AUS or B1 = Acid gasses, B2 = Acid NOTE: As a series of factors will influence the actual performance of the
gas or hydrogen cyanide(HCN), B3 = Acid gas or hydrogen cyanide(HCN), glove, a final selection must be based on detailed observation. - E = Sulfur dioxide(SO2), G = Agricultural chemicals, K = Ammonia(NH3), * Where the glove is to be used on a short term, casual or infrequent Hg = Mercury, NO = Oxides of nitrogen, MB = Methyl bromide, AX = Low basis, factors such as "feel" or convenience (e.g. disposability), may boiling point organic compounds(below 65 degC) dictate a choice of gloves which might otherwise be unsuitable following long-term or frequent use. A qualified practitioner should be consulted.
SECTION 9 PHYSICAL AND CHEMICAL PROPERTIES
Information on basic physical and chemical properties
Clear blue-aqua viscous liquid with citrus/floral fragrance; mixes with water.
(Water = 1)
n-octanol / water
pH (as supplied)
Melting point /
freezing point (°C)
Initial boiling point
and boiling range (°C)
Flash point (°C)
Upper Explosive Limit
(dyn/cm or mN/m)
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Lower Explosive Limit
Vapour pressure (kPa)
Gas group
Solubility in water
pH as a solution (1%)
Vapour density (Air =
SECTION 10 STABILITY AND REACTIVITY
Unstable in the presence of incompatible materials.
Product is considered stable.
Hazardous polymerisation will not occur.
Conditions to avoid
SECTION 11 TOXICOLOGICAL INFORMATION
Information on toxicological effects
Not normally a hazard due to non-volatile nature of product Ingestion may result in nausea, abdominal irritation, pain and vomiting Excessive use or prolonged contact may lead to defatting, drying and irritation of sensitive skin Skin Contact
Not considered to cause discomfort through normal use.
The liquid may produce eye discomfort causing transient smarting, blinking No adverse effects anticipated from normal use. Long-term exposure to the product is not thought to produce chronic effects adverse to health (as classified by EC Directives using animal models); nevertheless exposure by all routes should be minimised as a matter of course.
Dermal (rabbit) LD50: >2000 mg/kg[1] Eye (rabbit): 100 mg - mild Oral (rat) LD50: 20000 mg/kgd[2] Eye (rabbit): 500 mg/24h - mild Skin(human):104 mg/3d Intermit Mod Skin(human):500 mg/7days mild Dermal (rabbit) LD50: >6000 mg/kg**[2] Oral (rat) LD50: 3700 mg/kgd[2] Skin (human):0.75 mg/3d-I- mild Skin (rabbit): 10% - mild Dermal (rabbit) LD50: >2000 mg/kg[1] dermal (rat) LD50: >2000 mg/kg*[2] Oral (rat) LD50: >3000 mg/kg[1] Oral (rat) LD50: 5200 mg/kg*[2] sodium lauryl ether
dermal (rat) LD50: >2000 mg/kg[1] Skin (rabbit):25 mg/24 hr moderate Page 7 of 16
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Oral (rat) LD50: >5000 mg/kg*[2] Oral (rat) LD50: 1600 mg/kge[2] Oral (rat) LD50: 1600 mg/kge[2] Oral (rat) LD50: 1600 mg/kge[2] Oral (rat) LD50: 1600 mg/kge[2] Oral (rat) LD50: 4100 mg/kg[1] Oral (rat) LD50: >21300 mg/kg**[2] Eye (rabbit): non-irritating * Skin (rabbit): non-irritating * Oral (rat) LD50: >90000 mg/kg[2] 1. Value obtained from Europe ECHA Registered Substances - Acute toxicity 2.* Value obtained from manufacturer's SDS. Unless otherwise specified data extracted from RTECS - Register of Toxic Effect of chemical Substances The material may cause skin irritation after prolonged or repeated exposure and may produce a contact dermatitis (nonallergic). This form of dermatitis is often characterised by skin redness (erythema) and swelling the epidermis.
Histologically there may be intercellular oedema of the spongy layer (spongiosis) and intracellular oedema of the The acute oral toxicity of propylene glycol is very low, and large quantities are required to cause perceptible health damage in humans. Serious toxicity generally occurs only at plasma concentrations over 1 g/L, which requires extremely high intake over a relatively short period of time. It would be nearly impossible to reach toxic levels by consuming foods or supplements, which contain at most 1 g/kg of PG. Cases of propylene glycol poisoning are usually related to either inappropriate intravenous administration or accidental ingestion of large quantities by children.The potential for long-term oral toxicity is also low. Because of its low chronic oral toxicity, propylene glycol was classified by the U. S. Food and Drug Administration as "generally recognized as safe" (GRAS) for use as a direct food additive.
Prolonged contact with propylene glycol is essentially non-irritating to the skin. Undiluted propylene glycol is minimally irritating to the eye, and can produce slight transient conjunctivitis (the eye recovers after the exposure is removed). Exposure to mists may cause eye irritation, as well as upper respiratory tract irritation. Inhalation of the propylene glycol vapours appears to present no significant hazard in ordinary applications. However, limited human experience indicates that inhalation of propylene glycol mists could be irritating to some individuals It is therefore recommended that propylene glycol not be used in applications where inhalation exposure or human eye contact with the spray mists of these materials is likely, such as fogs for theatrical productions or antifreeze solutions for emergency eye wash stations.
Propylene glycol is metabolised in the human body into pyruvic acid (a normal part of the glucose-metabolism process, readily converted to energy), acetic acid (handled by ethanol-metabolism), lactic acid (a normal acid generally abundant during digestion), and propionaldehyde (a potentially hazardous substance).
Propylene glycol shows no evidence of being a carcinogen or of being genotoxic.
Research has suggested that individuals who cannot tolerate propylene glycol probably experience a special form of irritation, but that they only rarely develop allergic contact dermatitis. Other investigators believe that the incidence of allergic contact dermatitis to propylene glycol may be greater than 2% in patients with eczema.
One study strongly suggests a connection between airborne concentrations of propylene glycol in houses and development of asthma and allergic reactions, such as rhinitis or hives in children Another study suggested that the concentrations of PGEs (counted as the sum of propylene glycol and glycol ethers) in indoor air, particularly bedroom air, is linked to increased risk of developing numerous respiratory and immune disorders in children, including asthma, hay fever, eczema, and allergies, with increased risk ranging from 50% to 180%. This concentration has been linked to use of water-based paints and water-based system cleansers.
Patients with vulvodynia and interstitial cystitis may be especially sensitive to propylene glycol. Women suffering with yeast infections may also notice that some over the counter creams can cause intense burning. Post menopausal women who require the use of an eostrogen cream may notice that brand name creams made with propylene glycol often create extreme, uncomfortable burning along the vulva and perianal area. Additionally, some electronic cigarette users who inhale propylene glycol vapor may experience dryness of the throat or shortness of breath . As an alternative, some suppliers will put Vegetable Glycerin in the "e-liquid" for those who are allergic (or have bad reactions) to propylene glycol.
Adverse responses to intravenous administration of drugs which use PG as an excipient have been seen in a number of people, particularly with large dosages thereof. Responses may include "hypotension, bradycardia.
QRS and T abnormalities on the ECG, arrhythmia, cardiac arrest, serum hyperosmolality, lactic acidosis, and haemolysis". A high percentage (12% to 42%) of directly-injected propylene glycol is eliminated/secreted in urine unaltered depending on dosage, with the remainder appearing in its glucuronide-form. The speed of renal filtration decreases as dosage increases, which may be due to propylene glycol's mild anesthetic / CNS-depressant Page 8 of 16
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-properties as an alcohol. In one case, intravenous administration of propylene glycol-suspended nitroglycerin to an elderly man may have induced coma and acidosis.
Propylene glycol is an approved food additive for dog food under the category of animal feed and is generally recognized as safe for dogs with an LD50 of 9 mL/kg. The LD50 is higher for most laboratory animals (20 mL/kg) Similarly, propylene glycol is an approved food additive for human food as well. The exception is that it is prohibited for use in food for cats due to links to Heinz body anemia.
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.
Triclosan is readily absorbed in humans by the skin , through the oral mucous membranes (Lin 2000), through the gastrointestinal tract , and through mucosal tissues following intra-vaginal administration Triclosan was excreted into the urine and faeces essentially unchanged with some evidence of conjugation.
Triclosan has been detected in the liver and fat. In a 13-week dermal subchronic study of triclosan in rats signs of severe dermal irritation were seen in the treated groups, especially in the high-dose group. These signs were erythema, dema, desquamation, and eschar formation.
Microscopically, hyperplasia of sebaceous glands, inflammation, and focal necrosis were seen on the skin of treated animals. The dermal effects were reversible during the recovery period. There were no systemic effects that could be treatment-related, although liver masses were observed in two treated animals .
Skin Sensitisation:
Subchronic dermal studies were conducted by applying 0.4 mL of a 2.5% or 5% suspension of triclosan in gum
Arabic five times each week for four weeks to the shaved backs of male and female rats (5/sex) No local dermal irritation or systemic toxicity was reported. Human Skin Irritation and Sensitisation:
Studies were conducted on the skin of human volunteers to determine the compatibility of dermal application of triclosan . The subjects were topically treated with 0.5% triclosan in 1% soap solution according to the Draize method . In the soap control, 0/50 subjects had sensitization or irritation, while 2/50 subjects receiving 0.5% triclosan had a very mild reaction. The conclusion was that triclosan was not a sensitiser or irritant. Reproductive/Developmental Toxicity:
Reproductive studies were cited in which a NOEL of 50 mg/kg/day was reported for the dams based on effects on the pups. A NOEL based on developmental outcomes was listed as 150-300 mg/kg/day ; however, no reproductive tract or fertility abnormalities were reported Oral administration of triclosan to pregnant mice (gestation days 1-16) resulted in maternal and foetal toxicity at 50 and 100 mg/kg. The authors report no indications of teratogenesis in the mice, or in rats (50 and 100 mg/kg) or in rabbits (10, 25, 50, 100 mg/kg) following administration during gestation. In a two-generational dose study conducted in rats at doses of 0, 300, 1000, and 3000 ppm in the diet (equivalent to 0, 15, 50, 150 mg/kg), toxicity was noted in the neonates from dams consuming the highest dose, and reductions in survival were seen in f1 and f2 populations with increased kidney dilations. Triclosan has also been detected in human breast milk, and is probably associated with the fat due to its high Triclosan has also been shown to inhibit cell growth in MCF-7 and SK Br-3 human breast cancer cell lines resulting in cellular apoptosis . The authors demonstrated that triclosan reversibly inhibited mammalian fatty acid synthesis (enzyme from SK Br-3 cells and goose uropygial gland). Triclosan was shown also to induce apoptosis in Smulow- Glickman human gingival epithelial cells in vitro Genetic toxicity:The results of 18 mutagenicity tests were summarised, of which 13 were conducted by industry
and not reported in the literature. Only one test indicated that triclosan was a mutagen (mammalian spot test), and a repeat of that study was negative. Endocrine disruption: There have been several reports on endocrine disruptor activity of triclosan. In one study
triclosan was weakly androgenic as evidenced by altered fin length and sex ratio in Japanese Medaka fish starting at age 2 days. Additional studies indicated that triclosan was toxic and had weak oestrogenic activity in Medaka .
Oestrogen antagonism was induced in frogs following intraperitoneal administration of high doses of triclosan, while lower doses reduced testosterone in male frogs . Additional studies with frogs showed that triclosan bound to thyroid hormone receptor In another study triclosan exhibited oestrogenic activity as evidenced by competitive binding with estradiol at the estrogen receptor and supported growth of the oestrogen-dependent MCF-7 cell line. The same study demonstrated triclosan bound to the rat androgen receptor, demonstrating androgenic activity. Nomination Profile Supporting Information for Toxicological Evaluation by the National Toxicology Program July Page 9 of 16
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Side-reactions during manufacture of the parent compound may result in the production of trace amounts of polyhalogenated aromatic hydrocarbon(s). Halogenated phenols, and especially their alkali salts, can condense above 300 deg. C . to form polyphenoxyphenols or, in a very specific reaction, to form dibenzo-p-dioxins Polyhalogenated aromatic hydrocarbons (PHAHs) comprise two major groups. The first group represented by the halogenated derivatives of dibenzodioxins (the chlorinated form is PCDD), dibenzofurans (PCDF) and biphenyls (PCB) exert their toxic effect (as hepatoxicants, reproductive toxicants, immunotoxicants and procarcinogens) by interaction with a cytostolic protein known as the Ah receptor. In guinea pigs the Ah receptor is active in a mechanism which "pumps" PHAH into the cell whilst in humans the reverse appears to true. This, in part, may account for species differences often cited in the literature. This receptor exhibits an affinity for the planar members of this group and carries these to the cellular nucleus where they bind, reversibly, to specific genomes on DNA. This results in the regulation of the production of certain proteins which elicit the toxic response. The potency of the effect is dependent on the strength of the original interaction with the Ah receptor and is influenced by the degree of substitution by the halogen and the position of such substitutions on the parent compound.
The most potent molecule is 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) while the coplanar PCBs (including mono-ortho coplanars) possess approximately 1% of this potency. Nevertheless, all are said to exhibit "dioxin-like" behaviour and in environmental and health assessments it has been the practice to assign each a The most subtle and important biological effects of the PHAHs are the effects on endocrine hormones and vitamin homeostasis. TCDD mimics the effect of thyroxin (a key metamorphosis signal during maturation) and may disrupt patterns of embryonic development at critical stages. Individuals from exposed wildlife populations have been observed to have altered sexual development, sexual dysfunction as adults and immune system suppression.
Immunotoxic effects of the PHAHs (including the brominated congener, PBB) have been the subject of several studies. No clear pattern emerges in human studies however with T-cell numbers and function (a blood marker for immunological response) increasing in some and decreasing in others. Developmental toxicity (e.g. cleft palate, hydronephrosis) occurs in relatively few species; functional alterations following TCDD exposure leads to deficits in cognitive functions in monkeys and to adverse effects in the male reproductive system of rats. Three incidences have occurred which have introduced abnormally high levels of dioxin or dioxin-like congeners to humans. The explosion at a trichlorophenol-manufacturing plant in Seveso, Italy distributed TCDD across a large area of the country-side, whilst rice-oil contaminated with heat-transfer PCBs (and dioxin-like contaminants) has been consumed by two groups, on separate occasions (one in Yusho, Japan and another in Yu-cheng, Taiwan). The only symptom which can unequivocally be related to all these exposures is the development of chloracne, a disfiguring skin condition, following each incident. Contaminated oil poisonings also produced eye-discharge, swelling of eyelids and visual disturbances. The Babies born up to 3 years after maternal exposure (so-called "Yusho-babies") were characteristically brown skinned, coloured gums and nails and (frequently) produced eye-discharges. Delays in intellectual development have been noted. It has been estimated that Yu-cheng patients consumed an average level of 0.06 mg/kg body weight/day total PCB and 0.0002 mg/kg/day of PCDF before the onset of symptoms after 3 months. When the oil was withdrawn after 6 months they had consumed 1 gm total PCB containing 3.8 mg PCDF. Taiwanese patients consumed 10 times as much contaminated oil as the Japanese patients (because of later withdrawal); however since PCB/PCDF concentration in the Japanese oil was 10 times that consumed in Taiwan, patients from both countries consumed about the same amount of PCBs/PCDFs.
Preliminary data from the Yusho cohort suggests a six-fold excess of liver cancer mortality in males and a three-fold excess in women. Recent findings from Seveso indicate that the biological effects of low level exposure (BELLEs), experienced by a cohort located at a great distance from the plant, may be hormetic, i.e. may be protective AGAINST the development of cancer. The PHAHs do not appear to be genotoxic - they do not alter the integrity of DNA. This contrasts with the effects of the many polycyclic aromatic hydrocarbons (PAHs) (or more properly, their reactive metabolites). TCDD induces carcinogenic effects in the laboratory in all species, strains and sexes tested. These effects are dose-related and occur in many organs. Exposures as low as 0.001 ug/kg body weight/day produce carcinoma. Several studies implicate PCBs in the development of liver cancer in workers as well as multi-site cancers in animals. The second major group of PHAH consists of the non-planar PCB congeners which possess two or more ortho-substituted halogens. These have been shown to produce neurotoxic effects which are thought to reduce the concentration of the brain neurotransmitter, dopamine, by inhibiting certain enzyme-mediated processes.
The specific effect elicited by both classes of PHAH seems to depend on the as much on the developmental status of the organism at the time of the exposure as on the level of exposure over a lifetime. NOTE: Some jurisdictions require that health surveillance be conducted on workers occupationally exposed to
polycyclic aromatic hydrocarbons. Such surveillance should emphasise demography, occupational and medical history health advice, including recognition of photosensitivity and skin changes physical examination if indicated records of personal exposure including photosensitivity The material may cause skin irritation after prolonged or repeated exposure and may produce a contact dermatitis (nonallergic). This form of dermatitis is often characterised by skin redness (erythema) and swelling epidermis.
Histologically there may be intercellular oedema of the spongy layer (spongiosis) and intracellular oedema of the Page 10 of 16
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[Van Waters Rogers]* [Thompson Research] ** No significant acute toxicological data identified in literature search. for alkyl sulfates; alkane sulfonates and alpha-olefin sulfonates Most chemicals of this category are not defined substances, but mixtures of homologues with different alkyl chain lengths. Alpha-olefin sulfonates are mixtures of alkene sulfonate and hydroxyl alkane sulfonates with the sulfonate group in the terminal position and the double bond, or hydroxyl group, located at a position in the vicinity of the sulfonate group. Common physical and/or biological pathways result in structurally similar breakdown products, and are, together with the surfactant properties, responsible for similar environmental behavior and essentially identical hazard profiles with regard to human health.
Acute toxicity: These substances are well absorbed after ingestion; penetration through the skin is however poor.
After absorption, these chemicals are distributed mainly to the liver.
Acute oral LD50 values of alkyl sulfates in rats and/or mice were (in mg/kg): C10-16-, and C12-; 1000-2000 C12-14, C12-15, C12-16, C12-18 and C16-18-; >2000 C14-18, C16-18-; >5000 The clinical signs observed were non-specific (piloerection, lethargy, decreased motor activity and respiratory rate, diarrhoea). At necropsy the major findings were irritation of the gastrointestinal tract and anemia of inner organs.
Based on limited data, the acute oral LD50 values of alkane sulfonates and alpha-olefin sulfonates of comparable chain lengths are assumed to be in the same range.
The counter ion does not appear to influence the toxicity in a substantial way.
Acute dermal LD50 values of alkyl sulfates in rabbits (mg/ kg): C12-13 and C10-16-;>500 Apart from moderate to severe skin irritation, clinical signs included tremor, tonic-clonic convulsions, respiratory failure, and body weight loss in the study with the C12- alkyl sulfate and decreased body weights after administration of the C10-16- alkyl sulfates. No data are available for alkane sulfonates but due to a comparable metabolism and effect concentrations in long-term studies effect concentrations are expected to be in the same range as found for alkyl sulfates.
There are no data available for acute inhalation toxicity of alkyl sulfates, alkane sulfonates or alpha-olefin In skin irritation tests using rabbits (aqueous solutions, OECD TG 404): C8-14 and C8-16 (30%), C12-14 (90%), C14-18 (60%)- corrosive Under occlusive conditions: C12, and C12-14 (25%), C12-15-, C13-15 and C15-16 (5-7%) - moderate to strong irritants Comparative studies investigating skin effects like transepidermal water loss, epidermal electrical conductance, skin swelling, extraction of amino acids and proteins or development of erythema in human volunteers consistently showed a maximum of effects with C12-alkyl sulfate, sodium; this salt is routinely used as a positive internal control giving borderline irritant reactions in skin irritation studies performed on humans. As the most irritant alkyl sulfate it can be concluded that in humans 20% is the threshold concentration for irritative effects of alkyl sulfates in general. No data were available with regard to the skin irritation potential of alkane sulfonates. Based on the similar chemical structure they are assumed to exhibit similar skin irritation properties as alkyl sulfates or alpha- olefin sulfonates of comparable chain lengths.
In eye irritation tests, using rabbits, C12-containing alkyl sulfates (>10% concentration) were severely irritating and produced irreversible corneal effects. With increasing alkyl chain length, the irritating potential decreases, and C16-18 alkyl sulfate sodium, at a concentration of 25%, was only a mild irritant.
Concentrated C14-16- alpha-olefin sulfonates were severely irritating, but caused irreversible effects only if applied as undiluted powder. At concentrations below 10% mild to moderate, reversible effects, were found. No data were available for alkane sulfonates Alkyl sulfates and C14-18 alpha-olefin sulfonates were not skin sensitisers in animal studies. No reliable data were available for alkane sulfonates. Based on the similar chemical structure, no sensitisation is expected.
However anecdotal evidence suggests that sodium lauryl sulfate causes pulmonary sensitisation resulting in hyperactive airway dysfunction and pulmonary allergy accompanied by fatigue, malaise and aching. Significant symptoms of exposure can persist for more than two years and can be activated by a variety of non-specific environmental stimuli such as a exhaust, perfumes and passive smoking.
Absorbed sulfonates are quickly distributed through living systems and are readily excreted. Toxic effects may result from the effects of binding to proteins and the ability of sulfonates to translocate potassium and nitrate (NO3-) ions from cellular to interstitial fluids. Airborne sulfonates may be responsible for respiratory allergies and, in some instances, minor dermal allergies. Repeated skin contact with some sulfonated surfactants has produced sensitisation dermatitis in predisposed individuals Page 11 of 16
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Repeat dose toxicity: After repeated oral application of alkyl sulfates with chain lengths between C12 and C18,
the liver was the only target organ for systemic toxicity. Adverse effects on this organ included an increase in liver weight, enlargement of liver cells, and elevated levels of liver enzymes. The LOAEL for liver toxicity (parenchymal hypertrophy and an increase in comparative liver weight) was 230 mg/kg/day (in a 13 week study with C16-18 alkyl sulfate, sodium). The lowest NOAEL in rats was 55 mg/kg/day (in a 13 week study with C12-alkyl sulfate, sodium).
C14- and C14-16-alpha-olefin sulfonates produced NOAELs of 100 mg/kg/day (in 6 month- and 2 year studies). A reduction in body weight gain was the only adverse effect identified in these studies.
No data were available with regard to the repeated dose toxicity of alkane sulfonates. Based on the similarity of metabolic pathways between alkane sulfonates, alkyl sulfates and alkyl-olefin sulfonates, the repeated dose toxicity of alkane sulfonates is expected to be similar with NOAEL and LOAEL values in the same range as for alkyl sulfates and alpha-olefin sulfonates, i.e. 100 and 200-250 mg/kg/day, respectively, with the liver as potential target organ.
Genotoxicity: Alkyl sulfates of different chain lengths and with different counter ions were not mutagenic in
standard bacterial and mammalian cell systems both in the absence and in the presence of metabolic activation.
There was also no indication for a genotoxic potential of alkyl sulfates in various in vivo studies on mice (micronucleus assay, chromosome aberration test, and dominant lethal assay).
alpha-Olefin sulfonates were not mutagenic in the Ames test, and did not induce chromosome aberrations in vitro.
No genotoxicity data were available for alkane sulfonates. Based on the overall negative results in the genotoxicity assays with alkyl sulfates and alpha-olefin sulfonates, the absence of structural elements indicating mutagenicity, and the overall database on different types of sulfonates, which were all tested negative in mutagenicity assays, a genotoxic potential of alkane sulfonates is not expected.
Carcinogenicity: Alkyl sulfates were not carcinogenic in feeding studies with male and female Wistar rats fed
diets with C12-15 alkyl sulfate sodium for two years (corresponding to doses of up to 1125 mg/kg/day). alpha-Olefin sulfonates were not carcinogenic in mice and rats after dermal application, and in rats after oral No carcinogenicity studies were available for the alkane sulfonates.
Reproductive toxicity: No indication for adverse effects on reproductive organs was found in various oral studies
with different alkyl sulfates. The NOAEL for male fertility was 1000 mg/kg/day for sodium dodecyl sulfate. In a study using alpha-olefin sulfonates in male and female rats, no adverse effects were identified up to 5000 ppm.
Developmental toxicity: In studies with various alkyl sulfates (C12 up to C16-18- alkyl) in rats, rabbits and mice,
effects on litter parameters were restricted to doses that caused significant maternal toxicity (anorexia, weight loss, and death).
The principal effects were higher foetal loss and increased incidences of total litter losses. The incidences of malformations and visceral and skeletal anomalies were unaffected apart from a higher incidence of delayed ossification or skeletal variation in mice at > 500 mg/kg bw/day indicative of a delayed development. The lowest reliable NOAEL for maternal toxicity was about 200 mg/kg/day in rats, while the lowest NOAELs in offspring were 250 mg/kg/day in rats and 300 mg/kg/day for mice and rabbits.
For alpha-olefin sulfonates (C14-16-alpha-olefin sulfonate, sodium) the NOAEL was 600 mg/kg/day both for maternal and developmental toxicity.
No data were available for the reproductive and developmental toxicity of alkane sulfonates. Based on the available data, the similar toxicokinetic properties and a comparable metabolism of the alkyl sulfates and alkane sulfonates, alkane sulfonates are not considered to be developmental toxicants.
Although the database for category members with C<12 is limited, the available data are indicating no risk as the substances have comparable toxicokinetic properties and metabolic pathways. In addition, longer-term studies gave no indication for adverse effects on reproductive organs with different alkyl sulfates Toxicological data are available and well documented for representative toluenesulfonates, xylenesulfonates and cumenesulfonates (including sodium, potassium, ammonium and calcium salts). These data demonstrate that hydrotropes have a low order of acute toxicity by all relevant routes (LC50s range from 100s to 1000s mg/kg), are not genotoxic in vitro or in vivo, show no evidence of a carcinogenic response (or any other systemic toxicity) in 2-year dermal exposure studies, and failed to induce developmental, teratogenic or fertility (sex organ) effects.
Adverse effects after repeated long term dosing of hydrotropes to animals included epidermal hyperplasia at the site of application in dermal studies, and decreased relative spleen weight in females in oral studies. The critical adverse effect and corresponding systemic NOAEL is 763 mg a.i./kg bw based upon decreased relative spleen weight in female rats in a 90-day oral study. The NOAEL for local effects, based on epidermal hyperplasia at the site of application, was 440 mg a.i./kg bw for mice in 90-day dermal studies.
Hydrotropes can be classified as a negligible-to-slight irritant to skin and a slight-to-moderate irritant to eyes. The irritation potential of aqueous solutions of hydrotropes depends on concentration, and the irritation is lessened with rinsing. Hydrotropes are not considered to be skin sensitisers.
HERA Report (Hydrotropes) September 2005 Hydrotropes in this category were assessed for mutagen/ genotoxic potential in a variety of assays including the mouse micronucleus, Ames, mouse lymphoma, sister chromatid exchange and chromosome aberration assays. No positive results were seen in vitro or in vivo in any of the studies. For both mice and rats exposed dermally for two years, there was no evidence of carcinogenic potential.
Examination of the sex organs (such as prostate, testes or ovaries) from animals in 90-day feeding studies and 90-day and two year dermal studies yielded no evidence to suggest that these chemicals have an adverse affect Page 12 of 16
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on the reproductive organs.
* Nease Corporation MSDS No significant acute toxicological data identified in literature search. Alkyl ether sulfates (alcohol or alkyl ethoxysulfates) (AES) (syn: AAASD ,alkyl alcohol alkoxylate sulfates, SLES) are generally classified according to Comité Européen des Agents de Surface et leurs Intermédiaires Organiques (CESIO) as Irritant (Xi) with the risk phrases R38 (Irritating to skin) and R36 (Irritating to eyes). An exception has been made for AES (2-3E0) in a concentration of 70-75% where R36 is substituted with R41 (Risk of serious damage to eyes).
AES are not included in Annex 1 of the list of dangerous substances of Council Directive 67/548/EEC.
Acute toxicity: AES are of low acute toxicity. Neat AES are irritant to skin and eyes. The irritation potential of AES
containing solutions depends on concentration. Local dermal effects due to direct or indirect skin contact with AES containing solutions in hand-washed laundry or hand dishwashing are not of concern because AES is not a contact sensitiser and AES is not expected to be irritating to the skin at in-use concentrations. The available repeated dose toxicity data demonstrate the low toxicity of AES. Also, they are not considered to be mutagenic, genotoxic or carcinogenic, and are not reproductive or developmental toxicants. The consumer aggregate exposure from direct and indirect skin contact as well as from the oral route via dishware residues results in an estimated total body burden of 29 ug /kg bw/day.
AES are easily absorbed in the intestine in rats and humans after oral administration. Radiolabelled C11 AE3S and C12 AE3S were extensively metabolized in rats and most of the 14C-activity was eliminated via the urine and expired air independently of the route of administration (oral, intraperitoneal or intravenous). The main urinary metabolite from C11 AE3S is propionic acid-3-(3EO)-sulfate. For C12 and C16 AE3S, the main metabolite is acetic acid-2-(3EO)-sulfate. The alkyl chain appears to be oxidised to CO2 which is expired. The EO-chain seems to be resistant to metabolism.
AES are better tolerated on the skin than, e.g., alkyl sulfates and it is generally agreed that the irritancy of AES is lower than that of other anionic surfactants. Alkyl chain lengths of 12 carbon atoms are considered to be more irritating to the skin compared to other chain lengths. The skin irritating properties of AES normally decrease with increasing level of ethoxylation. Undiluted AES should in general be considered strongly irritating. Even at concentrations of 10% moderate to strong effects can be expected. However, only mild to slight irritation was observed when a non-specified AES was applied at 1% to the skin.
Subchronic toxicity: A 90-day subchronic feeding study in rats with 1% of AE3S or AE6S with alkyl chain lengths
of C12-14 showed only an increased liver/body weight ratio. In a chronic oral study with a duration of 2 years, SODIUM LAURYL ETHER
doses of C12-AE3S of 0.005 - 0.05% in the diet or drinking water had no effects on rats. The concentration of 0.5% sometimes resulted in increased kidney or liver weight.
Subchronic 21-day repeat dose dietary studies showed low toxicity of compounds with carbon lengths of C12-15, C12-14 and C13-15 with sodium or ammonium alkyl ethoxylates with POE (polyoxyethylene) n=3. One study indicated that C16-18 POE n=18 had comparable low toxicity. No-observed-adverse-effect levels (NOAELs) range from 120 to 468 mg/kg/day, similar to a NOAEL from a 90-day rat gavage study with NaC12-14 POE n=2(CAS RN 68891-38-3), which was reported to be 225 mg/kg/day. In addition, another 90-day repeat dose dietary study with NaC12-15 POE n=3 (CAS RN 68424-50-0) resulted in low toxicity, with a NOAEL of greater than approximately 50 mg/kg/day (calculated based on dose of 1000 ppm in diet). Effects were usually related to hepatic hypertrophy, increased liver weight, and related increases in haematological endpoints related to liver enzyme induction.
Reproductive and developmental toxicity: No evidence of reproductive and teratogenic effects was seen in a
two-generation study in rats fed with a mixture (55:45) of AES and linear alkylbenzene sulfonates. Dietary levels of 0.1, 0.5, and 1% were administered to the rats either continuously or during the period of major organogenesis during six pregnancies. No changes in reproductive or embryogenic parameters were observed.
Based on this study an overall no-observed-adverse-effect level (NOAEL) for systemic effects was 0.1%, which was 86.6 mg/kg/day for the F0 generation, and 149.5 mg/kg/day for the F1 generation. The NOAEL of 86.6 mg/kg/day was selected as the toxicology endpoint for the chronic risk assessment for the sulfate derivatives.
Carcinogenicity: Chronic dietary studies conducted with rats showed no incidence of cancer and no effects at the
concentrations tested (lowest dose tested was ca 75 mg/kg/day).
NOTE: Some products containing AES/ SLES have been found to also contain traces (up to 279 ppm) of 1,4-dioxane; this is formed as a by-product during the ethoxylation step of its synthesis. The U.S. Food and Drug Administration recommends that these levels be monitored.The U.S. Environmental Protection Agency classifies 1,4-dioxane to be a probable human carcinogen (not observed in epidemiological studies of workers using the compound, but resulting in more cancer cases in controlled animal studies), and a known irritant with a no-observed- adverse-effects level of 400 milligrams per cubic meter at concentrations significantly higher than those found in commercial products. Under Proposition 65, 1,4-dioxane is classified in the U.S. state of California to cause cancer. The FDA encourages manufacturers to remove 1,4-dioxane, though it is not required by federal law.
The material may produce moderate eye irritation leading to inflammation. Repeated or prolonged exposure to irritants may produce conjunctivitis.
Human beings have regular contact with alcohol ethoxylates through a variety of industrial and consumer products such as soaps, detergents, and other cleaning products . Exposure to these chemicals can occur through ingestion, inhalation, or contact with the skin or eyes. Studies of acute toxicity show that volumes well above a reasonable intake level would have to occur to produce any toxic response. Moreover, no fatal case of poisoning with alcohol ethoxylates has ever been reported. Multiple studies investigating the acute toxicity of alcohol ethoxylates have shown that the use of these compounds is of low concern in terms of oral and dermal toxicity . Clinical animal studies indicate these chemicals may produce gastrointestinal irritation such as ulcerations of the stomach, pilo-erection, diarrhea, and lethargy. Similarly, slight to severe irritation of the skin or eye was generated Page 13 of 16
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when undiluted alcohol ethoxylates were applied to the skin and eyes of rabbits and rats. The chemical shows no indication of being a genotoxin, carcinogen, or mutagen (HERA 2007). No information was available on levels at which these effects might occur, though toxicity is thought to be substantially lower than that of nonylphenol Alcohol ethoxylates are according to CESIO (2000) classified as Irritant or Harmful depending on the number of EO < 5 gives Irritant (Xi) with R38 (Irritating to skin) and R41 (Risk of serious damage to eyes) EO > 5-15 gives Harmful (Xn) with R22 (Harmful if swallowed) - R38/41 EO > 15-20 gives Harmful (Xn) with R22-41 >20 EO is not classified (CESIO 2000) Oxo-AE, C13 EO10 and C13 EO15, are Irritating (Xi) with R36/38 (Irritating to eyes and skin) .
AE are not included in Annex 1 of the list of dangerous substances of the Council Directive 67/548/EEC In general, alcohol ethoxylates (AE) are readily absorbed through the skin of guinea pigs and rats and through the gastrointestinal mucosa of rats. AE are quickly eliminated from the body through the urine, faeces, and expired air (CO2).Orally dosed AE was absorbed rapidly and extensively in rats, and more than 75% of the dose was absorbed. When applied to the skin of humans, the doses were absorbed slowly and incompletely (50% absorbed in 72 hours). Half of the absorbed surfactant was excreted promptly in the urine and smaller amounts of AE appeared in the faeces and expired air (CO2) ). The metabolism of C12 AE yields PEG, carboxylic acids, and CO2 as metabolites. The LD50 values after oral administration to rats range from about 1-15 g/kg body weight indicating a low to moderate acute toxicity.
The ability of nonionic surfactants to cause a swelling of the stratum corneum of guinea pig skin has been studied.
The swelling mechanism of the skin involves a combination of ionic binding of the hydrophilic group as well as hydrophobic interactions of the alkyl chain with the substrate. One of the mechanisms of skin irritation caused by surfactants is considered to be denaturation of the proteins of skin. It has also been established that there is a connection between the potential of surfactants to denature protein in vitro and their effect on the skin. Nonionic surfactants do not carry any net charge and, therefore, they can only form hydrophobic bonds with proteins. For this reason, proteins are not deactivated by nonionic surfactants, and proteins with poor solubility are not solubilized by nonionic surfactants. A substantial amount of toxicological data and information in vivo and in vitro demonstrates that there is no evidence for alcohol ethoxylates (AEs) being genotoxic, mutagenic or carcinogenic.
No adverse reproductive or developmental effects were observed. The majority of available toxicity studies revealed NOAELs in excess of 100 mg/kg bw/d but the lowest NOAEL for an individual AE was established to be 50 mg/kg bw/day. This value was subsequently considered as a conservative, representative value in the risk assessment of AE. The effects were restricted to changes in organ weights with no histopathological organ changes with the exception of liver hypertrophy (indicative of an adaptive response to metabolism rather than a toxic effect). It is noteworthy that there was practically no difference in the NOAEL in oral studies of 90-day or 2 years of duration in rats. A comparison of the aggregate consumer exposure and the systemic NOAEL (taking into account an oral absorption value of 75%) results in a Margin of Exposure of 5,800. Taking into account the conservatism in the exposure assessment and the assigned systemic NOAEL, this margin of exposure is considered more than adequate to account for the inherent uncertainty and variability of the hazard database and inter and intra-species extrapolations.
AEs are not contact sensitisers. Neat AE are irritating to eyes and skin. The irritation potential of aqueous solutions of AEs depends on concentrations. Local dermal effects due to direct or indirect skin contact in certain use scenarios where the products are diluted are not of concern as AEs are not expected to be irritating to the skin at in-use concentrations. Potential irritation of the respiratory tract is not a concern given the very low levels of airborne AE generated as a consequence of spray cleaner aerosols or laundry powder detergent dust.
In summary, the human health risk assessment has demonstrated that the use of AE in household laundry and cleaning detergents is safe and does not cause concern with regard to consumer use.
* [Emery Chemical Co.] No significant acute toxicological data identified in literature search. Serious Eye
STOT - Single
Respiratory or Skin
STOT - Repeated
– Data required to make classification available – Data available but does not fill the criteria for classification – Data Not Available to make classification SECTION 12 ECOLOGICAL INFORMATION
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citric acid,
sodium lauryl ether
DO NOT discharge into sewer or waterways.
Persistence and degradability
LOW (LogKOW = -8.995) LOW (LogKOW = -1.38) Mobility in soil
LOW (KOC = 18420) SECTION 13 DISPOSAL CONSIDERATIONS
Waste treatment methods
Recycle wherever possible or consult manufacturer for recycling options. Product / Packaging
Consult State Land Waste Management Authority for disposal. Bury residue in an authorised landfill. Recycle containers if possible, or dispose of in an authorised landfill. SECTION 14 TRANSPORT INFORMATION
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Land transport (ADG): NOT REGULATED FOR TRANSPORT OF DANGEROUS GOODS
Air transport (ICAO-IATA / DGR): NOT REGULATED FOR TRANSPORT OF DANGEROUS GOODS
Sea transport (IMDG-Code / GGVSee): NOT REGULATED FOR TRANSPORT OF DANGEROUS GOODS
SECTION 15 REGULATORY INFORMATION
Safety, health and environmental regulations / legislation specific for the substance or mixture
PROPYLENE GLYCOL(57-55-6) IS FOUND ON THE FOLLOWING REGULATORY LISTS
Australia Exposure Standards Australia Inventory of Chemical Substances (AICS) Australia Hazardous Substances Information System - Consolidated Lists 2,4,4'-TRICHLORO-2'-HYDROXYDIPHENYL ETHER(3380-34-5) IS FOUND ON THE FOLLOWING REGULATORY LISTS
Australia Hazardous Substances Information System - Consolidated Lists Australia Inventory of Chemical Substances (AICS) SODIUM CUMENESULFONATE(28348-53-0) IS FOUND ON THE FOLLOWING REGULATORY LISTS
Australia Inventory of Chemical Substances (AICS) SODIUM LAURYL ETHER SULFATE(9004-82-4) IS FOUND ON THE FOLLOWING REGULATORY LISTS
Australia Inventory of Chemical Substances (AICS) HYDROXYETHYLCELLULOSE(9004-62-0) IS FOUND ON THE FOLLOWING REGULATORY LISTS
Australia Inventory of Chemical Substances (AICS) LANOLIN, ETHOXYLATED(61790-81-6) IS FOUND ON THE FOLLOWING REGULATORY LISTS
Australia Inventory of Chemical Substances (AICS) WATER(7732-18-5) IS FOUND ON THE FOLLOWING REGULATORY LISTS
Australia Inventory of Chemical Substances (AICS) N (propylene glycol; water; hydroxyethylcellulose; lanolin, ethoxylated; sodium cumenesulfonate; 2,4,4'-trichloro- N (hydroxyethylcellulose; lanolin, ethoxylated) New Zealand - NZIoC Philippines - PICCS Y = All ingredients are on the inventory N = Not determined or one or more ingredients are not on the inventory and are not exempt from listing(see specific ingredients in brackets) SECTION 16 OTHER INFORMATION
Ingredients with multiple cas numbers
112099-35-1, 164325-69-3, 261921-78-2, 3380-34-5, 88032-08-0 Page 16 of 16
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15763-76-5, 28348-53-0, 32073-22-6, 65130-69-0 11121-04-3, 113096-26-7, 115284-60-1, 116958-77-1, 12627-22-4, 12627-23-5, 1335-72-4, 1335-73-5, 3088-31-1, 32057-62-8, sodium lauryl ether 37325-23-8, 39390-84-6, 39450-08-3, 42504-27-8, 51059-21-3, 51286-51-2, 53663-56-2, 56572-89-5, 57762-43-3, 57762-59-1, 66747-17-9, 68585-34-2, 68891-38-3, 73651-68-0, 74349-47-6, 76724-02-2, 9004-82-4, 91648-56-5, 95508-27-3, 98112-64-2 lanolin, ethoxylated 61790-81-6, 8039-09-6 Classification of the preparation and its individual components has drawn on official and authoritative sources as well as independent review by the Chemwatch Classification committee using available literature references.
A list of reference resources used to assist the committee may be found at: www.chemwatch.net The (M)SDS is a Hazard Communication tool and should be used to assist in the Risk Assessment. Many factors determine whether the reported Hazards are Risks in the workplace or 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.
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end of SDS
Source: http://www.schuelke.co.in/media-au-en/docs/SDS/MICROSHIELD-australia-SDS/MS-Triclosan_SDS.pdf
Medical abortion: teratogenic effects of misoprostol
Gynaecology Case Reports 323 Declaration of interest: Th e authors report no confl icts of interest. Th e cies continued to term, resulting in three infants (14.3%) born with authors alone are responsible for the content and writing of the paper. congenital malformations (Barnett 1996). Nevertheless, in 1997, a study involving 86 pregnant women who
rotherhamhospice.org.uk
Metabolic or drug induced: Haloperidol ORAL THRUSH: 500micrograms to 5mg oral nocte, ( ), OR: Good oral hygiene, and: Miconazole oral gel 24mg/ml Levomepromazine, oral or sc, from 6.25 mg od. qds treatment should be continued for 48hours after lesions have healed. Fluconazole 50mg daily Intestinal obstruction - contact Specialist Palliative