This report contains the collective views of an international group of
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    policy of the United Nations Environment Programme, the International
    Labour Organisation, or the World Health Organization.

    Published under the joint sponsorship of
    the United Nations Environment Programme,
    the International Labour Organisation,
    and the World Health Organization

    First draft prepared by Dr. A. Nakamura,
    National Institute for Hygienic Sciences, Japan

    World Health Orgnization
    Geneva, 1991

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    coordination of laboratory testing and epidemiological studies, and
    promotion of research on the mechanisms of the biological action of

    WHO Library Cataloguing in Publication Data

    Triphenyl phosphate.

        (Environmental health criteria ; 111)

        1.Organophosphorus compounds - adverse effects 2.Organophosphorus
        compounds - toxicity   I.Series

        ISBN 92 4 157111 X        (NLM Classification: QV 627)
        ISSN 0250-863X

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    1.1. Identity, physical and chemical properties, analytical methods
    1.2. Sources of human and environmental exposure
    1.3. Environmental transport, distribution, and transformation
    1.4. Environmental levels and human exposure
    1.5. Effects on organisms in the environment
    1.6. Effects on experimental animals and  in vitro  test systems
    1.7. Effects on humans


    2.1. Identity
    2.2. Physical and chemical properties
    2.3. Conversion factor
    2.4. Analytical methods
        2.4.1. Sample extraction
        2.4.2. Clean-up procedures
        2.4.3. Gas chromatography and mass spectrometry
        2.4.4. Contamination of analytical reagents
        2.4.5. Other analytical methods


    3.1. Production levels and processes
    3.2. Uses


    4.1. Transport and transformation in the environment
        4.1.1. Release to the environment
        4.1.2. Fate in water and sediment
        4.1.3. Biodegradation
        4.1.4. Water treatment
    4.2. Bioaccumulation
        4.2.1. Fish
        4.2.2. Chironomid larvae
        4.2.3. Environmental fate in artificial pond water


    5.1. Environmental levels
        5.1.1. Air
        5.1.2. Water
        5.1.3. Sediment and soil
        5.1.4. Fish
    5.2. General population exposure
        5.2.1. Food
        5.2.2. Drinking-water
        5.2.3. Human tissues
    5.3. Occupational exposure


    6.1. Unicellular algae and fungi
    6.2. Aquatic organisms
    6.3. Insects



    8.1. Single exposure
    8.2. Short-term exposure
    8.3. Skin irritation
    8.4. Reproduction
    8.5. Mutagenicity
    8.6. Carcinogenicity
    8.7. Neurotoxicity
    8.8.  In vitro  studies



    10.1. Evaluation of human health risks
         10.1.1. Exposure levels
         10.1.2. Toxic effects
    10.2. Evaluation of effects on the environment
         10.2.1. Exposure levels
         10.2.2. Toxic effects


    11.1. Recommendations for further research










Dr S. Dobson, Institute of Terrestrial Ecology, Monks Wood Experimental
   Station, Abbots Ripton, Huntingdon, Cambridgeshire, England  (Chairman)

Dr S. Fairhurst, Medical Division, Health and Safety Executive,
   Bootle, Merseyside, England  (Joint Rapporteur)

Ms N. Kanoh, Division of Information on Chemical Safety, National
   Institute of Hygienic Sciences, Setagaya-ku, Tokyo, Japan

Dr A. Nakamura, Division of Medical Devices, National Institute of
   Hygienic Sciences, Setagaya-ku, Tokyo, Japan

Dr M. Tasheva, Department of Toxicology, Institute of Hygiene and
   Occupational Health, Sofia, Bulgaria

Dr B. Veronesi, Neurotoxicology Division, US Environmental Protection
   Agency, Research Triangle Park, North Carolina, USA

Mr W.D. Wagner, Division of Standards Development and Technology
   Transfer, National Institute for Occupational Safety and Health,
   Cincinnati, Ohio, USA

Dr R. Wallentowicz, Exposure Assessment Application Branch, US
   Environmental Protection Agency, Washington, DC, USA  (Joint Rapporteur)

Dr Shen-Zhi Zhang, Beijing Municipal Centre for Hygiene and Epidemic
   Control, Beijing, China


Dr M. Beth, Berufsgenossenschaft der Chemischen Industrie (BG Chemie),
   Heidelberg, Federal Republic of Germany

Dr R. Kleinstück, Bayer AG, Leverkusen, Federal Republic of Germany


Dr M. Gilbert, International Programme on Chemical Safety, Division of
   Environmental Health, World Health Organization, Switzerland  (Secretary)


    Every effort has been made to present information in the criteria 
documents as accurately as possible without unduly delaying their 
publication.  In the interest of all users of the environmental health 
criteria documents, readers are kindly requested to communicate any 
errors that may have occurred to the Manager of the International 
Programme on Chemical Safety, World Health Organization, Geneva, 
Switzerland, in order that they may be included in corrigenda, which 
will appear in subsequent volumes. 

                                 *    *

    A detailed data profile and a legal file can be obtained from the 
International Register of Potentially Toxic Chemicals, Palais des 
Nations, 1211 Geneva 10, Switzerland (Telephone No. 7988400 or 7985850). 


    A WHO Task Group meeting on Environmental Health Criteria for 
Triphenyl Phosphate was held at the British Industrial Biological 
Research Association (BIBRA), Carshalton, United Kingdom, from 9 to 13 
October 1989.  Dr S.D. Gangolli, Director, BIBRA, welcomed the 
participants on behalf of the host institution and Dr M. Gilbert opened 
the meeting on behalf of the three cooperating organizations of the IPCS 
(ILO, UNEP, WHO). The Task Group reviewed and revised the draft criteria 
document and made an evaluation of the risks for human health and the 
environment from exposure to triphenyl phosphate. 

    The first draft of this document was prepared by Dr A. Nakamura, 
National Institute for Hygienic Sciences, Japan.  Dr M. Gilbert and Dr 
P.G. Jenkins, both members of the IPCS Central Unit, were responsible 
for the overall scientific content and editing, respectively. 


BCF   bioconcentration factor

EC    effective concentration

HPLC  high performance liquid chromatography

LC    lethal concentration

LD    lethal dose

ND    not detected

OPIDN organophosphate-induced delayed neuropathy

TAP   triaryl phosphate

TCP   tricresyl phosphate

TLC   thin-layer chromatography

TPP   triphenyl phosphate


1.1.  Identity, physical and chemical properties, analytical methods

    Triphenyl phosphate (TPP) is a non-flammable, non-explosive, 
colourless, crystalline substance.  Its partition coefficient between 
octanol and water (log Pow) is 4.61-4.76.  At normal ambient 
temperatures, it hydrolyses rapidly in alkaline solution, producing 
diphenyl phosphate and phenol, but very slowly in acidic or neutral 

    The analytical method of choice is gas-liquid chromatography with 
nitrogen-phosphorus sensitive or flame photometric detection.  The 
detection limit in water is about 20 ng/litre. 

1.2.  Sources of human and environmental exposure

    TPP is manufactured from phosphorus oxychloride and phenol.  It is 
used as a flame retardant in phenolic and phenylene-oxide-based resins 
for the manufacture of electrical and automobile components and as a 
non-flammable plasticizer in cellulose acetate for photographic films. 
It  is also a component of hydraulic fluids or lubricant oils and has a 
number of other minor uses. 

    Exposure of the general population through normal use can be 
regarded as minimal. 

1.3.  Environmental transport, distribution, and transformation

    Triaryl phosphates enter into the aquatic environment mainly via 
hydraulic fluid leakage as well as by leaching from plastics and, to a 
minor extent, from manufacturing processes. Because of its low water 
solubility and relatively high soil adsorption coefficient, TPP is 
rapidly adsorbed on river (or pond) sediments. Its biodegradation in 
aqueous environments is rapid. 

    The degradation of TPP involves a stepwise enzymatic hydrolysis to 
orthophosphate and phenolic moieties. 

    The bioconcentration factors (BCF) measured for several species of 
fish range from 6 to 18 900 and the depuration half-life ranges from 1.2 
to 49.6 h. 

    The release of TPP from production sites to the air represents a 
source of human exposure in the occupational environment. The combustion 
of plastics and volatilization from plastics or water surfaces may also 
be a major pathway to the atmosphere. 

1.4.  Environmental levels and human exposure

    TPP has been widely found in air, water, sediment, and aquatic 
organisms, but levels in environmental samples are low.  The maximum 
levels reported are 23.2 ng/m3 in air, 7900 ng/litre in river water, 
4000 ng/g in sediment, and 600 ng/g in fish. 

1.5.  Effects on organisms in the environment

    The growth of algae is completely inhibited at TPP concentrations of 
1 mg/litre or more but is stimulated at lower concentrations (0.1 and 
0.05 mg/litre).  The nitrogenase activity of  Anabaena flos-aquae 
decreases in a dose-dependent manner from 84% at 0.1 mg/litre to 68% at 
5.0 mg/litre. 

    TPP is the most acutely toxic of the various triaryl phosphates to 
fish, shrimps, and daphnids. The acute toxicity index of TPP for fish 
(96-h LC50) ranges from 290 mg/litre in bluegills to 0.36 mg/litre in 
rainbow trout. The large difference in EC0 values between trout and 
fathead minnows may be due to the difference in their ability to 
metabolize TPP.  Sublethal effects on fish include morphological 
abnormalities such as congestion, degeneration, and haemorrhage from the 
smaller blood vessels (mainly in the gills) and behavioural 
abnormalities.  The immobility of fish exposed to 0.21-0.29 mg per litre 
completely disappeared within 7 days when the fish were transferred to 
clean water. 

1.6.  Effects on experimental animals and in vitro test systems

    The oral LD50 of TPP has been estimated to be >6.4 g/kg in rats and 
>2.0 g/kg in chickens. 

    TPP doses ranging from 0.5 to 2 g/kg were well tolerated by rabbits 
after intramuscular injection and by chickens after oral administration. 
In a 35-day feeding study, depression of body weight gain and increase 
in liver weight were observed at a dose of TPP in male Holtzman rats. 

    TPP was not teratogenic in Sprague-Dawley rats at dose levels up to 
690 mg/kg body weight.  No reproduction studies have been reported. 

    There are no data on the mutagenicity of TPP from well-validated 
tests, and there has been no adequate carcinogenicity study. 

    TPP did not cause delayed neurotoxicity following single 
subcutaneous exposures in cats (up to 1 g/kg) or in a 4-month study in 
Sprague-Dawley rats at dose levels up to 1% in the feed. 

    No immunotoxic effects were reported from a 120-day study in rats 
fed dose levels up to 1% in the feed. 

1.7.  Effects on humans

    While a statistically significant reduction in red blood cell 
cholinesterase has been reported in some workers, there has been no 
evidence of neurological disease in workers in a TPP-manufacturing 
plant.  There have been no reports of delayed neurotoxicity in cases of 
TPP poisoning. Contact dermatitis due to TPP has been described. 


2.1.  Identity

Chemical structure:


Molecular formula: C18H15O4P

Relative molecular mass: 326.3

CAS chemical name: Phosphoric acid, triphenyl ester

CAS registry number: 115-86-6

RTECS registry number: TC8400000

Synonyms:  Triphenyl phosphate; Triphenyl-phosphate; TPP

Trade name:  Phosflex TPP(R),; Disflamoll TP(R),;  Celluflex TPP(R),

Manufacturers and suppliers (Modern Plastics Encyclopedia, 1975):

Ashland Chemical Co.; Celanese Co.; Daihachi Chemical Industry Co., 
Ltd.; East Coast Chemicals Co.;  B.F. Goodrich Chemical Co.;  Mobay 
Chemical Co.; Monsanto Chemical Co.; Rhone-Poulenc Co.; Showa Ether Co., 
Ltd.; Stauffer Chemical Co. 

2.2.  Physical and chemical properties

The physical properties of TPP are listed in Table 1.

Table 1.  Physical properties of TPP
Physical state                       crystalline solid
Colour                               colourless
Odour                                very slightly aromatic
Melting point (°C)                   49-50a; 49b; 49.2c
Boiling point (°C)                   245 (11 mmHg)a,b; 220 (5 mmHg)c; 
                                     234 (5 mmHg)d; 370e
Relative density                     1.185-1.202 (25 °C)c; 1.185 (25 °C)d; 
Refractive index (at 25 °C)          1.552-1.563c
Flash point (°C)                     220b; 225c
Viscosity (cSt)                      11 (50 °C); 9.9 (55 °C)c
Vapour pressure (mmHg)               0.15 (150 °C); 1.90 (200 °C)c; 
                                     1.0 (193.5 °C)e
Henry's Law constant                 1.8-3.6 x 10-7 atm-m3/mol
Solubility in organic solvents       soluble in benzene, chloroform, ether, 
                                     acetone; moderately soluble in ethanola
Solubility in water (mg/litre)       1.9f; 0.73g; 2.1 (±0.1)h
Octanol-water partition coefficient  4.63f; 4.61i; 4.76j
(log Pow)

a    Windholz (1983)
b    Hine et al. (1981)
c    Modern Plastics Encyclopedia (1975)
d    Lefaux (1972)
e    Sutton et al. (1960)
f    Saeger et al. (1979)
g    Hollifield (1979)
h    Ofstad & Sletten (1985)
i    Kenmotsu et al. (1980b)
j    Sasaki et al. (1981)
    TPP is non-flammable and non-explosive.  It begins to decompose at 
about 600 °C but is not completely degraded even at 1000 °C in inert 
gas.  Under these conditions, TPP yields aromatic hydrocarbons 
(naphthalene, biphenyl, phenanthrene, anthracene, etc.), oxygenated 
aromatic compounds (phenol, dibenzofuran, diphenyl ether) and phosphoric 
oxides (ortho- , pyro-, meta-, and poly-phosphoric acids). With a large 
excess of air, complete combustion to carbon dioxide is accomplished 
within the temperature range 800-900 °C (Lhomme et al., 1984). 

    At ordinary temperature, TPP is hydrolysed very slowly in acidic and 
neutral solutions but rapidly in alkaline solutions.  The hydrolysis 
rate constants and half-lives are summarized in Table 2. In studies by 
Barnard et al. (1961), alkaline hydrolysis of TPP yielded diphenyl 
phosphate, but further hydrolysis to monophenyl phosphate and phosphoric 
acid was not observed under the experimental conditions used.  Under 
strong acidic conditions and at high temperature (100 °C), TPP readily 
hydrolyses to give phosphoric acid (Barnard et al., 1966). 

    In studies by Finnegan & Matson (1972), the photolysis of TPP 
yielded biphenyl (2%), the recovered ester amounting to 48%. The quantum 
yield for biphenyl formation was 6 x 10-4.

2.3.  Conversion factor

    Triphenyl phosphate         1 ppm = 13.35 mg/m3 air

2.4.  Analytical methods

    Analytical methods for determining TPP in air, water, sediment, 
fish, and biological tissues are summarized in Table 3.  General 
procedures for TPP analysis are similar to those for tricresyl phosphate 
(TCP) (WHO, 1990).  The detection limit of TPP in water is approximately 
20 ng/litre. 

    Diphenyl phosphate, a hydrolysis product of TPP, has been determined 
in sediment by extraction with aqueous methanol, clean-up with XAD-2 
resin and C-18 bonded silica cartridge, butylation, and gas 
chromatographic determination (Muir et al., 1983b). 

    TPP is present in several commercial triaryl phosphates, e.g., 
Santicizer-140,(R) Pydraul 50E,(R) (Monsanto Co.), Fyrquel GT,(R) and 
Phosflex 41-P,(R) (Stauffer Chemical Co.) (Deo & Howard, 1978). When TPP 
is identified, other triaryl phosphates are often detected at the same 

2.4.1.  Sample extraction

    TPP is extracted from water, sediment, fish, and air along with TCP. 
WHO (1990) gives details of methods. 

Table 2.  Hydrolysis rate constants and half-lives of TPP in aqueous solution
                                                    Rate constants
Solution              Temper-  pH           K1           K2            K1'             Half-   Reference
                      ature                 first        second        pseudo-         life
                      (°C)                  order        order         first
                                            (sec-1)      (M-1.sec-1)   order
Water                 27      alkaline                   2.7 x 10-1                            Wolfe 
60% dioxane-water     0       alkaline                   2.35 x 10-3                           Barnard 
                      10.1    alkaline                   4.77 x 10-3                           et al. 
                      24.7    alkaline                   1.06 x 10-2                           (1961)
                      35      alkaline                   2.32 x 10-2                           Barnard 
                                                                                               et al. 
NaOH (0.1 mol/        22      13.0                                                     0.49 h  Muir et 
litre)/acetone (1:1)                                                                           al.         
H3BO4/NaOH buffer     25      9                                                        3 days  Mayer et  
                                                                                               al. (1981)
Buffered water        21 ± 2  8.2                                      9.3 x 10-2/day  7.5     Howard & 
                                                                                       days    Deo (1979)
                      9.5                                                              1.3     Howard &  
                                                                                       days    Deo (1979)
Dioxane-water (3:1)   100     neutral                                  6.0 x 10-8/day  130     Barnard et 
                                                                                       days    al. (1961)
KH2PO4/Na2HPO4        25      7                                                        19      Mayer et  
                                                                                       days    al. (1981)
KHC8H4O4/NaOH buffer  25      5                                                        28      Mayer et 
                                                                                       days    al. (1981)
Dioxane-water (3:2)   100     neutral       6 x 10-8                                           Barnard
                              0.122M HClO4  1.43 x 10-5                                        et al. 
                              1.21M HClO4   10.8 x 10-5                                        (1966)
                              3.02M HClO4   6.45 x 10-5                                        Barnard 
                                                                                               et al. 

Table 3.  Methods for the determination of TPP
Sample type  Sampling method                           Analytical  Limit of    Applicability  Reference
             extraction/clean-up                         method    detection

Workplace    collect with Millipore filter, extract      GC/FPD    1 µg per    TCP & TPP      US NIOSH 
air          with ethanol                                          sample                     (1982)

Environment  trap with glycerol-Florisil column, eluate  GC/FPD    1 ng/m3     simultaneous   Yasuda 
air          with methanol, add water, and extact with                         method for     (1980)         
             hexane                                                            trialkyl/aryl

Air          collect by aspiration through ethanol,      TLC       5 ng/plate  TCP & TPP      Druyan 
             hydrolyse with NaOH; the resultant phenols                                       (1975)
             are reacted with  p -O2NC6H4N2+ and
             separated with silica gel plate

Drinking-    adsorb with XAD-2 resin, eluate with        GC/NPD    1 ng/litre  method for     Lebel et 
water        acetone-hexane or acetone                   GC/MS                 low level      al. (1979,
                                                                               trialkyl/aryl  1981)

River or     extract with methylene chloride or benzene  GC/NPD    0.02 µg/    simultaneous   Kenmotsu et 
sea water                                                GC/FPD    litre       method for     al. (1980a,
                                                                   (TPP)       trialkyl/aryl  1981b, 
                                                                               phosphates     1982b)

                                                         GC/MS     0.05 µg/                   Muir et al. 
                                                                   litre                      (1981)
                                                                   (TCP)                      Ishikawa et 
                                                                                              al. (1985)

Farm pond    reflux with methanol-water (9+1) or meth-   GC/NPD    1 ng/g      simultaneous   Muir et al. 
sediment     ylene chloride-methanol (1+1), clean-up by                        method for     (1980, 1981)
             acid alumina column chromatography                                triaryl        

Table 3.  (contd.)
Sample type  Sampling method                           Analytical  Limit of    Applicability  Reference
             extraction/clean-up                         method    detection

River        extract with acetonitrile or acetone,       GC/FPD    5 ng/g      simultaneous   Kenmotsu et 
or sea       clean-up by charcoal or Florisil column     GC/MS                 method for     al.(1980a,
sediment     chromatography                                                    trialkyl/aryl  1981b, 1982a, 
                                                                               phosphates     1982b, 1983)
                                                                                              Ishikawa et 
                                                                                              al. (1985)

Fish         extract with hexane or methanol, clean-up   GC/NPD    1 ng/g      simultaneous   Muir et 
             by gel permeation column chromatography     GC/MS                 method for     al. (1980,
             and acid alumina column chromatograpy                             triaryl        1981, 1983)

Fish         extract with acetonitrile and methylene     GC/FPD    5 ng/g      simultaneous   Kenmotsu et 
             chloride, clean-up by acetonitrile-hexane   GC/MS                 method for     al. (1980a)
             graphy, concentrated sulfuric acid extrac-                        trialkyl/aryl
             tion and Florisil column chromatography                           phosphates   

Human        extract with benzene or acetone-hexane      GC/NPD    1 ng/g      simultaneous   Lebel & 
adipose      (15 + 85), clean-up by gel permeation       GC/FPD                method for     Williams 
tissues      chromatography                                                    trialkyl/aryl  (1983)
2.4.2.  Clean-up procedures

    Clean-up procedures for TPP are similar to those for TCP (WHO, 
1990). It is difficult to separate TPP from other triaryl phosphates by 
Florisil or gel permeation chromatography. 

2.4.3.  Gas chromatography and mass spectrometry

    TPP is analysed simultaneously with TCP.  GC and mass spectrometry 
procedures are described in WHO (1990). 

2.4.4.  Contamination of analytical reagents

    Triaryl phosphates (TAPs) are widely used as flame retardants in 
plastics and hydraulic fluids. Their wide-spread use and release into 
the environment produces trace contamination of reagents used for 
analysis. Trace amounts of TPP have been found in Super Q water 
(Williams & Lebel, 1981), Corning water (Lebel et al., 1981), hexane, 
acetonitrile, and methylene chloride (Daft, 1982). TAPs have also been 
found in cyclohexane (Bowers et al., 1981), hexane (Hudec et al., 1981), 
and analytical grade filters (Daft, 1982). Care must be taken to avoid 
contamination of reagents in order to obtain reliable data in trace 
analysis of TPP. 

2.4.5.  Other analytical methods

    A colorimetric method has been developed for determination of TPP in 
air (Druyan, 1975), but the interference by other TAPs was not 
investigated.  Thin-layer chromatography (TLC) has been used for the 
determination of TPP in air (Druyan, 1975) and in plastics (Peereboom, 
1960; Braun, 1965).  The octanol/water partition coefficient of TPP has 
been determined by reversed phase TLC (Renberg et al., 1980).  It is 
difficult to separate the various TAPs by TLC (Bloom, 1973). Tittarelli 
& Mascherpa (1981) described a highly specific HPLC detector for TAPs 
using a graphite furnace atomic absorption spectrometer.  In general, 
TLC and HPLC have not been used as widely as GLC for the analysis of 


3.1.  Production levels and processes

    TPP does not occur naturally in the environment. Figures concerning 
total world production are not available, but 7250 tonnes was produced 
in the USA in 1977 (Boethling & Cooper, 1985) and 3750 tonnes in Japan 
in 1984. 

    TPP is produced from phosphorus oxychloride and phenol.

3.2.  Uses

    TPP was used, in Japan in 1984, as a flame-retardant in phenolics 
and phenylene-oxide-based resin for the manufacture of electrical and 
automobile components (3200 tonnes), as a non-flammable plasticizer in 
cellulose acetate for photographic films (500 tonnes), and for other 
miscellaneous purposes (50 tonnes)a.  Other uses of TPP are as a non-
combustible substitute for camphor in celluloid (which renders 
acetylcellulose, nitrocellulose, airplane "dope", etc. stable and 
fireproof), for impregnating roofing paper, and as a plasticizer in 
lacquers and varnishes (Windholz, 1983). It is also used as a 
plasticizer in vinyl automotive upholstery (Ahrens et al., 1978) and in 
cellulose acetate articles (Pegum, 1966). 

    TPP is also found as a component of hydraulic fluids and lubricant 
oils (WHO, 1990; Table 6), and of other triaryl phosphate esters: methyl 
diphenyl phosphate (triphenyl phosphate content, ca. 5%);  2-ethylhexyl 
diphenyl phosphate (ca. 5%); trixylenyl phosphate (ca. 5%); iso-decyl 
diphenyl phosphate (ca. 45%); cresyl diphenyl phosphate (ca. 45%); 
isopropylphenyl diphenyl phosphate (ca. 45%) (Daft, 1982). 

a  Personal communication to IPCS from the Association of the Plasticizer
   Industry of Japan (1985).



     TPP has been found in various environmental media, but usually at 
 low levels. It may be released by leakage at sites of production and use 
 and by the combustion of plastics.  No figures are available on the 
 amounts released into the environment. 

     The solubility of TPP in water is low, and it is readily adsorbed 
 onto sediment. 

     The rate of biodegradation in water is dependent on water quality (1 
 mg/litre was degraded in 4 days in River Mississippi water).  Little or 
 no degradation occurs in heat-sterilized river water.  The degradation 
 pathway is reported to involve stepwise enzymatic hydrolysis. 

     Water treatment techniques, both for waste water and drinking-water, 
 reduce TPP levels by at least an order of magnitude. 

     Bioaccumulation data are available from laboratory studies, but 
 should be considered to represent a bioaccumulation potential.  
 Depuration, as measured by clearance rate constant, is higher for 
 rainbow trout than for fathead minnows by about 50%. 

4.1.  Transport and transformation in the environment

4.1.1.  Release to the environment

    The release of TPP into the air at production sites represents a 
potential source of human contamination.  It has been suggested that, 
since TPP in the reactor and purification vessels is hot, mist and 
vapour coming from leaks in the reactor and from the open receiving tank 
are the main source of TPP in the air (Sutton et al., 1960) (see also 
section 5.2).  Recent figures however are not available.  A low 
concentration (0.057 mg/m3) of TPP was detected near a zinc die cast
machine where hydraulic fluids were used (US NIOSH, 1980). 

    Combustion of plastics or volatilization from plastics or water 
surface may also be a major pathway to the atmosphere.  Vick et al. 
(1978) found TPP emitted in the vapour phase and on particulate matter 
from a utility plant.  The concentrations were not reported. 

    The entry of TPP into the aquatic environment is thought to occur 
principally via hydraulic fluid leakage, as well as by leaching from 
vinyl plastics and, to a minor extent, from manufacturing processes 
(Ahrens et al., 1978; Mayer et al., 1981; WHO, 1990). 

4.1.2.  Fate in water and sediment

    The solubility of TPP in water is low (Table 1).

    Monitoring studies have shown trialkyl and triaryl phosphates to be 
present in water and sediment sampled near major industrialized sites 
(Konasewich et al., 1978; Sheldon & Hites, 1978, 1979; Mayer et al., 

1981; Williams & Lebel, 1981; Aldous, 1982; Williams et al., 1982; 
Ishikawa et al., 1985).  The adsorption coefficient of TPP on marine 
sediment was found to be 59 (Kenmotsu et al., 1980b).  Muir et al. 
(1982) showed rapid equilibrium of TPP with the bottom sediment in a 
shallow pond (depth 0.5 m) within 10 h. 

4.1.3.  Biodegradation

    TPP (200 µg) was completely degraded within 4 days in 200 ml of 
River Mississippi (USA) water at room temperature (Saeger et al., 1979). 
Howard & Deo (1979) measured the degradation rate constants for TPP in 
non-sterilized natural water (Seneca River and Lake Ontario, USA). 
Little degradation occurred for the first two days, followed by a loss 
more rapid than in distilled water at comparable pH.  After two days, 
the pseudo-first-order rate constants at pH 8.2 were 0.64 and 0.34 days-1
for the two natural water samples, and 0.093 days-1 for distilled 
water.  The rapid degradation (99.2% in 7 days) of TPP (1 mg/litre) was 
also found in a river die-away study using Neya and Oh River water 
(Osaka, Japan), whereas no degradation was observed during 15 days in 
heat-sterilized river water (Hattori et al., 1981). In clear non-
sterilized sea water, the degradation was very slow (35.1% in 14 days) 
(Hattori et al., 1981). 

    Primary biodegradation rates from semicontinuous activated sludge 
studies generally show the same trend in degradation rates as river die-
away studies; TPP (3-13 mg per litre, 24-h feed) revealed 96% (± 2%) 
degradation (Saeger et al., 1979).  The ultimate biodegradability was 
measured using the apparatus and procedure developed by Thompson & 
Duthie and modified by Sturm; the theoretical carbon dioxide evolution 
from TPP (18.3 mg/litre) was 81.8% (Saeger et al., 1979). 

    The degradation pathway for TPP is reported to involve stepwise 
enzymatic hydrolysis to orthophosphate and phenolic moieties.  The 
phenol would be expected to undergo further degradation (Barrett et al., 
1969; Pickard et al., 1975). 

4.1.4.  Water treatment

    Data from FMC Corporation (USA) show that TPP (0.74 mg per litre) in 
waste water was reduced to 0.07 mg/litre in the effluent water by 
biological treatment (Boethling & Cooper, 1985).  TPP was reduced from 
16 µg/litre to 2 µg/litre by classical secondary treatment methods, and 
from 0.2 µg/litre to 0.03 µg/litre by standard techniques for drinking-
water treatment (Sheldon & Hites, 1979).  Fukushima & Kawai (1986) also 
reported that TPP (0.054-2.12 µg/litre) in untreated water was reduced 
to 0.005-0.082 µg/litre by conventional waste water treatment. 

4.2.  Bioaccumulation

4.2.1.  Fish

    Data on the bioconcentration and depuration of TPP are given in 
Table 4. None of the exposures were considered to be representative of 
realistic environmental levels. Moreover the bioconcentration factor 
(BCF) measured in the laboratory must be considered to represent a 
bioaccumulation potential rather than an absolute bioaccumulation factor 
(Veith et al., 1979). 

    Several equations have been presented to predict the 
bioconcentration factors of organic chemicals in various fish strains 
using octanol-water partition coefficient (Pow) or water solubility 
(Neely et al., 1974; Lu & Metcalf, 1975; Kanazawa, 1978; Veith et al., 
1979; Sasaki et al., 1982). 

    Of six tissues of fish exposed with 14C-triphenyl phosphate, liver 
had the highest concentration (10 µg/g at 4 h post-treatment) and also 
showed the highest rate of 14C-triphenyl phosphate depuration.  The 
rapid clearance from liver suggests extensive TPP metabolism.  Rates of 
uptake of radioactivity (µg/g tissue per h) by the six tissues were as 
follows: liver, 2.75; kidney, 2.01; caeca, 0.62; intestine, 0.53; 
muscle, 0.45; blood, 0.56 (Muir et al., 1980b). 

    Clearance of TPP was biphasic with more rapid rates of clearance in 
the first 6 days after transfer to clean water, especially in the case 
of rainbow trout (Muir et al., 1983a).  The clearance rate constant was 
higher for rainbow trout than for fathead minnows by about 50% (Muir et 
al., 1983a). 

Table 4.  Bioaccumulation and clearance of TPP by fish
Species    Temp  Flow/ Analy-  BCF          Exposure       Uptake   Clearance   Depur-    Reference
           (°C)  stat  tical   (k1/k2)      concentration  rate     rate        ation
                       methoda              (mg/litre)     (k1,     (k2 x 103,  half life   
                                                           h-1)     h-1)        (h)
Killfish    25   Stat  GC-FPD  157-390      1                                   1.2       Sasaki et al. 
 (Oryzeas                                                                                  (1982)
 latpes)                GC-FPD  250-500      0.25                                          Sasaki et al. 
                 Flow  GC-FPD  84-193       1                                             Sasaki et al. 

Rainbow     10   Stat  TR      1368 ± 329b  0.005-0.05              11.6-17.4   42.5      Muir et al. 
trout                                                                                     (1983a)
 (Salmo                 TR      573 ± 97c                   9.7c
 gairdneri)             TR      931 ± 122d                           17.7d
                       HER     324 ± 99c                            20.7
            10   Stat  TR      2590b        0.05           43.36    17.9 (fast)           Muir et al. 
                       TR      18 900b                              2.45 (slow)
            12   Stat  GC-FPD  271                                  12.96                 Sitthichaikasem

Fathead     10   Stat  TR      1743 ± 282b  0.005-0.05              7.6-14.0    49.6      Muir et al. 
minnows                                                                                   (1983a)
 (Pimephales            TR      561 ± 115c                           7.2c
 promelas)              TR      218 ± 55d                   15.4d
                       HER     420 ± 25c                                        30.0

Goldfish    25   Stat  GC-FPD  6-11                                                       Sasaki et al. 
 (Carassius                                                                                (1981)
a    GC-FPD = gas chromatography (flame photometric detector) after suitable extraction; 
     TR = total radioactivity; HER = hexane-extractable radioactivity.
b    BCF was calculated by the "initial rate method".
c    The static test method was used (Zitko, 1980).
d    K1 and k2 were derived by non-linear regression calculation.
4.2.2.  Chironomid larvae

    Muir et al. (1983b) studied the accumulation of TPP by  Chironomus 
 tentans  larvae exposed to water and sediment spiked with 14C-triphenyl 
phosphate. The overall accumulation has been described by the following 

        dCc/dt = k1(Cw) - k2(Cc) + k3(Cs)

where Cc is the concentration in the larvae, Cw the concentration in 
water, Cs the concentration in sediment, k1, k3 are uptake rate 
constants, and k2 is the elimination rate constant. 

The rate constant k3 has been described by the following equation:

       k3 = k1(Cw/Cs) x (CFs - CFw)/(CFw)

where CFs is the equilibrium concentration factor for larvae in sediment 
and CFw is the equilibrium concentration factor for larvae in water. 

The results are summarized in Table 5.
Table 5.  Uptake rate constants (k1) calculated by use of a first-order
kinetic model and concentration factors for uptake of TPP by Chironomid larvae
                     High concentration                Low concentration
                     (500 µg/kg sediment)              (50 µg/kg sediment)
System          k1(h-1)     CFw       CFs         k1(h-1)      CFw        CFs
Pond sediment   0.4 ± 0.1   6 ±  0    12 ± 10     0.6 ± 0.2    12 ±  4    18 ±  8
River sediment  2.1 ± 0.8   45 ± 17a  78 ± 34a    4.2 ± 1.6    88 ± 34    90 ± 41
Sand sediment   3.3 ± 1.0   64 ± 33b  173 ± 69b   10.4 ± 3.1   208 ± 62b  138 ± 17b

a    Significant difference (P = 0.05) between mean larval concentrations in water 
     and in sediment using the t-test.
b    Significant difference (P = 0.01) between mean larval concentrations in water 
     and in sediment using the t-test.

    The relative contribution of sediment and water to the body burdens 
observed in larvae (24-h exposure) was estimated by calculating uptake 
rates for water (k1)(Cw) and for sediment (k3)(Cs).  The results 
indicate that contributions from water and sediment were roughly 
equivalent for most sediments for a sediment-to-water ratio of 1:5. The 
authors noted however: 

     "A greater ratio of water to sediment would tend to increase 
     the contribution of uptake from water proportionally.  A 
     water-to-sediment ratio of 100:1 would reduce the contribution 
     of sediment uptake to 10%, and would make it difficult to show 
     significant differences between water and sediment 

    Initial elimination rate constants and half-lives of TPP for larvae 
exposed to different sediment-water systems are shown in Table 6. 

Table 6.  Elimination rate constants and half-lives of TPP for
Chironamid larvae
                    Elimination rate
    System          k2 (h-1)       Half-life (h)
Pond sediment       0.023 ± 0.012      30.4 ± 16.1
River sediment      0.011 ± 0.004      62.7 ± 24.5
Sand sediment       0.016 ± 0.010      44.4 ± 28.0
River water         0.039 ± 0.013      17.6 ±  6.0

4.2.3.  Environmental fate in artificial pond water

    The environmental fate of radiolabelled TPP (60 µg per litre) in 
artificial pond water was studied by Muir et al. (1982).  The 
radioactivity observed in each pond compartment is shown in Table 7. 
Small losses of TPP by volatilization were thought to occur, but this 
was not confirmed by direct measurement above the water surface.  
Despite differences in fish species and water temperatures between 
laboratory and field experiments, the observed body burdens of TPP were 
similar, for the first 24 h of the experiment, to those predicted on the 
basis of laboratory data. However, at 72 and 240 h, the predicted values 
were higher than those observed.  These results were considered to 
reflect more rapid clearance of TPP by fathead minnows than by rainbow 

Table 7.  Percentage of TPP radioactivity in the 
various compartments of a pond
Time(h)   Water  Sediment  Duckweed   Fish   Total
10        74     29        1.4        2.7    107.1
24        52     34        1.4        3.4    90.8
32        31     -         -          -      -
48        34     43        1.2        1.3    79.5
72        28     33        0.9        0.9    62.8
120       23     40        0.5        0.6    64.1
240       13     36        0.5        0.5    50.0



     TPP has been widely found in air, water, sediment, and aquatic 
 organisms, but only at low levels.  Higher levels have been found only 
 in sediments near industrialized areas. 

     Ambient air concentrations of TPP in rural areas range from 0.5 to 
 1.4 ng/m3  and in urban areas from 0.9 to 14.1 ng/m3. 

     TPP levels in surface water from 3 to 700 ng/litre have been 
 measured, values up to 7900 ng/litre occurring near facilities producing 
 either aryl phosphates or hydraulic fluids containing TPP. These high 
 values probably result from TPP bound to suspended sediment. Reported 
 drinking-water levels are several orders of magnitude lower (0.3-30 
 ng/litre), suggesting that TPP is removed by adsorption to filtration 
 media in water-treatment plants.  No TPP has been detected in potable 
 water from wells.  There is no information available on levels in 

     Levels of TPP in river and marine sediment range from 0.2 to 200 
 ng/g, but values of up to 4000 ng/g have been reported in sediments near 
 manufacturing sites for automobile parts. There has been one report of 
 TPP being detected in agricultural soils, but no values were given. 

     In fish and shellfish, TPP tissue levels from 2 to 150 ng per g have 
 been reported.  No TPP has been detected in human adipose tissue and 
 there are no data on TPP for any other species. 

     Exposure to humans can occur by several routes, including the 
 ingestion of contaminated drinking-water, fish, shellfish, and other 
 foodstuffs. US FDA total-diet studies have found average daily intake 
 levels of 0.3-4.4, 1.2-1.6, and 0.5-1.6 ng per kg body weight per day 
 for infants, toddlers, and adults, respectively. It should be noted that 
 TPP occurred in less than 1% of the foods in these diets. 

     Occupational exposure can occur in manufacturing industries and other
 areas such as automobile or aircraft facilities handling hydraulic fluids.  
 Levels of 0.008 to 29.6 mg/m3 have been detected in air, the highest 
 values occurring at TPP-manufacturing sites. 

5.1.  Environmental levels

    TPP has been found widely in air, water, sediment, and aquatic 
organisms. The levels of TPP in environmental samples are low (Table 8), 
although moderately high levels have often been found in sediment 
collected near heavily industrialized areas (Table 9 and 10). 

5.1.1.  Air

    Yasuda (1980) measured the distribution of various organic 
phosphorus compounds in the atmosphere above the eastern Seto Inland 
Sea, Japan, and found TPP at levels of 0.5-1.4 ng/m3 in 3 out of 4 
samples.  He also measured concentrations of phosphate esters in the 
atmosphere above the Dogo Plain and Ozu Basin of Western Shikoku, Japan, 

these being mainly agricultural areas.  TPP was detected only in the 
urban air of a middle-size city (Matsuyama) at levels of 0.9-14.1 ng/m3. 

5.1.2.  Water

    Although there have been many studies of TAPs in water, TPP has not 
often been detected in natural waters. According to the annual reports 
of the Environment Agency of Japan, TPP has not been detected in river 
or sea water at any sampling points in Japan.  Detection limits varied 
from 20 to 200 ng/litre at the various laboratories (EAJ, 1977, 1981).  
Kawai et al. (1978) detected TPP in river water sampled in Osaka, Japan, 
at levels of 50-700 ng per litre, and Ishikawa et al. (1985) detected 
levels of 13-31 ng/litre in 5 out of 16 samples of river water in 
Kitakyushu City, Japan, but none in sea water. Both cities are located 
in the most heavily industrialized area of Japan.  In Tokyo, Japan, TPP 
was not found in river or sea water (detection limit: 20 ng/litre) by 
Wakabayashi (1980), whereas a level of 3 ng/litre was detected in sea 
water by Sugiyama & Tanaka (1982). 

    High concentrations of TAPs have frequently been detected in river 
water sampled near producer and user sites.  Sheldon & Hites (1978) 
found 100-300 ng TPP/litre in 2 out of 5 samples of Delaware River (USA) 
water collected in winter, and 100-400 ng/litre in 11 out of 12 samples 
collected in summer.  The highest level (16 000 ng/litre) of TPP was 
found in a waste stream entering Philadelphia's NorthEast Sewage 
Treatment plant for industrial effluents (Sheldon & Hites, 1979). 
Concentrations of TPP in four samples of Kanawha River (USA) water 
collected 13 km downstream from the outfall of an aryl phosphate 
manufacturing plant ranged from 300 to 1200 ng/litre (Boethling & 
Cooper, 1985).  Mayer et al. (1981) also detected TPP (100-7900 
ng/litre) in Mississippi River (USA) water sampled at St. Louis 
(Missouri), where two phosphate ester hydraulic fluids were being 
produced by Monsanto Co. 

Table 8.  Concentrations of TPP in environmental air, water, sediment, and fish at various locations
Year   Location              Sample                  Concentrationa        Number of   Reference
1975   Japan (various        river and sea water     ND (20-200 ng/litre)  (0/100)     EAJ (1977)
       locations)            river and sea sediment  ND (2-50 ng/g)        (0/100)
                             fish                    ND (5-50 ng/g)        (0/100)

1976   Osaka (Japan)         river water             50-700 ng/litre       (11/13)     Kawai et al. 
1976   Shikoku (Japan)       atmosphere              0.9-14.1 ng/m3        (4/19)      Yasuda (1980)

1977   Eastern Seto          atmosphere              0.5-1.4 ng/m3         (3/4)
       Inland Sea (Japan)

1978   Eastern Ontario       drinking-water          0.3-2.6 ng/litre      (12/12)     Lebel et al. 
       water treatment                                                                 (1981)
       plant (Canada)

1978   Tokyo (Japan)         river water             ND (20 ng/litre)      (0/12)      Wakabayashi 
                             sea water               ND (20 ng/litre)      (0/3)       (1980)
                             river sediment          0.7-3.3 ng/g          (10/15)
                             sea sediment            0.2-0.3 ng/g          (2/3)

1979   Canada (various       drinking-water          0.3-8.6 ng/litre      (20/60)     Williams & 
       locations)                                                                      Lebel (1981)

1980   Great Lake (Canada)   drinking-water          0.2-4.8 ng/litre      (11/12)     Williams et 
                                                                                       al. (1982)
1980   Kitakyushu            river water             13-31 ng/litre        (3/16)      Ishikawa et 
       City (Japan)          sea water               ND (10 ng/litre)      (0/9)       al. (1985)
                             sea sediment            ND (5 ng/g)           (0/6)

1980   Seto Inland           fish and shellfish      2-6 ng/g              (12/41)     Kenmotsu et 
       Sea (Japan)                                                                     al. (1981a)
1981   Tokyo Bay             sea water               3 ng/litre                        Sugiyama & 
       (Japan)                                                                         Tanaka (1982)

NR     USA                   drinking-water          10-120 ng/litre                   Muir (1984)
a  Figures in parentheses are detection limits
   ND = not detected; NR = not reported

Table 9.  Concentration of TPP in water, sediment, and fish muscle at industrialized and non-industrialized sites in the USAa
Location                                      Water (ng/litre)   Sediment (ng/g)   Fish (ng/g)
Waukegan Harbor, Illinois                     ND (0/5)           10 (2/3)          ND (0/13)

Waukegan Bay, Illinois                        ND (0/4)           ND (0/3)          NR
Upper Saginaw River, Michigan                 100 (3/3)          10 (3/3)          ND (0/12)

Saginaw River at Lake Huron                   600-700 (4/4)      1000-4000 (3/3)   100 (1/10)

Illinois River, Grafton Illinois              100 (4/4)          ND (0/3)          ND (0/4)

Missouri River, Fenton, Missouri              ND (0/4)           ND (0/3)          ND (0/9)

Missouri River at Chesterfield, Missouri      100 (1/4)          ND (0/4)          NR

Missouri River, Halls Ferry, Missouri         100-200 (3/3)      ND (0/3)          NR

Mississippi River above St. Louise, Missouri  ND (0/5)           NR                500 (1/3)

Mississippi River at St. Louise, Missouri     100-7900 (9/15)    100 (2/6)         NR

Mississippi River below St. Louise, Missouri  100-400 (3/3)      ND (0/3)          100 (1/4)

Kanawha River, Winfield, W. Virginia          100-800 (3/3)      20-200 (3/6)      100-600 (13/27)

San Francisco Bay, California                 100 (2/5)          NR                NR
a  From: Mayer et al. (1981); measurements were made from November 1977 to May 1978; figures in 
   parentheses indicate number of samples (detected/analysed); detection limits were 100 ng/litre 
   (water), 10 ng/g (sediment), and 100 ng/g (fish); ND = not detected; NR = not reported

Table 10.  Concentrations of TPP near sites producing or using trialkyl/aryl phosphates
Year   Location                         Sample                 Concentration       Number of   Reference
1975   New Orleans (USA)                finished water         120 ng/litre        NR          Boethling 
                                                                                               & Cooper 
1976   Delaware River (USA)             river water (winter)   100-300 ng/litre    (2/5)       Sheldon & 
                                        river water (summer)   100-400 ng/litre    (11/11)     Hites 
1977   Delaware River (USA)             influent of sewage     16 000 ng/litre     NR          Sheldon & 
                                        treatment plant                                        Hites 
                                        effluent of sewage     2000 ng/litre       NR          (1979)
                                        treatment plant
                                        river water            200-300 ng/litre    (3/3)
                                        effluent of water      30 ng/litre         NR
                                        treatment plant

1978   Kanawha River (USA)              river water            300-1200 ng/litre   NR          Boethling 
                                                                                               & Cooper 
1980   FMC Corp. Plant (USA)            waste water            740 000 ng/litre    NR          Boethling 
                                        effluent water         7000 ng/litre       NR          & Cooper 

1980   Automobile manufacture (USA)     workplace air          0.008-0.057 mg/m3   (6/6)       US NIOSH 
1983   Saginaw River (USA)              river water            700 ng/g            (1/4)       Boethling 
                                                                                               & Cooper 
NR     TPP manufacturing plant (USA)    workplace air          0.5-29.6 mg/m3      (78/78)     Sutton et 
                                                                                               al. (1960)
NR     Waukegan Harbor, Illinois (USA)  fish (carp, goldfish)  60-150 ng/g         (3/3)       Lombardo & 
                                                                                               Egry (1979)
5.1.3.  Sediment and soil

    Relatively high concentrations of TPP have occasionally been found 
in sediments collected near heavily industrialized areas.  Mayer et al. 
(1981) found TPP levels of 1000-4000 ng/g in sediment from the Saginaw 
River (Lake Huron) sampled at 1.6-3.2 km downstream from several plants 
manufacturing automobile spare parts (Boethling & Cooper, 1985). They 
also detected TPP levels of 10-200 ng/g at Waukegan Harbor (Illinois), 
Upper Saginaw River (Michigan), the Mississippi River at St. Louis 
(Missouri), and the Kanawha River at Winfield (West Virginia) (Mayer et 
al., 1981).  According to the annual reports of the Environment Agency 
of Japan, TPP has not been found at any sampling points in Japan. The 
detection limits varied from 2 to 50 ng/g at the various laboratories 
(EAJ, 1977). Wakabayashi (1980) detected TPP levels of 0.7-3.3 ng/g in 
10 out of 15 river sediment samples, and 0.2-0.3 ng/g in 2 out of 3 sea 
sediment samples analysed in Tokyo. 

    Caines & Holden (1976) identified TPP in agricultural soils 
collected from vineyards in Scotland, but the concentration was not 

5.1.4.  Fish

    Lombardo & Egry (1979) found TPP levels of 60-150 ng/g in carp and 
goldfish caught near a site at Waukegan Harbor (USA) where aryl 
phosphate hydraulic fluids were used. Mayer et al. (1981) detected 
concentrations of 100-600 ng per g in 16 out of 82 samples collected in 
several rivers in the USA.  According to the annual reports of the 
Environment Agency of Japan, TPP has not been detected in fish caught at 
any sampling points in Japan.  The detection limits ranged from 5 to 50 
ng/g at the various laboratories (EAJ, 1977, 1981).  Kenmotsu et al. 
(1981a) found TPP levels of 2-6 ng/g in 12 out of 41 samples collected 
from Seto Inland Sea, Japan. 

5.2.  General population exposure

5.2.1.  Food

    Gilbert et al. (1986) analysed composite total-diet samples 
(representative of 15 different commodity food types encompassing an 
average adult diet for each of eight regions in the United Kingdom) for 
the presence of trialkyl and triaryl phosphates.  Of the food groups, 
offal, other animal products, and nuts consistently contained the 
highest levels, but the proportion of individual compounds in the 
different food groups varied.  Trioctyl phosphate was the major 
component in the carcass meat, offal, and poultry groups, and there were 
significant amounts of TPP and TBP.  Total phosphate intake was 
estimated to be between 0.07 and 0.1 mg per person per day. 

    Gunderson (1988) reported the presence of TPP in samples collected 
between April 1982 and April 1984 during FDA total-diet studies. The 
mean daily intakes of TPP were 0.3-4.4, 1.2-1.6, and 0.5-1.6 ng/kg body 
weight per day for infants, toddlers, and adults, respectively. 

5.2.2.  Drinking-water

    Lebel et al. (1981) analysed TAPs in drinking-water sampled from 
eastern Ontario water treatment plants and found TPP levels of 0.3-2.6 
ng/litre in all of the 12 samples collected.  An extended survey of 
drinking-water was conducted in Canada (Williams & Lebel, 1981).  TPP 
was detected at levels of 0.3-8.6 ng/litre in 7 out of 60 samples of 
treated potable water obtained at the treatment plants of 29 
municipalities. Higher levels of TPP were present in treated water 
obtained from river sources, compared with samples from lake sources, 
and TPP was not found in potable water from wells.  TPP was also 
detected in 11 out of 12 samples of drinking-water obtained from 12 
water treatment plants located around the Great Lakes (USA and Canada) 
at concentrations from 0.2 to 4.8 ng/litre (Williams et al., 1982).  
Sheldon & Hites (1979) reported a relatively high level of TPP (30 
ng/litre) in finished drinking-water sampled from a water treatment 
plant located near a sewage treatment plant handling industrial 

    In general, the concentration of TPP in drinking-water is 100- to 
1000-fold lower than that in river or lake water.  Due to its adsorption 
to sediment, TPP can efficiently be removed by filtration at water 
treatment plants. 

5.2.3.  Human tissues

    There has been only one report of TAPs being present in human 
adipose tissues (Lebel & Williams, 1983). TPP was not detected. 

5.3.  Occupational exposure

    Sutton et al. (1960) investigated the concentration of TPP in the 
air of a TPP-manufacturing plant.  The levels found at various locations 
are indicated in Table 11. 

Table 11.  Air concentrations of TPP at various 
locations in a manufacturing plant
Location              Number of    Range      Mean
                      samples      (mg/m3)    (mg/m3)
Reactor room             6         1.4-2.2    1.8

Purification area
 General room air        6         1.0-3.9    2.4
 Receiving tank         10         5.0-29.6   12.0

Flaker room
 General room air        6         1.8-3.7    2.6
 Flaker                 11         2.6-6.8    4.5

Bagging area
 General room air        5         2.2-7.8    4.1
 Bagger                 23         0.5-20.8   8.2
 Stacking bags          11         0.7-7.4    5.4

    TPP has been detected at concentrations of 0.008-0.057 mg/m3 in the 
air at automobile manufacturing plants where hydraulic fluids are used 
(US NIOSH, 1980). 



     The primary productivity of green algal cultures was inhibited (to 
 50%) by exposure to TPP (0.26 to 0.5 mg/litre) for 7 days, and the 
 nitrogenase activity of cyanobacteria (blue-green algae) was inhibited 
 at 5 mg/litre. Fungal spore germination was unaffected at 5 x 10-3

     The 48-h LC50  for Daphnia is 1.0 mg/litre and 96-h LC50 
 values for fish range from 0.36 to 290 mg/litre. The no-observed-effect 
 level for growth and survival of rainbow trout fry is 1.4 µg/litre. 

     There is no information on the toxicity of TPP to organisms living 
 in or ingesting sediment and none on terrestrial species other than 

6.1.  Unicellular algae and fungi

    TPP was the most toxic compound among six TAPs tested for effects on 
the primary productivity of algae (Wong & Chau, 1984).  The growth of 
green algae was completely inhibited at concentrations of 1 mg/litre or 
more but stimulated at lower concentrations (0.1 and 0.05 mg/litre) 
(Wong & Chau, 1984). The nitrogenase activity, measured by the acetylene 
reduction technique, of a cyanobacterium (blue-green alga:  Anabaena 
 flos-aquae)  was affected by TPP.  Additions of 0.1, 1.0, and 5.0 
mg/litre reduced the nitrogenase activity to 84, 77, and 68% of the 
control value, respectively (Wong & Chau, 1984).  These data are 
summarized in Table 12. 

    TPP did not show any toxicity, as measured by spore germination, to 
the fungus  Aspergillus niger  at a concentration of 5 x 10-3 
mol/litre.  However, it inhibited fungal respiration by 8-9% (Eto et 
al., 1975). 

6.2.  Aquatic organisms

Data on the toxicity of TPP to aquatic organisms are given in Table 13.

Table 12.  Toxicity of TPP and its products for freshwater unicellular algae
Organism        Chemical  Temper-  Species                    Effect                 Concen-    Reference
                          ature    (mg/litre)                                        tration   
                          (°C)                                                       (mg/litre)
Alga              TPP     20        Ankistrodesmus falcatus    7-day IC50 for         0.26       Wong & 
                                    acicularis                 primary productivity              Chau 
Green alga        TPP     20        Scenedesmus quadricaudata  7-day IC50 for         0.50       Wong & 
                                                              primary productivity              Chau 
Green alga        TPP               Selenastrum capricornutum  96-h EC50              2          Mayer
                  P50E              Selenastrum capricornutum  96-h EC50              5          et al. 
                  P115E             Selenastrum capricornutum  96-h EC50              > 1000    (1981)

Cyanobacterium    TPP     20        Anabaena flos-aquae        28-h Inhibition of     5          Wong & 
(blue-green alga)                  61% of control             acetylene reduction               Chau 
Lake Ontario      TPP     20                                  IC50 for primary       0.2        Wong & 
phytoplankton                                                 productivity                      Chau

Table 13.  Toxicity of TPP for aquatic organisms
Organisms          Age/size       Temper- pH   Flow/ Hard-  End-point    Parameter   Concent-   Reference
                                  ature        stat  ness   or                       ration    
                                  (°C)               (mg/   criteria                 (mg/litre)        
                                                     litre) used                               
Rainbow trout      Fry: 0.11 g,                stat                      96-h LC50   0.36       Palawski 
 (Salmo             24 mm, 12 days                                                               et al. 
 gairdneri)         past swim-up                                                                 (1983)
                   Fry: 0.11 g,                stat         immobility,  96-h LC50   0.30       Palawski 
                   24 mm, 12 days                           mortality,                          et al. 
                   past swim-up                             loss of                             (1983)
                   stage                                    equilibrium

                   Fry            12(±1)  7.2  stat  272    mortality    96-h LC50   0.40       Mayer et 
                                               flow  272    and growth   90-d EC0    >0.0014   al. (1981)
                   0.60 g         12      7.4  stat  40                  96-h LC50   0.37       Mayer &
Fathead minnow                                 stat                      96-h LC50   0.66       Mayer  
 (Pimephales        Egg and fry                 flow         mortality    90-d EC0    0.087-0.27 et al. 
 promelas)          Egg and fry                 flow         and growth   90-d EC0    >0.23     (1981)
                   1.00 g         22      7.3  stat  44                  96-h LC50   1.0        Mayer & 

Sheepshead minnow                              stat                      96-h LC50   0.32-0.56  Mayer et 
 (Cyprinodon                                                                                     al. (1981)

Bluegill           33-75 mm       23      7.6- stat  55                  96-h LC50   290        Dawson et 
 (Leptomis                                 7.9                                                   al. (1977)

Killifish          0.1-0.2 g      25           stat                      96-h LC50   1.2        Sasaki et 
 (Oryzias                                                                                        al. (1981)

Table 13.  Toxicity of TPP for aquatic organisms
Organisms          Age/size       Temper- pH   Flow/ Hard-  End-point    Parameter   Concent-   Reference
                                  ature        stat  ness   or                       ration    
                                  (°C)               (mg/   criteria                 (mg/litre)        
                                                     litre) used                               
Goldfish           0.8-2.8 g                   stat                      96-h LC50   0.70       Sasaki et 
 (Carassius                                                                                      al. (1981)

Channel catfish    0.23 g         22      7.5  stat  38                  96-h LC50   0.42       Mayer & 
 (Ictalurus                                                                                      Ellersieck 
 punctatus)                                                                                      (1986)

Tidewater          40-100 mm      20           stat                      96-h LC50   95         Dawson 
silverside                                                                                      et al. 
 (Menidia                                                                                        (1977)

Mysid shrimp                                   stat                      96-h LC50   0.18-0.32  Mayer 
 (Mysidopsis                                                                                     et al. 
 bahia)                                                                                          (1981)

Water flea                                     stat                      48-h EC50   1.0        Mayer 
                                                                                                et al. 
    The 96-h LC50 values for pure TPP to fish range from 0.36 mg/litre 
for the rainbow trout (Palawski et al., 1983) to 290 mg/litre for the 
bluegill (Dawson et al., 1977). 

    The growth and survival of rainbow trout fry were not affected when 
they were exposed to TPP at a concentration of 0.0014 mg/litre (Mayer et 
al., 1981). At 0.23 mg/litre, the survival of fathead minnow fry was 
significantly reduced, but neither the growth of the survivors nor 
hatchability was affected (Mayer et al., 1981; Palawski et al., 1983). 

    Sublethal effects of TPP on fish include morphological and 
behavioural abnormalities (Wagemann et al., 1974; Lockhart et al., 
1975).  Spinal curvature was observed in surviving rainbow trout exposed 
for 24-72 h at concentrations near the LC50 (Sasaki et al., 1981; 
Palawski et al., 1983). 

    Death of goldfish occurred in a 20-litre water tank in which a piece 
(18 x 38 cm) of car seat upholstery containing TPP had been immersed 
(Ahrens et al., 1978).  Goldfish exposed to TPP (concentration not 
stated) showed histopathological lesions characterized by congestion, 
degeneration, and haemorrhage of the smaller blood vessels, principally 
venules and capillaries.  Such vascular pathology was most pronounced in 
the gills.  Similar but less pronounced congestion of the smaller blood 
vessels was noted in the brain, spinal cord, pseudobranch and kidneys 
(Ahrens et al., 1978).  Immobility of fish exposed to 0.21-0.29 mg 
TPP/litre disappeared within 7 days after exposure had stopped 
(Palawski, et al., 1983). 

    Exposure of aquatic organisms to TPP would normally arise from 
spillage of hydraulic fluids containing this compound. Studies have been 
made of the effects of various products, especially Pydraul 50E and 
115E, Houghtosafe 1120, and Santicizer 154, on fish and aquatic 
invertebrates.  Where comparisons have been made between different 
components of the fluids, TPP has been shown to be responsible for most 
of the acute toxicity observed. However, certain characteristic 
sublethal symptoms seen with these hydraulic fluids (such as cataracts 
of the eye lens, effects on bone development and collagen content, 
haemorrhagic lesions of the dorsal and gill regions, and vertebral 
deformity) do not occur after exposure to TPP. They are therefore caused 
by other fluid components (Wagemann et al., 1974; Dawson et al., 1977; 
Nevins & Johnson, 1978; Mayer et al., 1981; Adams et al., 1983). 

6.3.  Insects

    In studies on 5th-instar small brown planthopper larvae  (Laodelphax 
 striatellus), the chemical being applied by contact, the 21-h LD50 was 
570.2 µg TPP per tube, but TPP-OH was without effect (Eto et al., 1975).  
The 24-h LD50 in similar studies on adult female (2-5 days old) house 
flies  (Musca domestica)  was >1000 µg TPP per jar (Plapp & Tong, 1966).  
When adult female (4-5 days old) green rice leafhoppers were treated 
topically, the 24-h LD50 for TPP was 4.6 mg/g and for TPP-OH was 11.53 
mg/g (Eto et al., 1975). 


    No data on the kinetics and metabolism of TPP in experimental 
animals are available.  Eto et al. (1975) reported that treated 
houseflies transform TPP into diphenyl  p -hydroxyphenyl phosphate 
(TPP-OH)  in vivo. 



     Acute toxicity data exist for several species of animals and 
 indicate low toxicity via the oral and dermal routes (1320 to 10 800 
 mg/kg and >7900 mg/kg, respectively).  No inhalation data are 
 available. TPP also exhibits low toxicity in short-term studies and is 
 not irritant to mouse skin.  In rats, no effects were seen in mothers or 
 offspring following repeated dietary exposure of 166-690 mg/kg per day 
 for a period of 91 days, including mating and gestation periods. 

     The neurotoxicity of TPP has been debated since the early studies of 
 Smith et al. (1930, 1932), which reported delayed neuropathy in cats and 
 monkeys exposed to TPP in acute and short-term studies.  However, Wills 
 et al. (1979) could demonstrate no ataxia or neuropathic damage in cats 
 exposed to 99.9%-pure TPP. Consequently, the validity of the Smith 
 studies has been questioned.  Other toxicity studies using behavioural 
 and morphological end-points have demonstrated that TPP administered 
 short-term to cats and chickens fails to produce neuro-toxic changes.  A 
 mixture of triaryl (including cresyl and phenyl) phosphates produced 
 neurochemical changes and minor peripheral nerve pathology in the caudal 
 nerve of rats; acute intraperitoneal injection of 150 mg or less 
 produced neither biochemical nor morphological change. 

     Negative results have been reported for several in vitro 
 mutagenicity studies.  No satisfactory studies are available on 

8.1.  Single exposure

    Acute toxicity data resulting from single exposure to TPP are 
summarized in Table 14.  Little information is available on the acute 
signs of toxicity. 

8.2.  Short-term exposure

    Sutton et al. (1960) reported a 35-day feeding study in male 
Holtzman rats with TPP at doses of 1 and 5 g/kg. Depression of body 
weight gain and an increase of liver weight were observed in the high-
dose group.  No haematological changes were found. 

Table 14.  Acute toxicity of triphenyl phosphate
Species     Route of     LD50    Reference
            adminis-     (mg/kg)
Rat         oral         3500      Hierholzer et al. (1957)
Rat         oral         3800      Antonyuk (1974)
Rat         oral         10 800    Johannsen et al. (1977)
Rat         oral         > 5000    US EPA (1986)

Mouse       oral         > 3000    Sutton et al. (1960)
Mouse       oral         1320      Antonyuk (1974)
Mouse       oral         > 5000    US EPA (1986)

Guinea-pig  oral         > 4000    Sutton et al. (1960)

Chicken     oral         > 2000    Smith et al. (1932)
Chicken     oral         > 5000    Johannsen et al. (1977)

Rabbit      dermal       > 7900    Johannsen et al. (1977)

    In studies by Hinton et al. (1987), TPP was fed to weanling Sprague-
Dawley rats (10 of each sex per group) at dose levels of 0, 2.5, 5, 7.5, 
or 10 g/kg for 120 days. The immunotoxicity evaluation included total 
protein analysis, electrophoretic analysis of serum proteins, lymphoid 
organ weights in relation to growth, and histopathology, together with 
expanded immunohistochemical evaluation of B- and T-lymphocyte regions 
in the spleen, thymus, and lymph nodes using immunoperoxidase staining. 
Assessment was made of the humoral response to a T-lymphocyte-dependent 
antigen, sheep red blood cells; it began at mid-term of the feeding 
period for the primary response and was followed by secondary and 
tertiary booster immunizations at intervals of 3 weeks. The kinetics of 
the response were measured by haemolysin assay of relative antibody 
titres at days 3, 4, 5, and 6 post injection. No significant effects on 
the response were noted for either sex at any of the dose levels tested. 
The only effects noted were a decreased rate of growth at high levels of 
TPP and increased levels of alpha- and ß-globulins (Hinton et al., 

    When Antonyuk (1974) administered TPP orally for 3 months to rats at 
doses of 380 or 1900 mg/kg, there were no deaths, no abnormal growths, 
and no inhibition of cholinesterase activity.  In another study, 
Antonyuk (1974) administered 650 to 1900 mg/kg orally to rats for 3 
months with no significant toxic effects. 

8.3.  Skin irritation

    No significant skin irritation was observed when a gauze pad soaked 
with approximately 0.5 ml of a 70% solution of TPP in alcohol was 
applied to the skin of mice for 72 h (Sutton et al., 1960). 

8.4.  Reproduction

    In studies by Welsh et al. (1987), male and female Sprague-Dawley 
(Spartan) rats (40 of each sex per group) were fed dietary levels of 0, 
2.5, 5, 7.5, or 10 mg TPP/kg (from 4 weeks post weaning for 91 days, 
through mating and gestation).  At these dietary levels, the daily 
intake of TPP during pregnancy was 0, 166, 341, 516, and 690 mg/kg body 
weight, respectively.  TPP exposure had no toxic effects on mothers or 
offspring at these dosages.  The types of developmental anomalies were 
similar in both treated and control animals, and no significant increase 
in the incidence of anomalies was seen in the treated groups as compared 
to control values. TPP was not teratogenic in Sprague-Dawley rats at the 
levels tested. 

8.5.  Mutagenicity

    Szybalski (1958) reported negative results with TPP in a paper disk 
method using streptomycin-dependent mutants of  E.coli. 

    TPP did not demonstrate mutagenic activity in microbial assays 
employing  Salmonella typhimurium  (TA 1535, TA 1537, TA 1538, TA 98, and 
TA 100 strains) and  Saccharomyces cerevisiae  (D4 strain) indicator 
organisms.  All studies were carried out both in the presence and 
absence of metabolic activation (Monsanto, 1979). 

    Negative results were also reported in Ames tests conducted with 
 Salmonella typhimurium  strains TA 98, TA 100, TA 1535, and TA 1537, in 
the absence or presence of rat liver S9 (Zeiger et al., 1987). 

    TPP was tested for its ability to induce mutations at the thymidine 
kinase (TK) locus in cultured L5178Y mouse lymphoma cells.  When tested 
with or without metabolic activation, TPP did not induce significant 
mutations at the TK locus (Monsanto, 1979). 

8.6.  Carcinogenicity

    Theiss et al. (1977) studied the occurrence of lung adenomas in 
strain A/St male mice, 6 to 8 weeks old, using doses of 80, 40, or 20 mg 
TPP/kg injected intraperitoneally 1, 3, and 18 times, respectively, into 
groups of 20 mice.  Twenty-four weeks after the first injection, the 
animals were sacrificed, and the frequency of lung tumours was compared 
with that in the control group of 50 animals treated with tricarpylin 
(vehicle).  The pulmonary adenoma response to TPP was not significantly 
greater than the response of the control mice.  This study was 
considered inadequate due to the low survival of animals in two of the 
three experimental groups and the short duration of the study. 

8.7.  Neurotoxicity

    In 1930, Smith and his associates found that single and multiple 
doses of technical grade TPP produced generalized delayed paralysis in 
cats and monkeys but not in chickens or rabbits (Smith et al., 1930). 

    Smith et al. (1932) attempted to ascertain the minimum lethal dose 
of TPP. Rabbits survived after an intramuscular injection of 1 g/kg; 
chickens also were unaffected after oral administrations of 0.5 to 2 

g/kg.  In cats, the minimum toxic dose by subcutaneous injection was 
about 0.2 g/kg and the reaction was of the delayed type; a neurotoxic 
action and flaccid paralysis were followed by death. 

    Johannsen et al. (1977) dosed chickens with cumulative doses of 60 
g/kg but failed to produce ataxia or neuropathology suggestive of 
organophosphate-induced delayed neuropathy (OPIDN). 

    In an attempt to re-evaluate the delayed neurotoxicity, Wills et al. 
(1979) reported that 99.9%-pure TPP did not produce any evidence of 
axonal degeneration, demyelination, or any other pathological changes at 
11 levels of the nervous system (from the cerebral cortex to peripheral 
nerves) when subcutaneously injected into cats at doses of 0.4, 0.7, or 
1.0 g/kg. Prostration occurred at the higher doses.  Wills et al. (1979) 
suggested that the samples of TPP used by Smith et al. (1930) may have 
contained impurities that were capable of producing axonal degeneration 
and demyelination. 

    Sobotka et al. (1986) fed young male Sprague-Dawley rats (10 per 
group) diets containing TPP at levels of 0, 2.5, 5, 7.5, or 10 g/kg, for 
4 months.  Treatment-related decreases in growth rate, in the absence of 
changes in food consumption, were found at all dietary levels above 2.5 
g/kg.  There was no evidence of neuromotor toxicity following subchronic 
dietary exposure to TPP. 

    In a study by Vainiotalo et al. (1987), a commercial cresyl diphenyl 
phosphate preparation was analysed and found to contain approximately 
35% triphenyl phosphate, 45% cresyl diphenyl phosphates, 18% dicresyl 
phenyl phosphates, and 2% tricresyl phosphates.  The product was almost 
free of the o-cresyl isomers, as revealed by the analysis of its 
alkaline hydrolysis products. A single intraperitoneal injection (150 or 
300 mg/kg) of this mixture caused the induction of microsomal cytochrome 
P-450 in the liver of Wistar rats, a concomitant increase in the 
activities of mixed function monooxygenases, and proliferation of smooth 
endoplasmic reticulum 24 h after the treatment.  The activity of 
pseudocholinesterase in blood was inhibited 4 h and 24 h after the 
injection but the effect leveled off.  Treatment with 300 mg/kg 
inhibited brain 2',3'-cyclic-nucleotide 3'-phosphohydrolase through the 
2-week observation period associated with demyelination in peripheral 

8.8.  In Vitro studies

     In vitro  TPP was found to cause significant direct inhibition of 
monocyte antigen presentation at non-cytotoxic concentrations as low as 
1 µmol/litre  (Esa et al., 1988). 


    Sutton et al. (1960) found no evidence of neurological disease or 
other abnormalities in 32 workers exposed to TPP vapour, mist, or dust 
(at a time-weighted air concentration of 3.5 mg/m3) for an average of 
7.4 years.  In six of these workers, who were exposed more regularly to 
TPP, there was a statistically significant asymptomatic reduction in 
erythrocyte cholinesterase values, but no plasma cholinesterase 

    In 39 workers exposed to an organophosphate ester mixture with about 
30% TPP and 70% different isopropyl TPPs, a significantly lower level of 
serum IgM and a lower activity (of borderline significance; p = 0.05) of 
erythrocyte cholinesterase, compared to controls, were reported. 
However, plasma cholinesterase activity and the other observed 
parameters were not significantly affected (Emmett et al., 1984). 

    A few individuals have been reported to show positive reactions in 
patch tests using cellulose acetate film containing both TCP and TPP. 
However, the causative agent could not be identified and may have been 
TCP (Hjorth, 1964).  A single case of allergy to spectacle frames could 
also have been due to TCP (Carlsen et al., 1986). 


10.1.  Evaluation of human health risks

    Animal data indicate that TPP has low toxicity.  It produces no 
irritant effect on animal skin.  Despite an early report to the contrary, 
TPP is not considered neurotoxic in animals or man.  The no-observed-
adverse-effect level on mothers and offspring from a 90-day rat study 
was at 690 mg/kg per day.  Both exposure of the general population and 
occupational exposure to TPP are low. 

    TPP is not mutagenic.

    The available data indicate no hazard to humans.

10.1.1.  Exposure levels

    Exposure of the general population to TPP through various 
environmental media, including drinking-water, is likely. The 
concentrations of TPP measured in drinking-water in Canada and the USA 
are extremely low.  TPP has often been detected in urban air, although 
the levels are low.  Vaporization of TPP from heated vinyl automotive 
upholstery under hot weather has been suggested, but no data on 
concentrations in cars are available.  In a survey of TAPs in human 
adipose tissues, TPP was not detected.  There are insufficient data to 
evaluate the significance of the general population exposure to TPP. 

    Significant air concentrations (0.5-29.6 mg/m3) have been reported 
in a TPP manufacturing plant, but recent figures are not available.  
More data on occupational exposure to TPP in manufacturing plants are 

10.1.2.  Toxic effects

    The toxicity profile of TPP is quite inadequate for a full 
evaluation of its hazard. 

    There is no evidence that TPP has mutagenic activity in bacteria or 
that it has carcinogenic activity, based on a study in one animal 
species. No evidence that TPP causes delayed neurotoxicity has so far 
been obtained in animal experiments. In a 35-day feeding study in rats, 
depression of body weight gain and increase in liver weight were 
observed at a dose of 5 g/kg. No adequate data are available on the 
effects of TPP on reproduction, i.e. function of gonads, fertility, 
parturition, and growth and development of offspring. 

    Contact dermatitis due to TPP has been described.

10.2.  Evaluation of effects on the environment

    Water concentrations of TPP in the environment are low and toxic 
effects on aquatic organisms are unlikely. Spills of hydraulic fluids 
containing TPP would be expected to cause local kills.  Since TPP is 
removed rapidly from the tissues of fish when exposure ends and 
bioconcentration factors are moderate, bioaccumulation is not considered 
to be a hazard. 

    High concentrations of TPP in sediment near production plants have 
been reported.  TPP bound to sediment has been shown to be bioavailable 
to one organism living in sediment, but no toxicity data on sediment-
living or sediment-ingesting species exist. There is, therefore, the 
possibility of effects on aquatic communities. 

10.2.1.  Exposure levels

    TPP is found in air, surface water, soil, sediment, and aquatic 
organisms sampled in heavily industrialized areas. The highest reported 
concentration of TPP in industrial water effluent is 16 µg/litre, while 
that in river water is 7.9 µg/litre.  Taking into account the rapid 
biodegradation of TPP in aqueous environments, normal concentrations of 
TPP in aqueous environments are unlikely to adversely affect aquatic 
organisms.  However, disposal of TPP-treated vinyl fabric upholstery 
into a pond would result in a sufficiently high concentration of TPP to 
kill fish. 

10.2.2.  Toxic effects

    Among the various triaryl phosphates, TPP is the most acutely toxic 
compound to fish, shrimps, and daphnids. The 96-h LC50 of TPP for fish 
ranges from 0.36 mg/litre in rainbow trout to 290 mg/litre in bluegill. 
Salmonids are generally sensitive to TPP, but the growth and survival of 
rainbow trout fry were not affected when they were exposed to TPP at a 
concentration of 0.0014 mg/litre.  Histopathological lesions in goldfish 
exposed to TPP consist of congestion, degeneration, and haemorrhage of 
the small blood vessels, principally venules and capillaries.  Such 
vascular pathology is most pronounced in the gills. 

    The growth of algae was completely inhibited at TPP concentrations 
of 1 mg/litre or more but was stimulated at lower concentrations (0.1 
and 0.05 mg/litre).  The nitrogenase activity of  Anabaena flos-aquae was 
significantly reduced, even at 0.1 mg/litre. 


11.1.  Recommendations for further research

    There is a need for skin sensitization,  in vitro cytogenicity, and 
pharmacokinetic studies on triphenyl phosphate. 

ADAMS, W.J., KIMERLE, R.A., HEIDOLPH, B.B., & MICHAEL, P.R. (1983)  Field 
comparison of laboratory-derived acute and chronic  toxicity data,  
Philadelphia, American Society of Testing and Materials, pp. 367-385 
(ASTM STP 802). 

Jr, & LISK, D.J. (1978) A water-extractable toxic compound in vinyl 
upholstery fabric.  Bull. environ. Contam. Toxicol., 20: 418-422. 

ALDOUS, C.N. (1982) Alterations in rat brain norepinephrine and dopamine 
levels and synthesis rates in response to five neurotoxic chemicals: 
acrylamide, 2,5-hexanedione, tri-o-tolyl phosphate, leptophos, and 
methyl mercuric chloride.  Diss. Abstr. Int., 43(5): 1441B. 

ANTONYUK, O.K. (1974) Hygienic evaluation of the plasticizer triphenyl 
phosphate added to polymer composition.  Gig. i Sanit., 8: 98-99. 

V.A. (1961) The reactions of organic phosphates. Part V. The hydrolysis 
of triphenyl and trimethyl phosphates.  J. Chem. Soc., 1961: 2670-2676. 

VERNON, C.A., & WELCH, V.A. (1966) Reactions of organic phosphates. Part 
VI. The hydrolysis of aryl phosphates.  J. Chem. Soc. (B), 1966: 227-235. 

BARRETT, H., BUTLER, R., & WILSON, I.B. (1969) Evidence for a 
phosphorylenzyme intermediate in alkaline phosphatase catalyzed 
reactions.  Biochemistry, 8: 1042-1047. 

(1974) Detection and estimation of tricresyl phosphate in mustard oil. 
 Forensic Sci., 3: 263-270. 

BLOOM, P.J. (1973) Application des chromatographies sur couch mince et 
gazliquide à l'analyse qualitative et quantitative des esters des acides 
phosphorique et phosphoreux.  J. Chromatogr., 75: 261-269. 

BOETHLING, R.S. & COOPER, J.C. (1985) Environmental fate and effects of 
triaryl and trialkyl/aryl phosphate esters.  Residue Rev., 94: 49-99. 

F.W. (1981) Trace impurities in solvents commonly used for gas 
chromatographic analysis of environmental samples.  J. Chromatogr., 206: 

BRAUN, D. (1965) [Qualitative analysis of plasticizers by using thin-
layer chromatography.]  Chimia, 19(2): 77-82 (in German). 

CAINES, L.A. & HOLDEN, A.V. (1976) Stream pollution by an organomercury 
compound.  Bull. environ. Contam. Toxicol., 16(4): 483-485. 

CARLSEN, L., ANDERSEN, K.E., & EGSGAARD, H. (1986) Triphenyl phosphate 
allergy from spectacle frames.  Contact dermatitis, 15: 274-277. 

Ciba-Geigy Corporation: Acute oral toxicity to rats and mice, EPA-OTS 
document 86-870000069. 

DAFT, J.L. (1982) Identification of aryl/alkyl phosphate residues in 
foods.  Bull. environ. Contam. Toxicol., 29: 221-227. 

acute toxicity of 47 industrial chemicals to fresh and saltwater fishes. 
 J. hazard. Mater., 1(4): 303-318. 

DEO, P.G. & HOWARD, P.H. (1978) Combined gas-liquid chromatographic mass 
spectrometric analysis of some commercial aryl phosphate oils.  J. Assoc. 
 Off. Anal. Chem., 61: 266-271. 

DRUYAN, E.A. (1975) [Separation and determination of tricresyl 
phosphate, triphenyl phosphate, phenol, o-, m-, and p-cresol by thin-
layer chromatography.]  Gig. i Sanit., 10: 62-65 (in Russian). 

EAJ (1977) [Environmental monitoring of chemicals.] Tokyo, Environment 
Agency Japan, pp. 212-214 (Environmental Survey Report Series No. 3) (in 

EAJ (1981) Environmental monitoring of chemicals: Environmental survey 
report of 1978, 1979 F.Y., Tokyo, Environment Agency Japan, pp. 171-183. 

TANAKA, F., SYNKOWSKI, D.R., & LEVINE, M.S. (1984) A clinical study of 
industrial workers exposed to organophosphate esters and a comparison 
group, Pittsfield, Massachusetts, General Electric Company (Prepared for 
the US Environmental Protection Agency, Washington). 

LEVINE, M.S. (1985) Industrial exposure to organophosphorus compounds. 
Studies of a group of workers with a decrease in esterase-staining 
monocytes.  J. occup. Med., 27(12): 905-914. 

ESA, A.H., WARR, G.A., & NEWCOMBE, D.S. (1988) Immunotoxicity of 
organophosphorous compounds. Clin. Immunol. Immunopathol., 49: 41-52. 

ETO, M., HASHIMOTO, Y., OZAKI, K., & SASAKI, Y. (1975) [Fungitoxicity 
and insecticide synergism of monothioquinol phosphate esters and related 
compounds.]  Botyu Kagaku, 40: 110-117 (in Japanese). 

FINNEGAN, R.A. & MATSON, J.A. (1972) Irradiation of triaryl phosphate 
esters. A new photochemical coupling reaction.  J. Am. Chem. Soc., 94: 

FUKUSHIMA, M. & KAWAI, S. (1986) [Present status and transition of 
selected organophosphoric acid triesters in the water area of Osaka 
city.]  Seitai Kagaku, 8: 13-24 (in Japanese). 

survey of trialkyl and triaryl phosphates in the United Kingdom total 
diet samples.  Food Addit. Contam., 3(2): 113-122. 

GUNDERSON, E.L. (1988) FDA total diet study, April 1982 - April 1984, 
dietary intakes of pesticides, selected elements and other chemicals.  J. 
 Assoc. Off. Anal. Chem., 71(6): 1200-1209. 

[Environmental fate of organic phosphate esters.]  Suishitu Odaku 
 Kenkyu, 4: 137-141 (in Japanese). 

HIERHOLZER, K., NOETZEL, H., & SCHMIDT, L. (1957) [Comparative 
toxicological study on triphenyl phosphate and tricresyl phosphate.] 
 Arzneimittelforschung,  7: 585-588. 

(1981) In: Clayton, G.D. & Clayton, F.E., ed. Patty's industrial hygiene 
and toxicology, 3rd revised ed., New York, Wiley-Interscience, Vol. 2A, 
pp. 2362-2363. 

(1987) Evaluation of immunotoxicity in a subchronic feeding study of 
triphenyl phosphate.  Toxicol. ind. Health, 3(1): 71-89. 

HJORTH, N. (1964) Contact dermatitis from cellulose acetate film. Cross-
sensitization between tricresyl phosphate (TCP) and triphenyl phosphate 
(TPP).  Contact dermatitis, 12: 86-100. 

HOLLIFIELD, H.C. (1979) Rapid nephelometric estimate of water solubility 
of highly insoluble organic chemicals of environmental interest.  Bull. 
 environ. Contam. Toxicol., 23: 579-586. 

HOWARD, P.H. & DEO, P.G. (1979) Degradation of aryl phosphates in 
aquatic environments. B ull. environ. Contam. Toxicol.,  22: 337-344. 

HUDEC, T., THEAN, J., KUEHL, D., & DOUDHERTY, R.C. (1981) Tris(dichloro-
propyl)phosphate, a mutagenic flame retardant: Frequent occurrence in 
human seminal plasma.  Science,  211: 951-952. 

ISHIKAWA, S., TAKETOMI, M., & SHINOHARA, R. (1985) Determination of 
trialkyl and triaryl phosphates in environmental samples.  Water Res., 
19: 119-125. 

R.W., & GRAHAM, P.R. (1977) Evaluation of delayed neurotoxicity and 
dose-response relationships of phosphate esters in the adult hen. 
 Toxicol. appl. Pharmacol.,  41: 291-304. 

KANAZAWA, J. (1978) Studies on formulation and residue analysis of 
pesticides.  J. Pestic. Sci.,  3: 185-193. 

KAWAI, S., FUKUSHIMA, M., ODA, K., & UNO, G. (1978) [Water pollution 
caused by organophosphoric compounds.]  Kankyo Gijyutsu,  7: 668-675 
(in Japanese). 

KENMOTSU, K., MATSUNAGA, K., & ISHIDA, T. (1980a) [Multiresidue 
determination of phosphoric acid triesters in fish, sea sediment and sea 
water.]  J. Food Hyg, Soc. Jpn,  21: 18-31 (in Japanese). 

KENMOTSU, K., MATSUNAGA, K., & ISHIDA, T. (1980b) [Studies on the 
mechanisms of biological activities of various environmental pollutants. 
V: Environmental fate of organic phosphoric acid triesters.]  Okayama-ken 
 Kankyo Hoken Senta Nemnpo,  4: 103-110 (in Japanese). 

KENMOTSU, K., MATSUNAGA, K., & ISHIDA, T. (1981a) [Studies on the 
biological toxicity of several pollutants in environments.]  Okayama-ken 
 Kankyo Hoken Senta Nempo,  5: 167-175 (in Japanese). 

KENMOTSU, K., MATSUNAGA, K., SAITO, N., & OGINO, Y. (1981b) [An 
environmental survey of chemicals. XVII. Multiresidue determination of 
organic phosphate esters in environment samples.]  Okayama-ken Kankyo 
 Hoken Senta Nempo,  5: 145-156 (in Japanese). 

[An environmental survey of chemicals. XIX. Determination of 
organophosphoric acid triesters (2).]  Okayama-ken Kankyo Hoken Senta 
 Nempo,  6: 126-132 (in Japanese). 

[Studies on the biological toxicity of several pollutants in 
environments. VII. GC/MS Spectrometric determination of organophosphoric 
acid triesters in sediment.]  Okayama-ken Kankyo Hoken Senta Nempo,  6: 
142-152 (in Japanese). 

(1983) [An environmental survey of chemical. XXII. GC/MS spectrometric 
determination of organophosphoric acid triesters in sediment (2).] 
 Okayama-ken Kankyo Hoken Senta Nempo,  7: 143-149 (in Japanese). 

KONASEWICH, D., TRAVERSY, W., & ZAR, H. (1978) Status report on organic 
and heavy metal contaminants in the Lakes Erie, Michigan, Huron and 
Superior basins.  Great Lakes Water Qual. Bd. 

LEBEL, G.L. & WILLIAMS, D.T. (1983) Determination of organic phosphate 
triesters in human adipose tissue.  J. Assoc. Off. Anal. Chem., 66: 

Isolation and concentration of organophosphorus pesticides from drinking 
water at the ng/L level, using macroreticular resin.  J. Assoc. Off. 
 Anal. Chem.,  62: 241-249. 

LEBEL, G.L., WILLIAMS, D.T., & BENOIT, F.M. (1981) Gas chromatographic 
determination of trialkyl/aryl phosphates in drinking water, following 
isolation using macroreticular resin.  J. Assoc. Off. Anal. Chem.,  
64: 991-998. 

LHOMME, V., BRUNEAU, C., SOYER, N., & BRAULT, A. (1984) Thermal behavior 
of some organic phosphates.  Ind. Eng. Chem. Prod. Res.  Dev.,  23: 

(1975) Chronic toxicity of a synthetic triaryl phosphate oil to fish. 
 Environ. Physiol. Biochem.,  5: 361-369. 

LOCKHART, W.L., METNER, D.A., BLOUW, A.P., & MUIR, D.C.G. (1982) 
Prediction of biological availability of organic chemical pollutants to 
aquatic animals and plants. In: Pearson, J.G., Foster, R.B., & Bishop, 
W.E., ed.  Aquatic toxicology and hazard assessment: Fifth conference, 
Philadelphia, American Society for Testing and Materials, pp. 259-272 
(ASTM STP 766). 

LOMBARDO, P. & EGRY, I.J. (1979) Identification and gas-liquid 
chromatographic determination of aryl phosphate residues in 
environmental samples.  J. Assoc. Off. Anal. Chem.,  62(1): 47-51. 

LU, P.-Y. & METCALF, R.L. (1975) Environmental fate and biodegradability 
of benzene derivatives as studied in a model aquatic ecosystem.  Environ. 
 Health Perspect.,  10: 269-284. 

MAYER, F.L., Jr, MAYER, K.S., & ELLERSIECK, M.R. (1986) Relation of 
survival to other endpoints in chronic toxicity tests with fish. 
 Environ. Toxicol. Chem.,  5(8): 737-748. 

SAEGER, V.W. (1981) Phosphate ester hydraulic fluids: An aquatic 
environmental assessment of Pydrauls 50E and 115E, In: Branson, D.R. & 
Dickson, K.L., ed.  Aquatic Toxicology and Hazard Assessment:  Fourth 
 Conference, Philadelphia, American Society for Testing and Materials, 
pp. 103-123 (ASTM STP 737). 

MOCHIDA, K., GOMYODA, M., FUJITA, T., & YAMAGATA, K. (1988) Tricresyl 
phosphate and triphenyl phosphate are toxic to cultured human, monkey, 
and dog cells.  Zentralbl. Bakterial. Mikrobiol. Hyg., B185(4-5): 

MODERN PLASTICS ENCYCLOPEDIA (1975) International Advertising Supplement 
52: 10A, p. 697, New York McGraw-Hill Inc. 

MONSANTO INDUSTRIAL CHEMICALS CO. (1979) Summary of the mutagenicity 
study, neurotoxicity study, teratology study, long-term feeding study 
and 90-day inhalation study which Monsanto has on the aryl phosphate, 
Saint-Louis, Missouri, Monsanto Industrial Chemicals Co. (Prepared for 
the US Environmental Protection Agency) (EPA-OTS document No. 40-

MUIR, D.C.G. (1984) Phosphate esters. In: Hutzinger, O., ed.  The 
 handbook of environmental chemistry, Berlin, Heidelberg, New York, 
Tokyo, Springer-Verlag, Vol. 3, Part C, pp. 41-66. 

MUIR, D.C.G., GRIFT, N.P., & SOLOMON, J. (1980a) Determination of 
several triaryl phosphates in fish and sediment samples.  Can. Plains 
 Proc., 9: 1-12. 

MUIR, D.C.G., GRIFT, N.P., BLOUW, A.P., & LOCKHART, W.L. (1980b) 
Environmental dynamics of phosphate esters. I. Uptake and 
bioaccumulation of triphenyl phosphate by rainbow trout.  Chemosphere,
9: 525-532. 

MUIR, D.C.G., GRIFT, N.P., & SOLOMON, J. (1981) Extraction and cleanup 
of fish, sediment, and water for determination of triaryl phosphates by 
gas-liquid chromatography.  J. Assoc. Off. Anal. Chem., 64: 79-84. 

MUIR, D.C.G., GRIFT, N.P., & LOCKHART, W.L. (1982) Comparison of 
laboratory and field results for prediction of the environmental 
behavior of phosphate esters.  Environ. Toxicol. Chem., 1: 113-119. 

MUIR, D.C.G., YARECHEWSKI, A.L., & GRIFT, N.P. (1983a) Environmental 
dynamics of phosphate esters. III. Comparison of the bioconcentration of 
four triaryl phosphates by fish.  Chemosphere, 12: 155-166. 

MUIR, D.C.G., TOWNSEND, B.E., & LOCKHART, W.L. (1983b) Bioavailability 
of six organic chemicals to Chironous tentans larvae in sediment and 
water.  Environ. Toxicol. Chem., 2: 269-281. 

NEELY, W.B., BRANSON, D.R., & BLAU, G.E. (1974) Partition coefficient to 
measure bioconcentration potential of organic chemicals in fish. 
 Environ. Sci. Technol., 8: 1113-1115.

NEVINS, M.J. & JOHNSON, W.W. (1978) Acute toxicity of phosphate ester 
mixtures to invertebrates and fish.  Bull. environ. Contam. Toxicol., 
19: 250-256. 

NOMEIR, A.A. & ABOU-DONIA, M.B. (1983) High-performanace liquid 
chromatographic analysis on radial compression column of the neurotoxic 
tri-o-cresyl phosphate and metabolites.  Anal. Biochem., 135: 296-303. 

OFSTAD, E.B. & SLETTEN, T. (1985) Composition and water solubility 
determination of a commercial tricresyl phosphate.  Sci. total Environ., 
43: 233-241. 

PALAWSKI, D., BUCKLER, D.R., & MAYER, F.L. (1983) Survival and condition 
of Rainbow trout  (Salmo gairdneri)  after acute exposures to methyl 
parathion, triphenyl phosphate, and DEF.  Bull. environ. Contam. 
 Toxicol., 30: 614-620. 

PEEREBOOM, J.W.C. (1960) The analysis of plasticizers by micro-
adsorption chromatography.  J. Chromatogr., 4: 323-328. 

PEGUM, J.S. (1966) Contact dermatitis from plastics containing triaryl 
phosphtes.  Br. J. Dermatol., 78: 626-631. 

PICKARD, M.A., WHELIHAN, J.A., & WESTLAKE, D.W.S. (1975) Utilization of 
triaryl phosphates by a mixed bacterial population.  Can. J. Microbiol.,
21: 140-145. 

PLAPP, F.W., Jr & TONG, H.H.C. (1966) Synergism of malathion and 
parathion against resistant insects: Phosphorus esters with synergistic 
properties.  J. econ. Entomol., 59(1): 11-15. 

RENBERG, L., SUNDSTROM, G., & SUNDH-NYGARD, K. (1980) Partition 
coefficients of organic chemicals derived from reversed phase thin layer 
chromatography. Evaluation of methods and application on phosphate 
esters, polychlorinated paraffins and some PCB-substitutes.  Chemosphere, 
9: 683-691. 

TUCKER, E.S. (1979) Environmental fate of selected phosphate esters. 
 Environ. Sci. Technol., 13: 840-844. 

SASAKI, K., TAKEDA, M., & UCHIYAMA, M. (1981) Toxicity, absorption and 
elimination of phosphoric acid triesters by Killifish and Goldfish. 
 Bull. environ. Contam. Toxicol., 27: 775-782. 

Bioconcentration and excretion of phosphoric acid triesters by Killifish 
 (Oryzeas laptipes). Bull. environ. Contam. Toxicol., 28: 752-759. 

SHELDON, L.S. & HITES, R.A. (1978) Organic compounds in the Delaware 
River.  Environ. Sci. Technol., 12: 1188-1194. 

SHELDON, L.S. & HITES, R.A. (1979) Sources and movement of organic 
chemicals in the Delaware River.  Environ. Sci. Technol., 13: 574-579. 

SITTHICHAIKASEM, S. (1978) Some toxicological effects of phosphate 
esters on rainbow trout and bluegill, Iowa State University (Ph. D. 

SMITH, M.I., EVOLVE, E., & FRAZIER, W.H. (1930) Pharmacological action 
of certain phenol esters with special reference to the etiology of so-
called ginger paralysis.  Public Health Rep., 45: 2509-2524. 

SMITH, M.I., ENGEL, E.W., & STOHLMAN, F.F. (1932) Further studies on the 
pharmacology of certain phenol esters with special reference to the 
relation of chemical constitution and physiologic action.  Natl. Inst. 
 Health Bull., 160: 1-53. 

(1986) Neuromotor function in rats during subchronic dietary exposure to 
triphenyl phosphate.  Neurobehav. Toxicol. Teratol., 8: 7-10. 

SUGIYAMA, H. & TANAKA, K. (1982) [Investigation of trace organic 
chemicals in the sea water of the Tokyo Bay by gas chromatography mass-
spectrometry.] Bull.  Kanagawa Prefect. environ. Center, 4: 33-38 (in 

E.C., ROUDABUSH, R.L., & FASSETT, D.W. (1960) Studies on the industrial 
hygiene and toxicology of triphenyl phosphate.  Arch. environ. Health, 
1: 45-58. 

SZYBALSKI, W. (1958) Special microbiological systems. II. Observations 
on chemical mutagenesis in microorganisms.  Ann. N.Y. Acad.  Sci., 76: 

Test for carcinogenicity of organic contaminants of United States 
drinking waters by pulmonary tumor response in strain A mice.  Cancer 
 Res., 37: 2717-2720. 

TITTARELLI, P. & MASCHERPA, A. (1981) Liquid chromatography with 
graphite furnace atomic absorption spectrophotometric detector for 
speciation of organophosphorous compounds.  Anal. Chem., 53: 1466-1499. 

US NIOSH (1980)  Industrial hygiene walk-through survey report on 
 organophosphorus exposures at Rochester products division, General 
 Motors Corporation, Rochester, Cincinnati, Ohio, National Institute for 
Occupational Safety and Health (PB82-104530). 

US NIOSH (1982) Industrial hygiene walk-through survey report on 
organophosphorus exposures at Chevron Chemical, Belle Chasse, Louisiana, 
Cincinnati, Ohio, National Institute for Occupational Safety and Health 
(Report No. IWA-89-10). 

(1987) Acute biological effects of commercial cresyl diphenyl phosphate 
in rats.  Toxicology, 44(1): 31-44. 

VASWANI, M., MAHAJAN, P.M., SETIA, R.C., & BHIDE, N.K. (1983) A simple 
colorimetric method for estimation of tricresyl phosphate in edible 
oils.  J. Oil Technol. Assoc. India, 15(1): 12-13. 

VEITH, G.D., DEFOE, D.L., & BERGSTEDT, B. (1979) Measuring and 
estimating the bioconcentration factor of chemicals in fish.  J. Fish 
 Res. Board Can., 36: 1040-1048. 

VICK, R.D., JUNK, G.A., AVERY, M.J., RICHARD, J., & SVEC, H.J. (1978) 
Organic emissions from combustion of combination coal/refuse to produce 
electricity.  Chemosphere, 7: 893-902. 

WAGEMANN, R., GRAHAM, B., & LOCKHART, W.L. (1974)  Studies on chemical 
 degradation and fish toxicity of a synthetic triaryl phosphate 
 lubrication oil, IMOL S-140, Ottawa, Environment Canada, Fisheries and 
Marine Service (Technical Report No. 486). 

WAKABAYASHI, A. (1980) [Environmental pollution and toxicological 
aspects of a triaryl phosphate synthetic oil].  Annual Report of the 
 Tokyo Metropolitan Research Institute for Environmental Protection, 11: 
110-113 (in Japanese). 

(1987) Teratogenic potential of triphenyl phosphate in Sprague-Dawley 
(Spartan) rats.  Toxicol. ind. Health, 3(3): 357-369. 

WHO (1990) Environmental Health Criteria 110: Tricresyl phosphate, 
Geneva, World Health Organization. 

WILLIAMS, D.T. & LEBEL, G.L. (1981) A national survey of tri(haloalkyl)-
, trialkyl-, and triaryl phosphates in Canadian drinking water.  Bull. 
 environ. Contam. Toxicol., 27: 450-457. 

(1982) Determination of mutagenic potential and organic contaminants of 
Great Lakes drinking water.  Chemosphere, 11: 263-276. 

(1979) Does triphenyl phosphate produce delayed neurotoxic effects? 
 Toxicol. Lett., 4: 21-24. 

WINDHOLZ, M., ed. (1983)  The Merck Index, 10th ed., Rahway, New Jersey, 
Merck and Co., Inc. 

WOLFE, N.L. (1980) Organophosphate and organophosphorothionate esters: 
Application of linear free energy relationships to estimate hydrolysis 
rate constants for use in environmental fate assessment.  Chemosphere, 
9: 571-579. 

WONG, P.T.S. & CHAU, Y.K. (1984) Structure-toxicity of triaryl 
phosphates in freshwater algae.  Sci. total Environ., 32(2): 157-65. 

YASUDA, H. (1980) [Concentration of organic phosphorus pesticides in the 
atmosphere above the Dogo plain and Ozu basin.]  J. Chem. Soc. Jpn, 1980: 
645-653 (in Japanese). 

SPECK, W. (1987)  Salmonella  mutagenicity tests: III. Results from the 
testing of 255 chemicals.  Environ. Mutagen., 9(Suppl. 9): 1-110. 

ZITKO, V. (1980) Proceedings of the 6th Annual Aquatic Toxicity 
Workshop,  Can. Tech. Rep. Fish. aquat. Sci., 575: 234-265. 


1. Identité, propriétés physiques et chimiques, méthodes d'analyse

   Le phosphate de triphényle (TPP) est une substance cristalline, 
ininflammable, inexplosible et incolore. Son coefficient de partage 
entre l'octanol et l'eau (log de Pow) est de 4,61-4,76. A la température 
ambiante ordinaire, il s'hydrolyse rapidement en milieu alcalin pour 
donner du phosphate de diphényle et du phénol, mais l'hydrolyse est très 
lente en milieu acide ou neutre. 

   Pour l'analyse, la méthode choix est la chromatographie gaz-liquide, 
avec détection au moyen d'un dispositif sensible à l'azote/phosphore ou 
par photométrie de flamme. La limite de détection dans l'eau est 
d'environ 20 ng/litre. 

2. Sources d'exposition humaine et environnementale

   Le phosphate de triphényle est produit à partir de l'oxychlorure de 
phosphore et du phénol. Il est utilisé comme retardateur de flamme dans 
les résines phénoliques et les résines à base d'oxydes de phénylène que 
l'on utilise pour la fabrication de pièces d'automobiles et de 
l'appareillage électrique; on l'emploie également comme plastifiant 
ininflammable dans l'acétate de cellulose servant à la confection des 
pellicules photographiques. Il entre également dans la compositision des 
liquides hydrauliques et des huiles lubrifiantes à côté d'un certain 
nombre d'autres usages de moindre importance. 

   On peut considérer qu'en utilisation normale, la population dans son 
ensemble n'encourt qu'une exposition minime. 

3. Transport, distribution et transformation dans l'environnement

   Les phosphates de triaryle pénètrent dans le milieu aquatique par 
suite de fuites de liquides hydrauliques, de la lixiviation de certains 
plastiques et en faibles quantités, lors des divers processus de 
fabrication. En raison de sa faible solubilité dans l'eau et de son 
coefficient d'adsorption au sol relativement élevé, le phosphate de 
triphényle se fixe rapidement sur les sédiments de rivières ou des 
étangs. En milieu aquatique, il subit une biodégradation rapide. 

   La dégradation du phosphate de triphényle comporte une hydrolyse 
enzymatique par étapes en orthophosphate et phénol. 

   Les facteurs de bioconcentration mesurés chez plusieurs espèces de 
poissons vont de 6 à 18 900 et la demi-vie d'élimination varie de 1,2 à 
49,6 heures. 

   La libération de cette substance dans l'air des unités de production 
constitue une source d'exposition humaine sur les lieux de travail. La 
combustion des matières plastiques et la volatilisation du phosphate de 
triphényle à partir de ces substances ou de la surface de l'eau peut 
également constituer une voie importante de pénétration dans 

4. Niveaux dans l'environnement et exposition humaine

   On trouve un peu partout du phosphate de triphényle dans l'air, 
l'eau, les sédiments et les organismes aquatiques, mais les prélèvements 
effectués n'en contiennent que de faibles quantités. Les teneurs les 
plus fortes qui aient été signalées sont de 23,2 ng/m3 dans l'air, 7900 
ng/litre dans des cours d'eau, 4000 ng/g dans des sédiments et de 600 
ng/g dans le poisson. 

5. Effets sur les êtres vivants dans leur milieu naturel

   La croissance des algues est complètement inhibée à des 
concentrations de 1 mg/litre ou davantage mais elle est en revanche 
stimulée à des concentrations plus faibles (0,1 et 0,05 mg/litre). 
L'activité de la nitrogénase d' Anabaena flos-aquae  diminue à mesure que 
la dose augmente, passant de 84% à 0,1 mg/litre à 68% à 5,0 mg/litre. 

   Le phosphate de triphényle est, parmi les phosphates de triaryle, 
celui qui présente la plus forte toxicité aiguë vis-à-vis des poissons, 
des crevettes et des daphnies. L'indice de toxicité aiguë de ce 
phosphate pour le poisson (CL50 à 96 h) va de 290 mg/litre pour  Lepomis 
 macrochirus, à 0,36 mg/litre pour la truite arc-en-ciel. La grande 
différence entre la truite et les vairons du genre Pimephales en ce qui 
concerne les valeurs de la CL50, pourraient être due à des différences 
dans leur aptitude à métaboliser le phosphate de triphényle. Parmi les 
effets sublétaux observés chez les poissons, on peut citer des anomalies 
morphologiques telles que congestion, dégénérescence et hémorragie au 
niveau des petits vaisseaux sanguins (essentiellement branchiaux) ainsi 
que des anomalies de comportement. L'immobilité des poissons exposés à 
0,21-0,29 mg/litre de phosphate de triphényle a complètement disparu 
dans les sept jours qui ont suivi le changement d'eau. 

6. Effets sur les animaux d'expérience et les systèmes d'épreuves in vitro

   On estime que la DL50 par voie orale est supérieure à 6,4 g/kg chez 
le rat et à 2,0 g/kg chez le poulet. 

   Des doses de phosphate de triphényle allant de 0,5 à 2 g/kg ont été 
bien tolérées par des lapins après injection intramusculaire et par des 
poulets après administration orale. Lors d'une étude d'alimentation de 
35 jours, on a observé après administration de cette substance à des 
rats Holtzman mâles, une réduction du gain de poids corporel et une 
augmentation du poids du foie. 

   On n'a pas observé d'effets tératogènes chez des rats Sprague-Dawley 
à des doses allant jusqu'à 690 mg/kg de poids corporel. On n'a pas 
publié d'études concernant la reproduction. 

   On ne dispose pas de données sur la mutagénicité du phosphate de 
triphényle qui résultent d'épreuves correctement validées et il n'y a 
pas eu non plus d'études de cancérogénicité convenables. 

   Après des injections sous-cutanées de phosphate de triphényle à des 
chats (jusqu'à 1 g/kg) on n'a pas observé de neurotoxicité retardée; on 
n'en a pas observé non plus après une étude de 4 mois sur des rats 
Sprague-Dawley qui en recevaient dans leur alimentation des doses allant 
jusqu'à 1% de la ration. 

   Aucun effet immunotoxique n'a été signalé après une étude de 120 
jours pendant laquelle des rats ont reçu du phosphate de triphényle dans 
leur nourriture à des doses allant jusqu'à 1%. 

7. Effets sur l'homme

   On a signalé une réduction statistiquement significative de la 
cholinestérase érythrocytaire chez certains travailleurs, mais aucun 
signe d'affection neurologique n'a été relevé chez des ouvriers qui 
travaillaient dans une unité de production de phosphate de triphényle. 
On n'a pas signalé non plus de neurotoxicité retardée parmi les cas 
d'intoxication par le phosphate de triphényle. On a décrit des cas de 
dermatite de contact dus au phosphate de triphényle. 


1. Evaluation des risques pour la santé humaine

   Les données tirées des études sur l'animal montrent que le phosphate 
de triphényle est peu toxique. Appliqué sur la peau d'animaux de 
laboratoire, il ne produit pas d'irritation. On estime que le phosphate 
de triphényle n'est pas neurotoxique pour l'homme ni l'animal, bien 
qu'un premier rapport ait pu affirmer le contraire. Lors d'une étude de 
90 jours sur des rats, on a évalué à 690 mg/kg par jour la dose sans 
effet nocif observable pour les mères et leur descendance. L'exposition 
professionnelle et l'exposition de la population dans son ensemble 
demeurent à un faible niveau. 

   Le phosphate de triphényle n'est pas mutagène.

   Selon des données disponibles, il ne présente aucun danger pour 

1.1 Niveaux d'exposition

   Il y a probablement un risque d'exposition de la population générale 
au phosphate de triphényle par l'intermédiaire des divers compartiments 
de l'environnement et notamment par l'eau de consommation. Toutefois les 
concentrations de phosphate de triphényle mesurées dans de l'eau de 
boisson au Canada et aux Etats-Unis se sont révélées extrêmement 
faibles. On en a souvent décelé la présence dans l'air des villes mais à 
faibles concentrations. On a pu craindre que l'échauffement des sièges 
d'automobiles en vinyle, lorsque la température extérieure est très 
élevée, puisse conduire à la vaporisation du phosphate de triphényle 
utilisé comme plastifiant, mais on ne dispose d'aucune donnée sur les 
concentrations présentes à l'intérieur des véhicules. Lors d'une enquête 
portant sur la teneur des tissus adipeux humains en phosphates de 
triaryle, on n'a pas décelé la présence de phosphate de triphényle. On 
ne dispose pas de données suffisantes pour se faire une idée de 
l'importance de l'exposition de la population générale au phosphate de 
triphényle. On a signalé des concentrations importantes de ce produit 
dans l'air d'une unité de production (0,5 à 29,6 mg/m3) mais on ne 
dispose pas de chiffres récents. Il serait bon d'avoir davantage de 
données sur l'exposition professionnelle au phosphate de triphényle dans 
les unités de production. 

1.2 Effets toxiques

   Le profil de toxicité du phosphate de triphényle ne permet guère 
d'évaluer de façon complète le danger qu'il représente. 

   On a noté aucun signe d'activité mutagène chez les bactéries ni 
d'ailleurs d'activité cancérogène, en se basant pour cela sur une étude 
relative à une seule espèce animale. L'expérimentation animale n'a pas 
pu jusqu'ici, mettre en évidence une neurotoxicité retardée attribuable 
à cette substance. Lors d'une étude d'alimentation de 35 jours sur des 
rats, on a relevé à la dose de 5 g/kg, une réduction du gain de poids 
corporel et une augmentation du poids du foie. On ne possède pas de 
données suffisantes sur les effets qu'il pourrait exercer sur la 

fonction de reproduction (gonades, fécondité, parturitions, croissance 
et développement de la progéniture). 

   On a décrit des cas de dermatite de contact attribuable au phosphate 
de triphényle. 

2. Evaluation des effets sur l'environnement

   Dans l'eau, la concentration du phosphate de triphényle est faible et 
il est peu probable qu'il exerce des effets toxiques sur les organismes 
aquatiques. Il peut y avoir mortalité locale par suite du déversement 
accidentel de liquides hydrauliques contenant du phosphate de 
triphényle. Cependant, comme ce phosphate s'élimine rapidement des 
tissus pisciaires lorsque cesse l'exposition et que les facteurs de 
bioconcentration sont moyens, on ne pense pas qu'il y ait véritablement 
risque de bioaccumulation. 

   On a fait état de fortes concentrations de phosphate de triphényle 
dans les sédiments proches des unités de production. Il a été montré en 
outre que le phosphate de triphényle lié aux sédiments pouvait être fixé 
par un organisme qui y était présent mais on ne possède aucune donnée de 
toxicité sur les espèces qui vivent dans les sédiments ou qui s'en 
nourrissent. Reste que des effets sur les populations aquatiques sont 

2.1 Niveaux d'exposition

   Dans les régions très industrialisées, les prélèvements effectués 
dans l'air, dans les eaux superficielles, dans le sol, les sédiments et 
parmi les organismes aquatiques indiquent la présence de phosphate de 
triphényle. La concentration la plus élevée qui ait été signalée dans 
des effluents industriels était de 16 µg/litre; dans un cours d'eau, 
elle était de 7,9 µg/litre. Si l'on prend en considération la 
biodégradation rapide du phosphate de triphényle dans le milieu 
aquatique, il est peu probable que les concentrations que l'on rencontre 
normalement puissent se révéler nocives pour les organismes qui y 
vivent. Toutefois la décharge dans des mares de déchets de garnitures de 
sièges en vinyle traité par du phosphate de triphényle, pourrait donner 
lieu à des concentrations mortelles pour les poissons. 

2.2 Effets toxiques

   Parmi les divers phosphates de triaryle, le phosphate de triphényle 
est celui dont la toxicité aiguë est la plus forte pour les poissons, 
les crevettes et les daphnies. La CL50 à 96 h varie de 0,36 mg/litre 
pour la truite arc-en-ciel à 290 mg/litre pour Lepomis macrochirus. Les 
salmonidés sont en général sensibles au phosphate de triphényle mais on 
a constaté qui ni la croissance ni la survie des alevins de truite arc-
en-ciel ne souffraient d'une exposition à cette substance à la 
concentration de 0,0014 mg/litre. Chez des poissons rouges exposés à du 
phosphate de triphényle, on a constaté un certain nombre d'anomalies 
histologiques: congestion, dégénérescence et hémorragie au niveau des 
petits vaisseaux sanguins, principalement les veinules et les 
capillaires. Cette pathologie vasculaire est plus prononcée au niveau 
des branchies. 

   La présence de concentrations de phosphate de triphényle de l'ordre 
de 1 mg/litre ou davantage a complètement inhibé la croissance de 
certaines algues alors que des concentrations plus faibles (0,1 et 0,05 
mg/litre) avaient l'effet contraire. L'activité de la nitrogénase 
d' Anabaena flos-aquae  a été sensiblement réduite, même à la 
concentration de 0,1 mg/litre. 


1. Recommandations relatives aux recherches à effectuer

 a) Etudes à entreprendre sur la sensibilisation cutanée.

 b) Nécessité d'une étude de cytogénicité  in vitro.

 c) Nécessité d'études pharmacocinétiques selon les différentes voies


1. Identidad, propiedades físicas y químicas y métodos analíticos

   El trifenilfosfato (TFF) es una sustancia no inflamable, no 
explosiva, incolora y cristalina. Su coeficiente de reparto en octanol y 
agua (log Poa) es de 4,61-4,76. A temperatura ambiente normal se 
hidroliza rápidamente en solución alcalina, dando difenilfosfato y 
fenol, y muy lentamente en soluciones ácidas o neutras. 

   El método analítico más apropiado es la cromatografía gas-líquido con 
un detector sensible al nitrógeno-fósforo o uno fotométrico de llama. El 
límite de detección en el agua es de unos 20 ng/litro. 

2. Fuentes de exposición humana y ambiental

   El TFF se fabrica a partir de oxicloruro de fósforo y fenol. Se 
utiliza como pirorretardante en resinas fenólicas y de óxido de fenileno 
en la producción de componentes eléctricos y del automóvil y como 
plastificante no inflamable en acetato de celulosa para películas 
fotográficas. También es un componente de fluidos hidráulicos o aceites 
lubricantes y tiene otros usos de menor importancia. 

   La exposición de la población general por el uso normal puede 
considerarse mínima. 

3. Transporte, distribución y transformación en el medio ambiente

   Los triarilfosfatos entran en el medio acuático principalmente por 
escapes de fluidos hidráulicos, así como por lixiviación a partir de los 
plásticos y, en menor medida, a partir de los procesos de fabricación. A 
causa de su baja solubilidad en agua y su coeficiente de adsorción en el 
suelo relativamente alto, el TFF se adsorbe con rapidez en los 
sedimentos de los ríos (o de las charcas). Su biodegradación en el medio 
acuoso es rápida. 

   El TFF se degrada mediante una hidrólisis enzimática escalonada que 
lo divide en ortofosfato y componentes fenólicos. 

   Los factores de bioconcentración (FBC) medidos en varias especies de 
peces oscilan entre 6 y 18 900, y la semivida de depuración va de 1,2 a 
49,6 h. 

   La liberación de TFF desde los lugares de producción al aire 
representa una fuente de exposición humana en el ambiente de trabajo. La 
combustión de plásticos y la volatilización a partir de ellos o de las 
superficies acuáticas también pueden ser importantes vías de ingreso en 
la atmósfera. 

4. Niveles medioambientales y exposición humana

   El TFF se ha detectado con frecuencia en el aire, el agua, los 
sedimentos y los organismos acuáticos, pero los niveles en muestras 
medioambientales son bajos. Los niveles máximos detectados son de 23,2 
ng/m3 en el aire, 7900 ng/litro en agua de río, 4000 ng/g en sedimentos 
y 600 ng/g en peces. 

5. Efectos sobre los seres vivos del medio ambiente

   Las concentraciones de TFF iguales o superiores a 1 mg/litro inhiben 
completamente el crecimiento de las algas, pero la concentraciones más 
bajas (0,1 y 0,05 mg/litro) lo estimulan. La actividad de la nitrogenasa 
de  Anabaena flos-aquae  decrece en función de la dosis desde 84% a 0,1 
mg/litro hasta 68% a 5,0 mg/litro. 

   De los distintos triarilfosfatos, el TFF es el más tóxico para los 
peces, los camarones y los dáfnidos. El índice de toxicidad aguda del 
TFF para los peces (CL50 96 h) oscila entre 290 mg/litro en  Lepomis 
 macrochirus  y 0,36 mg/litro en la trucha arco iris. La gran diferencia 
entre los valores de CE0 de la trucha y de  Pimephales promelas  puede 
deberse a su distinta capacidad para metabolizar el TFF. Entre los 
efectos subletales que produce en los peces figuran anomalías 
morfológicas como congestión, degeneración y hemorragias de los vasos 
sanguíneos más pequeños (principalmente de las branquias) y anomalías en 
el comportamiento. La inmovilidad de los peces expuestos a 
concentraciones de 0,21-0,29 mg/litro desapareció totalmente al cabo de 
siete días cuando se los puso en agua limpia. 

6. Efectos en los animales de experimentación y en sistemas de prueba
 in vitro 

   Se ha calculado que por vía oral la DL50 del TFF en ratas es > 6,4 
g/kg y en pollos es > 2,0 g/kg. 

   Los conejos y los pollos toleraron bien dosis de TFF de 0,5 a 2,0 
g/kg por vía intramuscular y oral respectivamente. En un estudio de 
alimentación de 35 días en machos de rata Holtzman, con una dosis de TFF 
se observó una disminución en la ganancia de peso corporal y un aumento 
del peso del hígado. 

   Con dosis de TFF de hasta 690 mg/kg de peso corporal no se produjeron 
efectos teratogénicos en ratas Sprague-Dawley. No se conocen estudios 
sobre la reproducción. 

   No hay datos acerca de la capacidad mutagénica del TFF obtenidos en 
ensayos bien contrastados y no se han hecho estudios adecuados de 

   La aplicación a gatos de una única dosis subcutánea de TFF (de hasta 
1 g/kg) no causó neurotoxicidad diferida; tampoco se observó en un 
estudio de cuatro meses en ratas Sprague-Dawley con dosis de hasta el 1% 
en el alimento. 

   No se comunicaron efectos inmunotóxicos tras un estudio de 120 días 
en ratas a las que se administraron dosis de hasta el 1% en el alimento. 

7. Efectos en la especie humana

   Se ha comunicado que, si bien algunos trabajadores de instalaciones 
de producción de TFF han mostrado una reducción estadísticamente 
significativa de la colinesterasa eritrocítica, no hay manifestaciones 
de enfermedades neurológicas. No hay informes de neurotoxicidad diferida 
en casos de intoxicación por TFF. Se han descrito casos de dermatitis de 
contacto debida al TFF. 

1. Evaluación de los riesgos para la salud humana

   Los datos obtenidos en animales indican que el TFF tiene una 
toxicidad baja. No produce efectos irritantes en la piel de los 
animales. A pesar de un primer informe en sentido contrario, no se 
considera que el TFF sea neurotóxico para los animales o el hombre. El 
nivel sin efecto adverso observado fue, en las madres y en las crías, de 
690 mg/kg al día en un estudio de 90 días realizado en ratas. La 
exposición al TFF es baja tanto en la población general como en los 

   El TFF no tiene efectos mutagénicos.

   Los datos disponibles indican que no entraña peligro para los seres 

1.1 Niveles de exposición

   Puede considerarse probable la exposición de la población general al 
TFF por conducto de distintos medios ambientales, incluida el agua de 
bebida. Se han medido concentraciones extraordinariamente bajas de TFF 
en el agua de bebida del Canadá y los EE.UU. Con frecuencia se ha 
detectado TFF en el aire urbano, aunque los niveles son bajos. Se ha 
hablado de vaporización de TFF al calentarse el vinilo de la tapicería 
de los automóviles, pero no se dispone de datos sobre la concentración 
en los coches. En un estudio de los triarilfosfatos en el tejido adiposo 
humano no se detectó TFF. Estos datos no bastan para evaluar la 
importancia de la exposición de la población general al TFF. 

   Se ha comunicado la existencia de concentraciones importantes (0,5-
29,6 mg/m3) en el aire de unas instalaciones de producción de TFF, pero 
no se dispone de cifras recientes. Se necesitan más datos sobre la 
exposición profesional al TFF en los lugares de fabricación. 

1.2 Efectos tóxicos

   Los datos de que se dispone sobre la toxicidad del TFF son totalmente 
insuficientes para una valoración completa del riesgo que representa. 

   No hay pruebas de que el TFF tenga actividad mutagénica en bacterias 
ni de que tenga actividad carcinogénica, de acuerdo con un estudio sobre 
una especie animal. De momento no se han obtenido pruebas de que el TFF 
cause neurotoxicidad diferida en animales de experimentación. En un 
estudio de alimentación de 35 días en ratas se observó una disminución 
en la ganancia de peso corporal y un aumento de peso del hígado con una 
dosis de 5 g/kg. No se dispone de datos adecuados en cuanto a los 
efectos del TFF en la reproducción, es decir, en la función de las 
gónadas, la fertilidad, el parto y el crecimiento y desarrollo de la 

   Se han descrito casos de dermatitis de contacto causada por el TFF. 

2. Evaluación de los efectos en el medio ambiente 

   Las concentraciones de TFF en el agua ambiental son bajas y los 
efectos tóxicos en los organismos acuáticos son poco probables. Los 
vertidos de fluidos hidráulicos con TFF podrían tener efectos letales a 
nivel local. Puesto que el TFF se elimina rápidamente de los tejidos de 
los peces al terminar la exposición y los factores de bioconcentración 
son moderados, no se considera que la bioacumulación sea un peligro. 

   Se ha informado de la presencia de altas concentraciones de TFF en 
sedimentos cercanos a instalaciones de producción. Se ha demostrado que 
cierto organismo que vive en los sedimentos puede utilizar el TFF fijado 
por éstos, pero no hay datos de toxicidad sobre las especies que viven 
en los sedimentos o se alimentan de ellos. Existe, por consiguiente, la 
posibilidad de efectos en las comunidades acuáticas. 

2.1 Niveles de exposición

   El TFF se halla en el aire, el agua superficial, el suelo, los 
sedimentos y los organismos acuáticos recogidos en zonas muy 
industrializadas. La concentración más alta de TFF en efluentes de aguas 
industriales que se ha comunicado es de 16 µg/litro, mientras que en 
aguas fluviales es de 7,9 µg/litro. Teniendo en cuenta la rápida bio-
degradación del TFF en el medio acuoso, es poco probable que las 
concentraciones normales de TFF en él afecten de manera adversa a los 
organismos acuáticos. Sin embargo, si se arrojase a una charca tejido de 
tapicería de vinilo tratado con TFF se produciría una concentración 
suficientemente alta para matar a los peces. 

2.2 Efectos tóxicos

   Entre los diferentes triarilfosfatos, el TFF es el compuesto más 
tóxico para peces, camarones y dáfnidos. Los valores de la CL50 en 96 
horas de TFF para los peces varían entre 0,36 mg/litro en la trucha arco 
iris y 290 mg/litro en  Lepomis macrochirus. Aunque los salmónidos en 
general son sensibles al TFF, el crecimiento y la supervivencia de los 
alevines de trucha arco iris no se vieron afectados cuando éstos se 
expusieron a una concentración de TFF de 0,0014 mg/litro. Los ejemplares 
de  Carassius auratus  expuestos al TFF presentaron lesiones 
histopatológicas consistentes en congestión, degeneración y hemorragia 
de los vasos sanguíneos pequeños, principalmente vénulas y capilares. 
Esta patología vascular es más pronunciada en las branquias. 

   Las concentraciones de TFF iguales o superiores a 1 mg/litro 
inhibieron completamente el crecimento de las algas, pero a 
concentraciones más bajas (0,1 y 0,05 mg/litro) lo estimularonn. La 
actividad de la nitrogenasa de  Anabaena flos-aquae  se redujo de forma 
significativa, incluso a una concentración de 0,1 mg/litro. 

1. Recomendaciones para futuras investigaciones

 a) Se deberían realizar estudios de sensibilización cutánea.

 b) Es necesario realizar un estudio de citogenicidad  in vitro.

 c) Se precisan estudios farmacocinéticos de las diferentes vías.

    See Also:
       Toxicological Abbreviations
       Triphenyl phosphate (ICSC)