Trichloroethylene

79-01-6

Amines * as stabilizers 0.001 - 0.01 %

* Combinations of
epoxides * and
esters * 0.2 - 2.0 % total (Fawell & Hunt 1988).

Solvent used for degreasing metals and as a dry-cleaning agent. 
It has been used as an anaesthetic by inhalation, although this
use is now infrequent. 
Solvent in food processing.

Odour threshold: 10 mg/l in water (Verschueren 1983).

131.38

Relative volatility (nBuAc=1) = 6.99

28.65 % (air), 71.27 % (water), 0.08 % (sediment).

Equilibrium distribution:
         mass %
air     99.67
water    0.31
solid    0.02
(Anon 1988)

Photooxidation half-life in air:
1.1d - 11.3d, 
based upon measured rate data for the vapor phase reaction with 
hydroxyl radicals in air (Howard 1991).

First-order hydrolysis half-life:
10.7mo, based upon a first order rate constant (k=0.065 mo-1)
at 25 °C (Howard 1991).

Aerobic half-life:
6mo - 1yr,
scientific judgement based upon acclimated aerobic soil 
screening test data (Howard 1991).

Anaerobic half-life:
98d - 4.5yr,
scientific judgement based upon anaeobic sediment grab sample 
data (Howard 1991).

Biodegradation:
2.4% by BOD
period: 14d
substance: 100 mg/l
sludge: 30 mg/l
(MITI 1992)

Degradation of trichloroethylene:
*--------------------------------------------------------------*
ENVIRONMENT  INIT.CONC   REDOX-      TEMP   DEGRADATION   REF.
             mg/l        COND.       °C     %/day    t1/2
*--------------------------------------------------------------*
soil            5        anaerobic   25      -       33-90   a
aquifer material 0.085   anaerobic   20       <3/7     -     b
water (mixed cult.) 0.012 methanogen 35       25/112  270    c
water           0.034    methanogen  35       12/112  620    c
water           0.127    methanogen  35       46/112  127    c
water           0.011    aerobic     20        0/175 >175    c
water           0.031    aerobic     20        0/175 >175    c
water           0.081    aerobic     20        0/175 >175    c
water           0.178    methanogen  35       40/57    78    d
water (deion.)  1.0      aerobic     25         -     320    e
water           0.08     aerobic + methane 20 81/0.3   <2    f
water           0.65     aerobic     20       69/4      2.4  f
soil            1.0      aerobic + natural gas  -       0.03 g
water (adapted) 1.436    aerobic      -       97/11     -    h
water          50        aerobic      -       44/14     -    h
water          36        aerobic/anaerobic    56/16     -    h
water           5        aerobic     25       64/7      -    i
water          10        aerobic     25       38/7      -    i
water (adapted) 5        aerobic     25       86/7      -    i
water          10        aerobic     25       84/7      -    i
soil            0.82     aerobic + propane      -      5-9   j
soil            0.9      aerobic     20       14/2      -    k
soil            0.18     aerobic     20        0/2      -    k
aquifer material 0.6 - 0.8 aerobic   17       <2/7       <1.2l
soil            0.15     aerobic + methane    95/7      -    m
*--------------------------------------------------------------*
a) Barrio-Lage et al. 1987 h) Kästner 1986 (1000000000 org./ml)
b) Wilson et al. 1983b     i) Tabak et al. 1981
c) Bouwer et al. 1981      j) Wilson & White 1986
d) Bouwer & McCarty 1983a  k) Wilson et al. 1981
e) Dilling et al. 1975     l) Wilson et al. 1983
f) Fogel et al. 1986       m) Wilson & Wilson 1985
g) Anon. 1987b             (Anon. 1987b).

Trichloroethylene is absorbed into the body through the lungs,
gastrointestinal tract and the skin. 
Following oral
administration of 5, 10 and 25 mg/kg to male rats,
trichloroethylene appeared rapidly in the blood, with
concentrations peaking after 6 - 10 min. 
This compound is
easily absorbed across the gastrointestinal tract in man, and
many cases of acute poisoning following oral ingestion have
been reported (Fawell & Hunt 1988).

Trichloroethylene is absorbed through the skin in man, although
the significance of this route of exposure for dilute aqueous
solutions is still unclear (Fawell & Hunt 1988).

Trichloroethylene is distributed primarily to the adipose
tissue, due to its high fat solubility (Fawell & Hunt 1988).

Transplacental diffusion has been demonstrated in humans, and
trichloroethylene was detected in foetal blood (Fawell &  Hunt 
1988).

This compound is readily metabolized by rodents, primates and
man. 
In the liver, metabolic breakdown of trichloroethylene is
thought to involve transformation by mixed function oxidase
enzymes to a reactive epoxide. 
The instability of this epoxide
has been attributed to its non-symmetrical arrangement of
chlorine atoms. 
A rearrangement of the epoxide results in the
formation of chloral. 
This may be either oxidized to
trichloroacetic acid, or reduced to trichloroethanol.

Trichloroethanol products may also be conjugated to form
glucoronides. 
The identification of HAAE
(N-(hydroxyacetyl)-aminoethanol) and oxalic acid in the urine
of rats and mice after a single oral dose of radiolabelled
trichloroethylene indicates that dechlorination reactions may
also occur in the breakdown of this compound. 
However, in man
the principal metabolites following absorption of
trichloroethylene appear to be trichloroacetic acid and
trichloroethanol (Fawell & Hunt 1988).

Recent studies suggest that trichloroethylene may also be
metabolized to some extent in the kidney, to form a cysteine
conjugate. 
The production of reactive intermediated during this
process may explain the nephrotoxicity and
nephrocarcinogenicity of trichloroethylene observed in rats
(Fawell & Hunt 1988).

Trichloroethylene metabolism appears to be a dose-dependent
process in rats and man (Fawell & Hunt 1988).

Alcohol in the blood inhibits metabolism of this compound and
may cause 'Degreaser's flush'. 
Symptoms include drowsiness and
reddening of the face and upper body (Fawell & Hunt 1988).

The major route of elimination is via the lungs. 
The rest is
eliminated in the urine. 
Following metabolism of
trichloroethylene, the elimination of various metabolites in
the urine occurs at different rates. 
The slower excretion rate
of trichloroacetic acid compared to trichloroethanol may be due
to its higher affinity for proteins (Fawell & Hunt 1988).

Confirmed to be non-accumulative or low accumulative 
(Anon. 1984).

Trichloroethylene appears to be of low reproductive toxicity.

There were no significant effects on fertility, teratogenicity
or neonatal development in rodents. 
Delayed ossification of the
sternum and displacement of the right ovary were observed in
the offsping of treated Long-Evans rats, but these do not
represent important embryotoxic effects 
(Schwetz et al. 1975,Dorfmueller et al. 1979, Taylor et al. 
1985, Ghantous et al.1986, Manson et al. 1984, Zenick et al. 
1984, Borzelleca & Carchman 1982, Fawell & Hunt 1988).

The toxicology of trichloroethylene has been well studied and
it appears to be of low acute and chronic toxicity. 
The
principal target organs are the CNS and liver, although recent
evidence suggests that trichloroethylene may be nephrotoxic in
rodents following long-term exposure
(Fawell & Hunt 1988,Tucker et al. 1982, Torkelson & Rowe 1982,
Adams et al. 1951, Kjellstrand et al. 1982, Kanje et al. 1981,
Stott et al. 1982, Kjellstrand et al. 1981, Aranyi et al. 1986, 
Sanders et al. 1982, WHO 1985, Feldman et al. 1985, 
Vernon & Ferguson 1969, James, 1963, Hayden et al. 1976, 
Wells 1982, Buben & O'Flaherty 1985, US NTP 1983, 
Kyrklund et al. 1983, Silverman & Williams 1975, 
Mitchell & Parsons-Smith 1969, Barret et al. 1982,
Vyskocil 1953).

In 1976 the National Cancer Institute study found an increase
in liver tumours in C6B3F1 mice following chronic oral exposure
to trichloroethylene. 
An increase in forestomach tumours in
Swiss mice and lung tumours in NMRI mice from oral and
inhalation exposure have also been reported. 
The carcinogenic
potential of trichloroethylene appears to be affected by the
presence of stabilisers. 
There was no evidence of
hepatocarcinogenicity in Osborne-Mendel rats. 
However, a number
of renal adenocarcinomas have been recently reported in rats
following long-term oral administration, which are rare in
untreated controls. 
Epidemiology studies are insufficient to
assess whether trichloroethylene causes cancer in man
(WHO 1985, Dekant et al. 1986a, Henschler et al. 1984, Fukuda
et al., Henschler et al. 1980, Van Duuren et al. 1983, Tu et al.
1985, Blair et al. 1979, Tola et al. 1980, Paddle 1983, Fawell
& Hunt 1988).

There is conflicting evidence that trichloroethylene is
mutagenic. 
Both positive and negative results were reported in
the Ames test with and without metabolic activation.

Trichloroethylene does no appear to be mutagenic in yeast in
the absence of metabolic activation, but the position is
unclear in the presence of S-9. 
Under certain conditions of
growth, trichloroethylene disrupts mitotic segregation in the
fungus Aspergillus nidulans. 
Unscheduled DNA synthesis and
chromosome aberrations were reported in human lymphocytes
following exposure to this compound. 
The metabolite
S-1,2-dichlorovinylcysteine was mutagenic in the Ames test
without metabolic activation. 
The differences in mutagenicity
observed in these studies may be partly explained by the purity
and nature of the additives present in the samples tested. 
Both
epichlorohydrin and epoxybutane, two stabilizers found in
technical grade trichloroethylene, were mutagenic in vitro. 
At
present, there are inadequate data to evaluate the mutagenic
potential of this chemical (Waskell 1978, Bartsch et al. 1979, 
Cerna & Kypenova, Greim et al. 1975, Bronzetti et al. 1978, 
Callen et al. 1980, Rossi et al. 1983, Crebelli et al. 1985, 
Slacik-Erben et al. 1980, Bergman 1983, Walles 1986, Perocco & 
Prodi 1981, Konietzko et al. 1978, Dekant et al. 1986b).

EC50, Eisenia foetida, 1000 mg/kg, 28d (Anon 1986b).

EC50, Brassica rapa sativa rapifera, 1000 mg/kg, 14d;
EC50, Avena sativa, 1000 mg/kg, 14d (Anon 1986b).

EC50, Photobacterium phosphoreum, 115 mg/l, 15 min;
EC50, assimilationtest, 530 mg/l, 24hr (Anon 1986b).

Toxicity threshold (cell multiplication inhibition test):
bacteria (Pseudomonas putida): 65 mg/l
(Bringmann & Kühn 1980a).

EC50 (24hr) 410 mg/l, rpd, Tetrahymena pyriformis (Yoshioka et
al. 1985).

LC50, 48hr, 132 mg/l, Tubificidae
LC50, 48hr, 64 mg/l, Chironomus gr. thummi
LC50, 48hr, 75 mg/l, Erpobdella octoculata
LC50, 48hr, 56 mg/l, Lymnaea stagnalis
LC50, 48hr, 42 mg/l, Dugesia cf. lugubris
LC50, 48hr, 75 mg/l, Hydra oligactis
LC50, 48hr, 110 mg/l, Corixa punctata
LC50, 48hr, 49 mg/l, Ischura elegans
LC50, 48hr, 70 mg/l, Nemoura cinerea
LC50, 48hr, 42 mg/l, Cloeon dipterum
(Slooff 1983).

Toxicity threshold (cell multiplication inhibition test):
green algae (Scenedesmus quadricauda): >1000 mg/l
protozoa (Entosiphon sulcatum): 1200 mg/l
(Bringmann & Kühn 1980a).

Atmosperic contamination with trichloroethylene has been
implicated as a possible factor in the depletion of the ozone
layer (Fawell & Hunt 1988).

Since trichloroethylene is virtually insoluble in water, and
has a specific gravity heaviere then water, any pollution of
groundwater is likely to persist. 
There is no indication that
trichloroethylene is produced from chlorination of natural
waters (Fawell & Hunt 1988).