Tris(2-chlorethyl)-phosphat

Organophosphate

Waste-water effluent contaminant

log Kow = 1.78

log Kow = 1.43

1.78

0.5

1.425 at 68 °F (NTP, 1992) - Denser than water; will sink

1.39 g/cu cm at 25 °C

Relative density (water = 1): 1.4

1.39 @25 °C

Clear, transparent liquid

Low viscosity liquid

1 to 5 mg/mL at 68 °F (NTP, 1992)

In water, 7.82X10+3 mg/L at 20 °C

In water, 7,000 mg/L, temp not specified.

Insoluble in benzene. Soluble in most organic solvents.

Slightly soluble in carbon tetrachloride

Very slightly soluble in aliphatic hydrocarbons; soluble in alcohols, esters, ketones and aromatic hydrocarbons.

450 °F (NTP, 1992)

216 °C (Cleveland open cup)

232 °C (450 °F) (Closed cup)

202 °C c.c.

Danger

H302: Harmful if swallowed [Warning Acute toxicity, oral]

P203, P264, P270, P273, P280, P301+P317, P318, P330, P391, P405, and P501 (click each P-code to see the statement)

Danger

H302 (97.3%): Harmful if swallowed [Warning Acute toxicity, oral]

P203, P264, P270, P273, P280, P301+P317, P318, P330, P391, P405, and P501 (click each P-code to see the statement)

Chemical: Ethanol, 2-chloro-, 1,1′,1′′-phosphate

Hazard Traits - Carcinogenicity; Genotoxicity; Hepatotoxicity and Digestive System Toxicity; Nephrotoxicity and Other Toxicity to the Urinary System; Neurotoxicity; Reproductive Toxicity

Status: Cease Manufacture Update: 31-10-2012 https://echa.europa.eu/registration-dossier/-/registered-dossier/5193

Substance: Tris(2-chloroethyl) phosphate

Tris(2-chloroethyl) phosphate: Does not have an individual approval but may be used under an appropriate group standard

This chemical is combustible. (NTP, 1992)

Combustible. Gives off irritating or toxic fumes (or gases) in a fire. Vapour/air mixtures are explosive.

SYMPTOMS: Symptoms of exposure to this compound may include discomfort, itching, reddening, swelling and dermatitis. It may also cause skin, eye, mucous membrane and upper respiratory tract irritation. This compound may be a weak cholinesterase inhibitor over time.

Causes slight eye irritation; Skin absorption is minimal; In high dose animal studies, findings include testicular damage, some inhibition of cholinesterase, and central nervous system effects including seizures. CNS effects may be due to cholinesterase inhibition or direct toxicity to brain. [HSDB] The average of two baseline respective cholinesterase activity determinations three days apart, with no exposures to enzyme inhibiting pesticides for at least 30 days, is recommended for each worker prior to exposure to cholinesterase inhibitors because of large inter-individual differences in published baseline values. To be established at least once a year. Removal from workplace exposures is recommended until the cholinesterase activity returns to within 20% of baseline. [TLVs and BEIs]

DHHS/NTP; Toxicology & Carcinogenesis Studies of Tris(2-chloroethyl) phosphate in F344/N Rats and B6C3F1 Mice (Gavage Studies) p.5 Technical Report Series No. 391 (1991) NIH Publication No. 91-2846

WHO; Environ Health Criteria 209: Flame Retardants: Tris(chloropropyl) Phosphate and Tris(2-chloroethyl)Phosphate p.65 (1998). EHC are designed for scientists and administrators responsible for the establishment of safety standards and regulations and provide basic scientific risk evaluations of a wide range of chemicals and groups of chemicals.

European Chemicals Bureau; IUCLID Dataset, Tris (2-Chloroethyl) phosphate (2000 CD-ROM edition) contains information on use, toxicology, and environmental effects of this chemical as supplied to the European Union by industry..[Available from, as of June 17, 2009: http://esis.jrc.ec.europa.eu/]

IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Volume 48 (1990). Some Flame Retardants and Textile Chemicals, and Exposures in the Textile Manufacturing Industry.[Available from, as of July 22, 2009: http://monographs.iarc.fr/ENG/Monographs/vol48/volume48.pdf]

IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Volume 71 (1999). Re-Evaluation of Some Organic Chemicals, Hydrazine and Hydrogen Peroxide.[Available from, as of July 22, 2009: http://monographs.iarc.fr/ENG/Monographs/vol71/volume71.pdf]

Pursuant to section 8(d) of TSCA, EPA promulgated a model Health and Safety Data Reporting Rule. The section 8(d) model rule requires manufacturers, importers, and processors of listed chemical substances and mixtures to submit to EPA copies and lists of unpublished health and safety studies. Ethanol-, 2-chloro-, phosphate (3:1) is included on this list.

Fires involving this material can be controlled with a dry chemical, carbon dioxide or Halon extinguisher. A water spray may also be used. (NTP, 1992)

Use water spray, powder, foam, carbon dioxide.

Fresh air, rest.

Rinse and then wash skin with water and soap.

Rinse with plenty of water for several minutes (remove contact lenses if easily possible).

Rinse mouth. Refer for medical attention .

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.

Biological Exposure Indices (BEI) [ACGIH] - Acetylcholinesterase activity in red blood cells = 70% of individual's baseline; Butylcholinesterase activity in serum or plasma = 60% of individual's baseline; Sample at end of shift; [TLVs and BEIs]

Powder, water spray, foam, carbon dioxide.

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.

Advice for firefighters: Wear self contained breathing apparatus for fire fighting if necessary.

SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a POTW is acceptable only after review by the governing authority. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must meet Hazardous Material Criteria for disposal.

Accidental Release Measures. Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid breathing vapours, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided. Methods and materials for containment and cleaning up: Soak up with inert absorbent material and dispose of as hazardous waste. Keep in suitable, closed containers for disposal.

SMALL SPILLS AND LEAKAGE: If you spill this chemical, FIRST REMOVE ALL SOURCES OF IGNITION. Then, use absorbent paper to pick up all liquid spill material. Your contaminated clothing and absorbent paper should be sealed in a vapor-tight plastic bag for eventual disposal. Solvent wash all contaminated surfaces with 60-70% ethanol followed by washing with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal and plant life; and conformance with environmental and public health regulations.

Waste treatment methods. Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Contaminated packaging: Dispose of as unused product.

Personal protection: filter respirator for organic gases and vapours adapted to the airborne concentration of the substance. Do NOT let this chemical enter the environment. Collect leaking and spilled liquid in covered containers as far as possible. Absorb remaining liquid in sand or inert absorbent. Then store and dispose of according to local regulations.

Tris(2-chloroethyl) phosphate was not detected (detection limit 1 ng/g) in adipose samples obtained at autopsy from up to eight male and eight female cadavers from each of six municipalities (Cornwall, London, St Catharines, Toronto, Welland, Windsor) in Ontario, Canada(1).

LC50; Species: Oryzias latipes (Medaka); Conditions: freshwater, static, 10 °C; Concentration: 245000 ug/L for 24 hr /formulated product/

LC50; Species: Oryzias latipes (Medaka); Conditions: freshwater, static, 20 °C; Concentration: 230000 ug/L for 24 hr /formulated product/

LC50; Species: Oryzias latipes (Medaka); Conditions: freshwater, static, 30 °C; Concentration: 66000 ug/L for 24 hr /formulated product/

LC50; Species: Oryzias latipes (Medaka); Conditions: freshwater, static, 10 °C; Concentration: 230000 ug/L for 48 hr /formulated product/

For more Ecotoxicity Values (Complete) data for TRIS(2-CHLOROETHYL) PHOSPHATE (8 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 390(SRC), determined from a structure estimation method(2), indicates that tris(2-chloroethyl) phosphate is expected to have moderate mobility in soil(SRC). Volatilization of tris(2-chloroethyl) phosphate from moist soil surfaces is expected to be an important fate process(SRC) given an estimated Henry's Law constant of 3.3X10-6 atm-cu m/mole(SRC), based upon its vapor pressure, 6.13X10-2 mm Hg(3), and water solubility, 7000 mg/L(4). Tris(2-chloroethyl) phosphate is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(3). A 4% of theoretical BOD using activated sludge in the Japanese MITI test(5) suggests that biodegradation is not an important environmental fate process in soil(SRC).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 390(SRC), determined from a structure estimation method(2), indicates that tris(2-chloroethyl) phosphate is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected(3) based upon an estimated Henry's Law constant of 3.3X10-6 atm-cu m/mole(SRC), derived from its vapor pressure, 6.13X10-2 mm Hg(4), and water solubility, 7000 mg/L(5). Using this Henry's Law constant and an estimation method(3), volatilization half-lives for a model river and model lake are 19 and 140 days, respectively(SRC). Tris(2-chloroethyl) phosphate may undergo hydrolysis in the environment based on an estimated hydrolysis half-life of 20 days at pH 5 to 9(2). According to a classification scheme(6), measured BCF values of 0.6-5.1 in fish(7-9), suggest bioconcentration in aquatic organisms is low(SRC). A 4% of theoretical BOD using activated sludge in the Japanese MITI test(7) suggests that biodegradation is not an important environmental fate process in water(SRC).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), tris(2-chloroethyl) phosphate, which has a vapor pressure of 6.13X10-2 mm Hg at 25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase tris(2-chloroethyl) phosphate is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 16 hours(SRC), calculated from its rate constant of 2.2X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Tris(2-chloroethyl) phosphate does not contain chromophores that absorb at wavelengths >290 nm(4) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC).

Tris(2-chloroethyl) phosphate was found in fruit and fruit juice samples for infants at an average and range of 0.0002 and 0-0.002 ppm, respectively(1); samples were collected from 10 US cities during the 1979 fiscal year(1). In a ten-year US Market Basket Survey of ready-to-eat foods (1982-1991), tris(2-chloroethyl) phosphate was found twice in peaches at an average concentration of 1.113 ug/g and once in purple plums at a concentration of 0.007 ug/g(2). Tris(2-chloroethyl) phosphate was detected in one sample of oils and fats associated with toddler food at 0.500 ug/g during a 1980-1982 US Total Diet Survey(3).

IDENTIFICATION AND USE: (Tris(2-chloroethyl) phosphate is a Clear, transparent liquid. It is used primarily as an additive plasticizer and viscosity regulator with flame-retarding properties for polyurethane, polyesters, polyvinyl chloride and other polymers. HUMAN EXPOSURE AND TOXICITY: Tris(2-chloroethyl) phosphate did not consistently demonstrate detectable unscheduled DNA synthesis with and without metabolic activation and failed to show a dose-response relationship in human WI-38 cells. ANIMAL STUDIES: In repeat dose studies Tris(2-chloroethyl) phosphate caused adverse effects on the brain (hippocampal lesions in rats), liver and kidneys. Non-irritant to eyes, but conflicting reports in the literature on skin irritation, has not been tested for sensitization potential. Not teratogenic. It adversely affects the fertility of male rats and mice. In vitro mutagenicity test results were inconsistent and an in vivo micronucleus test gave equivocal results. Tris(2-chloroethyl) phosphate causes benign and malignant tumors at various organ sites in rats and mice. A very high oral dose caused some inhibition of plasma cholinesterase and brain neuropathy target esterase, but did not cause delayed neurotoxicity. In rats, a high dose caused convulsions, brain lesions and impaired performance. Metabolites in rats and mice include bis(2-chloroethyl)carboxymethyl phosphate; bis(2-chloroethyl) hydrogen phosphate; and bis(2-chloroethyl)-2-hydroxyethyl phosphate glucuronide excreted mainly via the urine.

The average daily intake of tris(2-chloroethyl) phosphate for infants was found to be 0.0287 ug through fruit and fruit juice(1). The average daily intake of tris(2-chloroethyl) phosphate for toddlers was found to be 0.385 ug through oils and fats(2). The daily intake of tris(2-chloroethyl) phosphate per unit of body weight for infants and toddlers in 1979 was found to be 0.016 and 0.009 ug/kg, respectively; for infants in 1980 was 0.004 ug/kg(1); for toddlers in 1981-82 was 0.028 ug/kg(2). The average daily intake of tris(2-chloroethyl) phosphate was reported as (ug/g (Age)) 0.0049 (6-11 mo); 0.0065 (2 yrs); 0.0021 (14-16 yrs female); 0.0011 (14-16 yrs male); 0.0018 (25-30 yrs female); 0.0013 (25-30 yrs male); 0.0031 (60-65 yrs female)and 0.0026 (60-65 yrs male), according to an FDA Total Diet Study from Jun 1984-Apr 1986(3).

Tris(2-chloroethyl) phosphate was detected at unreported concentrations in the blood of white-tailed eagles and in shag egg; all samples were collected in Norway(1).

Tris(2-chloroehtyl) phosphate concentrations were reported in female herring gull (Larus argentatus) tissue and egg components from samples collected Apr 2010 at Lake Huron colony site on Chantry Island(1).[Table#4051]

EPA has released the first beta version (version 0.5) of the Interactive Chemical Safety for Sustainability (iCSS) Dashboard. The beta version of the iCSS Dashboard provides an interactive tool to explore rapid, automated (or in vitro high-throughput) chemical screening data generated by the Toxicity Forecaster (ToxCast) project and the federal Toxicity Testing in the 21st century (Tox21) collaboration. /The title compound was tested by ToxCast and/or Tox21 assays; See the data in Chemical Explorer/[USEPA; ICSS Dashboard Application; Available from, as of June 27, 2014: http://actor.epa.gov/dashboard/]

The following link will take the user to the National Toxicology Program (NTP) Test Agent Search Results page, which tabulates all of the "Standard Toxicology & Carcinogenesis Studies", "Developmental Studies", and "Genetic Toxicity Studies" performed with this chemical. Clicking on the "Testing Status" link will take the user to the status (i.e., in review, in progress, in preparation, on test, completed, etc.) and results of all the studies that the NTP has done on this chemical.[Available from, as of September 2, 2014: http://ntp-apps.niehs.nih.gov/ntp_tox/index.cfm?fuseaction=ntpsearch.searchresults&searchterm=115-96-8]

Ground water test wells down-gradient from the land application of primary wastewater effluent at Fort Devens, MA showed 0.28 and 0.81 ug/L of tris(2-chloroethyl) phosphate(1). Tris(2-chloroethyl) phosphate was in the leachate from the Osaka North Port Sea-Based Solid Waste Disposal Site at 0.4-300 ug/L(2). The mean concentrations of tris(2-chloroethyl phosphate in roof runoff water in Straussberg and Muenchelberg, Germany were 669 and 907 ng/L, respectively; sampled in July, 2001(3). Tris(2-chloroethyl) phosphate was detected, not quantified, in two of three samples from Swedish municipal landfill in Gryta, Vasteras, sampled in May 1990(4). Effluent wastewater samples collected in July 2001 from three municipal sewage treatment plants and one industrial sewage treatment plant that discharge their treated wastewater into the Oder River in Germany had mean tris(2-chloroethyl) phosphate concentrations of 352 ng/L and not detected (detection limit 1 ng/L), respectively(3). Sewage sludge in Japan was found to contain small amounts of tris(2-chloroethyl) phosphate(5). The concentration of tris(2-chloroethyl) phosphate in sludge samples taken from 11 sewage treatment plants located throughout Sweden was 0.6-110 ng/g dry weight, samples were collected 2002 to 2003(6). The concentration of tris(2-chloroethyl) phosphate in influent and effluent samples taken concurrently from these same plants was 90-1000 and 350-890 ng/L, respectively(6). Tris(2-chloroethyl) phosphate was detected at median values of 0.30-0.33 ug/L in influent samples and median concentration of 0.22 ug/L in effluent samples from three waste water treatment plants located in Galicia, Spain; samples were collected Nov 2007, Feb, Jun and Sep 2008(7). Tris(2-chloroethyl) phosphate was detected at <0.025-0.30 ng/L in influent samples and <0.025-0.70 ng/L in effluent samples from water treatment plants located in Spain(8). Tris(2-chloroethyl) phosphate was detected at 2000-2500 ng/L in influent samples and 1600-2200 ng/L in effluent samples from water treatment plants located in Norway(8).

Pursuant to section 8(d) of TSCA, EPA promulgated a model Health and Safety Data Reporting Rule. The section 8(d) model rule requires manufacturers, importers, and processors of listed chemical substances and mixtures to submit to EPA copies and lists of unpublished health and safety studies. Ethanol-, 2-chloro-, phosphate (3:1) is included on this list.

The present study was conducted to clarify the acute effect of tris(2-chloroethyl)phosphate (TRCP), an organophosphate flame-retardant, on spontaneous ambulatory activity (AA) in male ICR mice and to examine the neurochemical mechanism of this effect. Single dose administration of 200 mg/kg i.p. of TRCP increased AA in ICR mice. Neither the nicotinic cholinergic antagonist mecamylamine (MA) nor the muscarinic cholinergic antagonist scopolamine (SCP) affected the AA response to TRCP. On the other hand, the benzodiazepine agonist diazepam (DZ), the GABAA agonist muscimol (MUS) and the GABAB agonist baclofen (BAC) all attenuated the effect of TRCP. DZ and MUS blocked the increase of AA within the first 10 min after administration of TRCP. These drugs did not attenuate the AA-increasing effect of SCP, suggesting that the mechanism of TRCP action is distinct from that of SCP. MUS and BAC did, but DZ did not, inhibit the AA increasing effect of the dopaminergic agonist apomorphine (APO), suggesting that dopamine is involved in the control of AA, and that GABA can affect AA through interaction with dopaminergic neurons. These results suggest that TRCP acts as a GABA antagonist and not as a cholinergic agonist, and that TRCP increases AA in ICR mice through a GABAergic mechanism.

... Tris(2-chloroethyl) phosphate (TCEP) ... /was/ incubated with human liver S9 fraction and microsomes. ... TCEP was poorly metabolized into its diester and a product of oxidative dehalogenation. ...

Tris(2-chloroethyl) phosphate (TRCP), a flame retardant, produces a dose-, sex-, and species-dependent lesion in the hippocampal region of the brain following subchronic oral administration. This lesion is more common and more severe in female F344 rats than in male F344 rats, and is not observed in B6C3F1 mice. The present investigation of the metabolism of TRCP was designed to detect sex and species variations that might account for differences in toxicity. Elimination of TRCP-derived radioactivity was more rapid in mice, which excreted greater than 70% of an oral dose of 175 mg/kg in urine in 8 hr vs approximately 40% for male or female rats. However, the metabolic profile of TRCP-derived radioactivity in urine was similar for both species. The major metabolite in female rat urine was identified as bis(2-chloroethyl) carboxymethyl phosphate. This metabolite co-chromatographed with the major metabolite found in both male rat and mouse urine. Two additional metabolites identified in female rat urine were bis(2-chloroethyl) hydrogen phosphate and the glucuronide of bis(2-chloroethyl) 2-hydroxyethyl phosphate. These metabolites also cochromatographed with metabolites found in male rat and mouse urine. TRCP metabolism in rats was not induced or inhibited by nine daily 175 mg/kg doses. Toxicity, as evidenced by seizures, was potentiated in male rats pretreated with inhibitors of aldehyde dehydrogenase.

The hepatic microsomal fraction from male rats, but not female rats, metabolized TCEP. Liver slices and blood plasma, however, of both sexes metabolized the compound, demonstrating that at least part of the metabolism is extramicrosomal. Liver slices and microsomes from both male and female humans metabolized TCEP, but plasma and whole blood did not.

In a study on male B6C3F1 mice, more than 70% of an oral dose of 175 mg (14)C-labelled TCEP/kg body weight was excreted in urine within 8 hr. Identified urinary metabolites of TCEP in mice were bis(2-chloroethyl) carboxymethyl phosphate, bis(2-chloroethyl) hydrogen phosphate and bis(2-chloroethyl) 2-hydroxyethyl phosphate glucuronide.

Tris(2-chloroethyl) phosphate (TRCP) is a flame retardant that has a wide variety of industrial applications. In subchronic studies, oral administration of TRCP to rats and mice has been reported to produce dose-, sex-, and species-dependent lesions in the hippocampal brain region. The present investigation has examined the metabolism, elimination, and regional brain distribution of (14)C TRCP in male and female rats. (14)C TRCP was administered by gavage (0, 175, 350, or 700 mg/kg) and urine, feces, exhaled volatiles, CO2, and selected tissues were collected. Regional brain distribution of (14)C was determined 2 hr following single doses of TRCP to male and female rats, and 24 hr after a single dose and the last of 14 daily doses of TRCP to female rats. Results of these studies indicate that TRCP is readily absorbed from the gastrointestinal tract, distributed to all brain regions, and that metabolism and excretion are nearly complete in 72 hr. Most of the TRCP-derived radioactivity was excreted in urine (up to 85%), with feces, volatiles, and CO2 combined accounting for less than 10% of the dose. Predominant signs of toxicity associated with TRCP administration (350 and 700 mg/kg) were seizures within 2 hr of treatment, when most of the TRCP-derived radioactivity present in brain tissue was in the form of the parent compound. Traces of inextractable (14)C were detected at later times, but this material was not concentrated in brain relative to other tissues. ...

... Elimination of TRCP-derived radioactivity was more rapid in mice, which excreted greater than 70% of an oral dose of 175 mg/kg in urine in 8 hr vs approximately 40% for male or female rats. ...

Material does not appear to be absorbed through the skin.

The distribution and excretion of (14)C-labelled TCEP in 5-week-old male Wistar rats orally dosed with 50 umol/kg body weight. The label was concentrated by various tissues, especially the liver and kidney, during the first 6 hr following administration and then rapidly decreased. Most of the label was excreted by 24 hr and by 168 hr less than 1% remained in tissues. Urine accounted for 96%, feces for 6%, and expired air for 2% of the label.

For more Absorption, Distribution and Excretion (Complete) data for TRIS(2-CHLOROETHYL) PHOSPHATE (7 total), please visit the HSDB record page.

Flame retardant in plastics, especially in flexible foams used in automobiles and furniture, and in rigid foams used for building insulation. [IARC]

Plastic Composites Manufacturing [Category: Industry]

... Used primarily as an additive plasticiser and viscosity regulator with flame-retarding properties for polyurethane, polyesters, polyvinyl chloride and other polymers.

Flame-retardant plasticizer

Used in rigid polyurethane and polyisocyanurate foams, carpet backing, flame-laminated and rebonded flexible foam, flame-retardant coatings, most classes of thermosets, adhesives (gv), cast acrylic sheet, and wood-resin composites such as particle board.

Emulsions of tris(2-chloroethyl) phosphate, blended with a binder such as a vinyl or acrylic emulsion, can be used for applications such as the backcoating of upholstery. It can be used as a secondary plasticizer in polyvinyl chloride to suppress the flammability resulting from plasticizers such as phthalates. Where a particularly high degree of flame retardancy is required, it can be used in combination with the aromatic phosphate plasticizers. Such formulations can serve as an alternative to the use of antimony oxide in plasticized vinyl polymers.

(1972) Probably greater than 4.54X10+5 grams

Production volumes for non-confidential chemicals reported under the Inventory Update Rule.[Table#4053]

Ethanol, 2-chloro-, phosphate is listed as a High Production Volume (HPV) chemical (65FR81686). Chemicals listed as HPV were produced in or imported into the U.S. in >1 million pounds in 1990 and/or 1994. The HPV list is based on the 1990 Inventory Update Rule. (IUR) (40 CFR part 710 subpart B; 51FR21438).

Production volume for non-confidential chemicals reported under the 2006 Inventory Update Rule. Chemical: Ethanol, 2-chloro-, phosphate (3:1). Aggregated National Production Volume: 500,000 to < 1 million pounds.

For more U.S. Production (Complete) data for TRIS(2-CHLOROETHYL) PHOSPHATE (6 total), please visit the HSDB record page.

Ethanol, 2-chloro-, 1,1',1''-phosphate: ACTIVE

It is a plasticizer for cellulose cmpd and in them it acts as a flameproofer because of its chlorine content and its phosphoric radical. ... Particularly suitable for manufacture of noninflammable varnishes and plastics, particularly materials based on ethylcellulose, nitrocellulose, and cellulose acetate.

Excellent flameproofer for polyester resins, polyacrylates, and polyurethanes. It is compatible to some extent with polyvinyl chloride, but plasticizing efficiency is low and there is a tendency to exudation. Primary plasticizer must be used together with it.

Compatible with essentially all polymers containing polar groups.