りん酸トリフェニル

Other Classes -> Organophosphates, Other

Organophosphate

Waste-water effluent contaminant

Plastics -> ABS

Plastics -> Other functions -> Flame retardant

Plastics -> Plasticisers

log Kow = 4.59

4.59

3.9

Odorless

Phenol-like odor

1.2055 (NTP, 1992) - Denser than water; will sink

Density: 1.2055 g/cu cm at 50 °C

Bulk density: 10.5 lb/gal

Relative density (water = 1): 1.27

1.2055

1.268 @ 60°C

Flame retardants

Flame Retardants -> Organophosphorus flame retardant (OP)

Crystals from ligroin; prisms from alcohol; needles from diethyl ether

Colorless, crystalline powder

Needles

Insoluble (NTP, 1992)

In water, 1.9 mg/L at 25 °C

Insoluble in water

Soluble in ethanol; very soluble in ether, benzene, carbon tetrachloride, chloroform

Soluble in benzene, chloroform, ether, acetone; moderately soluble in alcohol

For more Solubility (Complete) data for Triphenyl phosphate (7 total), please visit the HSDB record page.

428 °F (NTP, 1992)

220 °C

428 °F (220 °C) (Closed cup)

220 °C c.c.

428 °F

428 °F

This chemical does not meet GHS hazard criteria for 0.6% (9 of 1488) of reports.

Warning

H400 (83.4%): Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard]

P273, P391, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 1488 reports by companies from 25 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Warning

Chemical: Phosphoric acid, triphenyl ester

Hazard Traits - Endocrine Toxicity; Neurotoxicity; Reproductive Toxicity

Phosphoric acid, triphenyl ester is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of Phosphoric acid, triphenyl ester are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)

T - indicates a substance that is the subject of a final TSCA section 4 test rule.

Status: Active Update: 21-07-2022 https://echa.europa.eu/registration-dossier/-/registered-dossier/15972

Substance: Triphenyl phosphate

Cholinesterase inhibition, but no cumulative toxicity, was observed in animal studies. A study of 33 workers (employed for an average of 7.4 years) in a plant manufacturing TPP found no adverse health effects. A slight reduction in erythrocyte cholinesterase activity was found in six workers. One case of occupational allergic contact dermatitis has been documented. [ACGIH] In high-dose animal studies, adverse effects include delayed paralysis similar to that seen with tri-o-cresyl phosphate. [HSDB]

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. Phosphoric acid, triphenyl ester is included on this list. Effective date: 10/4/82; Sunset date: 10/4/92.

Organophosphates, such as TRIPHENYL PHOSPHATE, are susceptible to formation of highly toxic and flammable phosphine gas in the presence of strong reducing agents such as hydrides. Partial oxidation by oxidizing agents may result in the release of toxic phosphorus oxides.

This compound is not very flammable but any fire involving this compound may produce dangerous vapors. You should evacuate the area. All firefighters should wear full-body protective clothing and use self-contained breathing apparatuses. You should extinguish any fires involving this chemical with a dry chemical, carbon dioxide, foam, or halon extinguisher. (NTP, 1992)

Use water spray, powder, foam, carbon dioxide.

Fresh air, rest. Refer for medical attention.

Remove contaminated clothes. Rinse and then wash skin with water and soap.

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

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.

(General first aid procedures)

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.

Keep container tightly closed in a dry and well-ventilated place.

Store in an area without drain or sewer access. Provision to contain effluent from fire extinguishing.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. 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: Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for disposal.

Sweep spilled substance into covered containers. If appropriate, moisten first to prevent dusting. Carefully collect remainder. Then store and dispose of according to local regulations. Personal protection: particulate filter respirator adapted to the airborne concentration of the substance. Do NOT let this chemical enter the environment.

If triphenyl phosphate is spilled ... : ventilate area of spill. For small quantities, sweep onto paper or other suitable material, place in appropriate container and burn in a safe place (such as a fume hood). Large quantities may be reclaimed; however, if this is not practical, dissolve in a flammable solvent (such as alcohol) and atomize in a suitable combustion chamber equipped with an appropriate effluent gas cleaning device.

SMALL SPILLS AND LEAKAGE: Should a spill occur while you are handling this chemical, you should dampen the solid spill material with alcohol, then transfer the dampened material to a suitable container. Use absorbent paper dampened with alcohol to pick up any remaining material. Seal the absorbent paper, and any of your clothes, which may be contaminated, in a vapor-tight plastic bag for eventual disposal. Solvent wash all contaminated surfaces with alcohol followed by washing with a strong soap and water solution. Do not reenter the contaminate area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.

SRP: 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 air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.

Product: Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contaminated packaging: Dispose of as unused product.

1. By making packages of triphenyl phosphate in paper or other flammable material and burning in a suitable combustion chamber... with an appropriate effluent gas cleaning device. 2. By dissolving... in a flammable solvent... and atomizing in a suitable combustion chamber... with an... effluent gas cleaning device.

Personal protection: particulate filter respirator adapted to the airborne concentration of the substance. Do NOT let this chemical enter the environment. Sweep spilled substance into covered containers. If appropriate, moisten first to prevent dusting. Carefully collect remainder. Then store and dispose of according to local regulations.

Concentration of triphenyl phosphate at five work environments in Kuopio, Finland(1).

Concentration of triphenyl phosphate at five work environments in Kuopio, Finland(1).

Concentration of triphenyl phosphate at two work environments in Kuopio, Finland(1).

Triphenyl phosphate concentrations were reported in hair, fingernail, toenail and blood samples in 50 individuals from Indiana University's Bloomingdale campus, sampled in July-August, 2014, the compound was not detected in blood samples.(1).

During a study of the level of triaryl/alkyl phosphates in human adipose tissue, no conclusions for triphenyl phosphate were drawn because trace levels of triphenyl phosphate were identified in the method blanks; however, triphenyl phosphate was detected in two human adipose tissue samples (13.6 and 11.2 ng/g) at levels significantly above the method blanks(1). Triphenyl phosphate concentrations were hair, fingernail, toenail and blood samples, respectively, in 50 individuals from Indiana University's Bloomingdale campus, sampled in July-August, 2014(2).

A series of symmetrical trisubstituted phosphorus esters was tested as synergists for malathion and other organophosphorus insecticides against resistant and normal strains of Chrysomya putoria and Musca domestica. Triphenyl phosphate synergized the insecticides more effectively against insecticide-resistant than normal insect strains.

LC50; Species: Menidia beryllina /(Inland silverside)/; Conditions: static bioassay; Concentration: 95 mg/L for 96 hr

LC50; Species: Carassius auratus (Goldfish) weight 0.8-2.8 g; Conditions: static bioassay; Concentration: 0.70 mg/L for 96 hr

LC50; Species: Ictalurus punctatus (Channel catfish) weight 0.23 g; Conditions: static bioassay, 22 °C, pH 7.5, hardness 38 mg/L; Concentration: 0.42 mg/L for 96 hr

LC50; Species: Gammarus pseudolimnaeus (Scud) age 60-90 day mid-instar larvae; Conditions: freshwater, static, 17 °C; Concentration: 250 ug/L for 96 hr (95% confidence interval: 160-390 ug/L) /99% purity formulation/

For more Ecotoxicity Values (Complete) data for Triphenyl phosphate (24 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), a Koc range of 2,514 to 3,561(2) indicates that triphenyl phosphate is expected to have slight mobility in soil(SRC). Volatilization of triphenyl 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, 2.00X10-6 mm Hg(3), and water solubility, 1.9 mg/L(4). However, adsorption to soil is expected to attenuate volatilization(SRC). Triphenyl phosphate is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(3). Mineralization half-lives of 37 and 32 days under aerobic and anaerobic conditions, respectively, using a loamy sand(2) suggest that biodegradation may be an important environmental fate process in soil(SRC).

AQUATIC FATE: Based on a classification scheme(1), a Koc range of 2,514 to 3,561(2) indicates that triphenyl 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, 2.00X10-6 mm Hg(4), and water solubility, 1.9 mg/L(5). Estimated volatilization half-lives for a model river and model lake are 20 and 152 days, respectively. However, volatilization from water surfaces is expected to be attenuated by adsorption to suspended solids and sediment in the water column. The estimated volatilization half-life from a model pond is 400 days if adsorption is considered(6). According to a classification scheme(7), bioconcentration factors ranging from 132(8) to 573(9) suggest that bioconcentration in aquatic organisms is high(SRC). Biodegradation half-lives of 2-4 days in river die-away tests(10) suggest that biodegradation may be 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), triphenyl phosphate, which has a vapor pressure of 2.00X10-6 mm Hg at 25 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase triphenyl 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 12 hours(SRC), calculated from its rate constant of 1.1X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase triphenyl phosphate may be removed from the air by wet and dry deposition(SRC). Triphenyl phosphate does not absorb light at wavelengths >290 nm(4) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC).

Triphenyl phosphate has been detected in a composite grain product sample (flours, breads, and cereals); however, this food sample may have been contaminated during analysis through laboratory reagents that contain triphenyl phosphate(1). Triphenyl phosphate was detected in 8 out of 230 ready to eat foods in the US at an average concentration of 0.2803 ug/g(2). The compound was tested for but not detected in 228 fresh potato samples sold at 34 farm markets in Alberta, Canada(3).

The substance can be absorbed into the body by inhalation.

inhalation, ingestion

Safe in the present practices of use and concentration. Ingredient, concentration, and use information are available in documents discoverable at https://cir-reports.cir-safety.org

IDENTIFICATION AND USE: Triphenyl phosphate (TPP) is a solid. It is used as fire-retarding agent, and a plasticizer for cellulose acetate and nitrocellulose. Triphenyl phosphate also has been found as one component of lubricating oil and hydraulic fluids. HUMAN STUDIES: It causes a delayed peripheral neuritis involving motor neurons, resulting in a flaccid paralysis, particularly of the distal muscles. No sensory disturbances. Potential symptoms of overexposure are minor changes in blood enzymes. In workers engaged in the manufacture of TPP there was some inhibition of plasma cholinesterase but no correlation of this effect with degree of exposure or with minor gastrointestinal or neuromuscular symptoms. A case of TPP allergy from spectacle frames was reported. TPP increased both 17beta-estradiol (E2) and testosterone concentrations in human H295R cells in vitro. In addition, transcription of four major steroidogenic genes was up-regulated and that of two sulfotransferase genes was down-regulated. Increase of TPP concentration in house dust was associated with a 10% increase in prolactin and a 19% decrease in sperm concentration in exposed men. ANIMAL STUDIES: Topical application of TPP to rats and mice caused no skin irritation. Because cholinesterase was not inhibited after topical application of TPP, it was concluded that percutaneous absorption was limited. TPP caused generalized delayed illness and paralysis in cats and primates. Administration of 0.2 g/kg of TPP s.c. caused paralysis in cats and fatal doses ranged between 0.3-1.0 g/kg. In mice choline esterase activity was reduced after doses of 10 to 500 mg/kg bw to 87.1 to 30.4% of control. No cholinergic or other symptoms were reported. TPP acted in vitro as antagonist of estrogen receptor inhibiting binding of E2 to estrogen receptor. Zebrafish retinoic acid receptor (RAR) may be involved in mediating TPP-induced developmental toxicity. Perinatal exposure to TPP exacerbates the development of obesity in male and female rats. TPP mutagenicity was negative at doses of 0, 100, 333, 1000, 3333, and 10,000 ug/plate in four Salmonella typhimurium strains (TA98, TA100, TA1535, and TA1537) in the presence and absence of metabolic activation. In vitro TPP was found to cause significant direct inhibition of monocyte antigen presentation at non-cytotoxic concentrations as low as 1 umol/L. ECOTOXICITY STUDIES: Vertebral damage and spinal curvature were observed in rainbow trout exposed to TPP for 96 hr. The growth of green algae was completely inhibited at concentrations of 1 mg/L or more but stimulated at lower concentrations (0.1 and 0.05 mg/L). TPP could increase the thyroid hormone concentrations in the early life stages of zebrafish by disrupting the central regulation and hormone synthesis pathways.

The average daily intake (AVDI) of triphenyl phosphate in 8 population groups in 1982-1984 was determined according to the FDA's monitoring program for chemical contaminants in the U.S. food supply (Total Diet Study or Market Basket Study). In 6-11 month old infants, the AVDI was 0.3 ng/kg-body weight-per day. In 2 yr old toddlers, the AVDI was 4.4 ng/kg-body weight-per day. In 14-16 year old females, the AVDI was 1.6 ng/kg-body weight-per day. In 14-16 year old males, the AVDI was 1.2 ng/kg-body weight-per day. In 25-30 year old females, the AVDI was 0.8 ng/kg-body weight-per day. In 25-30 year old males, the AVDI was 1.6 ng/kg-body weight-per day. In 60-65 year old females, the AVDI was 0.5 ng/kg-body weight-per day. In 60-65 year old males, the AVDI was 0.5 ng/kg-body weight-per day(1).

/AQUATIC SPECIES/ 1 ppm ... in water caused death of all six exposed goldfish within 8 hr. At concentration of 3 ppm or 5 ppm, all fish died within 5 hr and 1 hr, respectively. /Histological changes similar to mice and rats TPP poisoning/ congestion, degeneration, and hemorrhage from smaller blood vessels, pronounced mostly in liver, kidney, and brain.

/AQUATIC SPECIES/ Vertebral damage and spinal curvature were observed in rainbow trout exposed to triphenyl phosphate for 96 hr.

/AQUATIC SPECIES/ ...The growth of green algae was completely inhibited at concentrations of 1 mg/L or more but stimulated at lower concentrations (0.1 and 0.05 mg/L). The nitrogenase activity, measured by the acetylene reduction technique, of a cyanobacterium (blue-green alga: Anabaena flosaquae) was affected by TPP. Additions of 0.1, 1.0, and 5.0 mg/L reduced the nitrogenase activity to 84, 77, and 68% of the control value, respectively.

/AQUATIC SPECIES/ The toxicities of five phosphate ester compounds - Fyrquel GT, Kronitex 200, Phosflex 31P, Pydraul 50E and Santicizer 148-were evaluated in acute toxicity tests with rainbow trout (Salmo gairdneri), fathead minnows (Pimephales promelas), channel catfish (Ictalurus punctatus) and bluegills (Lepomis macrochirus) and in 90 day partial life-cycle tests with fathead minnows. Nominal exposure concentrations were 0, 0.06, 0.12, 0.25, 0.5 and 1.0 mg/L in the partial life-cycle tests with Fyrquel GT, Kronitex 200, Phosflex 31P and Pydraul 50E, and 0, 0.05, 0.09, 0.19, 0.38 and 0.75 mg/L in the test with Santicizer 148. The 96 hr LC50 values for rainbow trout, fathead minnows, channel catfish and bluegills exposed to the five phosphate esters ranged from <0.3 to >72 mg/L. The LC50 values may be directly related to the percentage of triphenyl phosphate contained in each of the compounds. The phosphate esters generally showed similar chronic toxicities to fathead minnows, and adverse toxic effects occurred at nominal exposure concentrations of 0.38 to 1.0 mg/L. Comparison of available environmental concentration data for phosphate esters with the effect concentrations obtained for fish in the present study indicated that phosphate ester compounds may not now pose a threat to fish populations. /SRP: Formulated products/

For more Ecotoxicity Excerpts (Complete) data for Triphenyl phosphate (6 total), please visit the HSDB record page.

Triphenyl phosphate was reported at median concentrations of 4.3 and 0.22 ng/g in plasma and feathers, respectively, of White-tailed Eagle (Haliaeetus albicilla) nestlings in Trondelag, Norway; sampling was conducted in 2011 just prior to fledging at between 6 to 9 weeks of age(1).

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. Phosphoric acid, triphenyl ester is included on this list. Effective date: 10/4/82; Sunset date: 10/4/92.

Firemaster 550 (FM550) is an additive flame retardant formulation of brominated and aryl phosphate ester (APE) components introduced as a major replacement product for the commercial polybrominated diphenyl ether mixture (known as PentaBDE) used primarily in polyurethane foam. However, little is known about the potential effects of FM550-based ingredients during early vertebrate development. Therefore, we first screened the developmental toxicity of each FM550 component using zebrafish as an animal model. Based on these initial screening assays, we found that exposure to the brominated components as high as 10 uM resulted in no significant effects on embryonic survival or development, whereas exposure to triphenyl phosphate (TPP) or mono-substituted isopropylated triaryl phosphate (mono-ITP)-two APEs comprising almost 50% of FM550-resulted in targeted effects on cardiac looping and function during embryogenesis. As these cardiac abnormalities resembled aryl hydrocarbon receptor (AHR) agonist-induced phenotypes, we then exposed developing embryos to TPP or mono-ITP in the presence or absence of an AHR antagonist (CH223191) or AHR2-specific morpholino. Based on these studies, we found that CH223191 blocked heart malformations following exposure to mono-ITP but not TPP, whereas AHR2 knockdown failed to block the cardiotoxic effects of both components. Finally, using a cell-based human AHR reporter assay, we found that mono-ITP (but not TPP) exposure resulted in a significant increase in human AHR-driven luciferase activity at similar nominal concentrations as a potent reference AHR agonist (beta-naphthoflavone). Overall, our findings suggest that two major APE components of FM550 induce severe cardiac abnormalities during early vertebrate development.

Using zebrafish as a model, we previously reported that developmental exposure to triphenyl phosphate (TPP) - a high-production volume organophosphate-based flame retardant - results in dioxin-like cardiac looping impairments that are independent of the aryl hydrocarbon receptor. Using a pharmacologic approach, the objective of this study was to investigate the potential role of retinoic acid receptor (RAR) - a nuclear receptor that regulates vertebrate heart morphogenesis - in mediating TPP-induced developmental toxicity in zebrafish. We first revealed that static exposure of zebrafish from 5-72h post-fertilization (hpf) to TPP in the presence of non-toxic concentrations of an RAR antagonist (BMS493) significantly enhanced TPP-induced toxicity (relative to TPP alone), even though identical non-toxic BMS493 concentrations mitigated retinoic acid (RA)-induced toxicity. BMS493-mediated enhancement of TPP toxicity was not a result of differential TPP uptake or metabolism, as internal embryonic doses of TPP and diphenyl phosphate (DPP) - a primary TPP metabolite - were not different in the presence or absence of BMS493. Using real-time PCR, we then quantified the relative change in expression of cytochrome P450 26a1 (cyp26a1) - a major target gene for RA-induced RAR activation in zebrafish - and found that RA and TPP exposure resulted in an approximate 5-fold increase and decrease in cyp26a1 expression, respectively, relative to vehicle-exposed embryos. To address whether TPP may interact with human RARs, we then exposed Chinese hamster ovary cells stably transfected with chimeric human RARalpha-, RARbeta-, or RARgamma to TPP in the presence of RA, and found that TPP significantly inhibited RA-induced luciferase activity in a concentration-dependent manner. Overall, our findings suggest that zebrafish RARs may be involved in mediating TPP-induced developmental toxicity, a mechanism of action that may have relevance to humans.

The organophosphate flame retardant, triphenyl phosphate (TPHP), has been detected with increasing frequency in environmental samples and its primary metabolite is considered to be diphenyl phosphate (DPHP). Information on the adverse effects of these compounds in avian species is limited. Here, we investigate the effects of TPHP and DPHP on cytotoxicity and mRNA expression, as well as in vitro metabolism of TPHP, by use of a chicken embryonic hepatocyte (CEH) screening assay. After 36 hr of exposure, CEH cytotoxicity was observed following exposure to >10 uM TPHP (LC50 = 47 +/- 8 uM), whereas no significant cytotoxic effects were observed for DPHP concentrations up to 1000 uM. Using a custom chicken ToxChip polymerase chain reaction (PCR) array, the number of genes altered by 10 uM DPHP (9 out of 27) was greater than that by 10 uM TPHP (4 out of 27). Importantly, 4 of 6 genes associated with lipid/cholesterol metabolism were significantly dysregulated by DPHP, suggesting a potential pathway of importance for DPHP toxicity. Rapid degradation of TPHP was observed in CEH exposed to 10 uM, but the resulting concentration of DPHP accounted for only 17% of the initial TPHP dosing concentration. Monohydroxylated-TPHP (OH-TPHP) and two (OH)2-TPHP isomers were identified in TPHP-exposed CEH, and concentrations of these metabolites increased over 0 to 36 hr. Overall, this is the first reported evidence that across 27 toxicologically relevant genes, DPHP altered more transcripts than its precursor, and that TPHP is also metabolized via a hydroxylation pathway in CEH.

Study deals with metabolic ring-hydroxylation of triphenyl phosphate in houseflies to give a quinol phosphate. A total of 530 mg triphenyl phosphate was applied to about 27,000 houseflies. Metabolites were extracted after 24 hr. In vivo transformation of triphenyl phosphate into diphenyl p-hydroxyphenol phosphate was confirmed.

Triphenyl phosphate was incubated with rat liver microsomal without NADPH and soluble fractions and found by gas chromatography that triphenyl phosphate was decomposed to diphenyl-phosphate as the major metabolite. Therefore, arylesterase in the microsomes contributes to triphenyl phosphate metabolism. The metabolic reactions were inhibited almost completely by SKF-525A and carbon monoxide in the absence of NADPH whereas KCN, NaN3, dipyridyl and EDTA showed little effect. Therefore, mixed function oxidase system in the microsomes plays a central role in the metabolism of triphenyl phosphate.

Triphenyl phosphate (TPHP) is primarily used as either a flame retardant or plasticizer, and is listed as an ingredient in nail polishes. However, the concentration of TPHP in nail polish and the extent of human exposure following applications have not been previously studied. We measured TPHP in ten different nail polish samples purchased from department stores and pharmacies in 2013-2014. Concentrations up to 1.68% TPHP by weight were detected in eight samples, including two that did not list TPHP as an ingredient. Two cohorts (n=26 participants) were recruited to assess fingernail painting as a pathway of TPHP exposure. Participants provided urine samples before and after applying one brand of polish containing 0.97% TPHP by weight. Diphenyl phosphate (DPHP), a TPHP metabolite, was then measured in urine samples (n=411) and found to increase nearly seven-fold 10-14 hr after fingernail painting (p<0.001). To determine relative contributions of inhalation and dermal exposure, ten participants also painted their nails and painted synthetic nails adhered to gloves on two separate occasions, and collected urine for 24 hr following applications. Urinary DPHP was significantly diminished when wearing gloves, suggesting that the primary exposure route is dermal. /These/ results indicate that nail polish may be a significant source of short-term TPHP exposure and a source of chronic exposure for frequent users or those occupationally exposed.

The material is poorly absorbed through the intact skin... .

The bioconcentration ratio of triphenyl phosphate was large compared with those of other phosphates in both species. Triphenyl phosphate originally present in the water was absorbed and metabolized completely by killifish within 72 hr, while goldfish absorbed triphenyl phosphate at a very slow rate, but accumulated TPP for a longer period. Thus, the ability to metabolize triphenyl phosphate is high in killifish while it is very low in goldfish.

The rate of uptake of (14)C-ring labeled triphenyl phosphate by rainbow trout was lower in river than in dechlorinated city water. Liver accumulated the highest residues of triphenyl phosphate compared to other tissues. A bioaccumulation ratio of 2590 was found, based on experimentally determined uptake and clearance rates.

The potential for prenatal exposure has recently raised concerns over the health risks of endocrine disruptors; however, knowledge about human prenatal exposure to organophosphorus flame retardants (OPFRs) is lacking. In this study, 2-ethylhexyl diphenyl phosphate (EHDPP), tributyl phosphate (TBP), triphenyl phosphate (TPHP), and tris(2-chloroethyl) phosphate (TCEP) were detected in the majority of chorionic villus samples, with median concentrations of 13.6, 18.8, 11.1, and 0.51 ng/g of dry weight (dw), respectively, significantly higher than those in the matching maternal decidua samples (5.96, 10.8, 1.44, and 0.26 ng/g of dw, respectively). The ratios of concentrations in chorionic villi (containing embryos) to those in maternal deciduae (CMRs) were 4.17, 3.82, 2.81, and 2.00 for EHDPP, TPHP, TBP, and TCEP, respectively, which correlated with their log Kow values (p = 0.003). The results of transthyretin (TTR) binding assays indicated that the stronger the binding ability to TTR, the higher the CMRs. The median concentrations of the metabolites diphenyl phosphate (DPHP), dibutyl phosphate (DBP), and bis(2-chloroethyl) phosphate (BCEP) were 4.11, 429, and 157 ng/g of dw in chorionic villi, higher than those in deciduae (1.64, 181, and 25.4 ng/g of dw, respectively). The ratios of DPHP/TPHP and DPHP/EHDPP were 0.20 and 0.43 in chorionic villi and 1.24 and 2.03 in deciduae, respectively, much lower than those of DBP/TBP and BCEP/TCEP (20.9 and 165.6 in chorionic villi and 13.1 and 35.3 in deciduae, respectively), suggesting that the difference in metabolism between the deciduae and chorionic villi would affect their maternal transfer.

Topical application of triphenyl phosphate to rats and mice caused no skin irritation. Because cholinesterase was not inhibited after topical application of triphenyl phosphate ... percutaneous absorption was limited.

CIR ingredient: Triphenyl Phosphate

Used as a plasticizer, fire-retardant, and substitute for camphor in celluloid; also used in lubricating oils and hydraulic fluids; [ACGIH]

Noncombustible substitute for camphor in celluloid; rendering acetylcellulose, nitrocellulose, airplane "dope", etc., stable and fireproof; impregnating roofing paper; plasticizer in lacquers and varnishes.

Fire-retarding agent, plasticizer for cellulose acetate and nitrocellulose.

/Triphenyl phosphate/ has been used as a plasticizer in automobile upholstery, as a fireproofing agent, as a noncombustible substitute for camphor in celluloid, and for impregnating roofing paper. Triphenyl phosphate also has been found as one component of lubricating oil and hydraulic fluids.

An early application was as a flame retardant for cellulose acetate safety film. It is also used in cellulose nitrate, various coatings, triacetate film and sheet, and rigid urethane foam. It has been used as a flame-retardant additive for engineering thermoplastics such as polyphenylene oxide-high impact polystyrene and ABS-polycarbonate blends.

2023: 1,000,000 - <5,000,000 lb

(1975) GREATER THAN 9.08X10+5 GRAMS

Phosphoric acid, triphenyl ester 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 volumes for non-confidential chemicals reported under the Inventory Update Rule.[Table#4002]

Production volume for non-confidential chemicals reported under the 2006 Inventory Update Rule. Chemical: Phosphoric acid, triphenyl ester. Aggregated National Production Volume: 10 to < 50 million pounds.

Non-confidential 2016 Chemical Data Reporting (CDR) information on the production and use of chemicals manufactured or imported into the United States. Chemical: Triphenylphosphate:

Prepared from P2O5 and phenol: Prahl, United States of America patent 2805240 (1957); by reaction of triethyl phosphite with chloramine-T ... .

Interaction of phenol and phosphorous oxychloride.

Prepared by reacting phosphorus pentoxide and phenol and by reaction of triethyl phosphate and chloramine-T. On a larger scale phosphorus oxychloride and phenol are reacted in an esterification tank with heating. The hydrogen chloride formed is trapped and condensed, while the crude triphenyl phosphate runs into a large tank where it is purified.

Grade: Technical

Pydraul 50 E (35% triphenyl phosphate)

... Usually produced in the form of flakes or shipped in heated vessels as a liquid.

Cosmetics product ingredient: Triphenyl phosphate

Information on 3 consumer products that contain Triphenyl phosphate in the following categories is provided:

Plastics -> Other functions -> Flame retardant

Plastics -> Polymer Type -> ABS

Plastics -> Plasticisers

HYDRAULIC FLUIDS

Textiles, apparel, and leather manufacturing

Phosphoric acid, triphenyl ester: ACTIVE

Though it easily supercools, triphenylphosphate can crystallize when present in films, imparting a milky appearance to them. Any excess of triphenylphosphate should ... be avoided; the addition of phthalates prevents crystallization.

... Lessens the inflammability of plastics in which it is incorporated, particularly cellulose acetate films. It is an excellent plasticizer for ethylcellulose and a very good fireproofing agent for vinyl and acrylic materials.