MONOGRAPH FOR UKPID
TETRACHLOROETHYLENE
Henrietta Wheeler
National Poisons Information Service (London Centre)
Medical Toxicology Unit
Guy's & St Thomas' Hospital Trust
Avonley Road
London
SE14 5ER
UK
This monograph has been produced by staff of a National Poisons
Information Service Centre in the United Kingdom. The work was
commissioned and funded by the UK Departments of Health, and was
designed as a source of detailed information for use by poisons
information centres.
Peer review group: Directors of the UK National Poisons Information
Service.
1 SUBSTANCE/PRODUCT NAME
1.1 Origin of substance
Tetrachloroethylene is a synthetic chemical with no natural sources
(Ware, 1988).
1.2 Name
1.2.1 Brand/trade name
Ankilostin; Antisal 1; Dee-Solv; Didakeno; Dowclean EC; Dow-per; ENT
1860; Fedal-Un; Nema; Perawin; Perclene; Percosolv; Perklone; PerSec;
Perwin; Tetlen; Tetracap; Tetralax; Tetraleno; Tetravec; Tetroguer;
Tetropil.
1.2.2 Generic name
Tetrachloroethylene.
1.2.3 Synonyms
Carbon bichloride, carbon dichloride, ethylene tetrachloride, PCE,
per, perc, perchlor, perchlorethylene, perchloroethylene, percosolve,
perk, tetrachlorethylene, tetrachloroethylene,
1,1,2,2-tetrachloroethylene, tetrachloroelthylenum.
1.2.4 Common names/street names
1.3 Chemical group/family
Halogenated aliphatic hydrocarbon.
1.4 Substance identifier and/or classification by use
Halogenated aliphatic hydrocarbon.
1.5 Reference numbers
CAS 127-18-4
RTECS/NIOSH KX 3850000
EINECS 2048259
UN 1897
1.6 Manufacturer
Not applicable.
1.7 Supplier/importer/agent/ licence holder
Not applicable.
1.8 Presentation
1.8.1 Form
Halogenated aliphatic hydrocarbon.
1.8.2 Formulation details
1.8.3 Pack sizes available
1.8.4 Packaging
The European Economic Commission regulations state that the label
should read that tetrachloroethylene is harmful if inhaled or
swallowed, and should be kept out of reach of children. Contact with
the eyes must be avoided (WHO, 1984).
1.9 Physico-chemical properties
Chemical structure C2Cl4
Physical state liquid
Colour Clear and colourless
Odour ether-like odour at 50 ppm. Odour threshold
0.3 ppm in water; 1.0 ppm in air.
Solubility
Water at 25°C 150 mg/L. Organic solvents: miscible with alcohol,
ethyl, ether, chloroform benzene, solvent hexane, and most of the
fixed and volatile oils.
Autoignition temperature No data available
Important chemical interactions
Mixtures of tetrachloroethylene and dinitrogen tetroxide are explosive
when subject to shock (Commission of the European Communities, 1986).
tetrachloroethylene reacts violently or explosively with certain
alkali or alkaline earth metals. Granular barium in contact with
tetrachloroethylene is susceptible to detonation. A mixture of lithium
shavings and tetrachloroethylene is impact-sensitive and will explode,
possibly violently. When heated together, potassium and
tetrachloroethylene explode at 97-99°C. A tetrachloroethylene sodium
mixture does not explode under similar conditions (Commission of the
European Communities, 1986; Sax, 1984).
Major products of combustion/pyrolysis
Tetrachloroethylene is slowly decomposed by light and by various
metals in the presence of moisture (Commission of the European
Communities, 1986; Reynolds, 1993). Tetrachloroethylene decomposes
upon heating above 150°C forming phosgene and hydrochloric acid.
Trichloroacetyl chloride is described as a major degradation product
and phosgene a lesser one (Commission of the European Communities,
1986).
Explosion limits No data
Flammability non-flammable
Boiling point 121.2°C
Density 1.6227 g/ml (at 20°C)
Vapour pressure 18.47 mmHg (at 25°C)
Relative vapour density 5.83
Flash point None
1.10 Hazard/risk classification
1.11 Uses
Tetrachloroethylene was first commercially produced in USA in 1925.
Tetrachloroethylene has been the solvent of choice in the dry cleaning
industry since the 1950s (Blair et al, 1979) and is used extensively
in textile processing as a scouring solvent to remove the oil from the
fabrics (Ellenhorn and Barceloux, 1988; Sax, 1984; Torkelson, 1994;
Ware, 1988). It is used in manufacturing fluorocarbons, as a drying
agent for metals and some other solids, as a fumigant for insects and
rodents (Gehring et al, 1991), as a heat transfer medium, and as a
degreasing solvent (Sax, 1984; Torkelson, 1994). It is also used in
aerosol cleaners, ignition wire driers, spot removers, fabric and wood
cleaners (Ellenhorn and Barceloux, 1988; Finkel et al, 1983; Sax,
1984; Torkelson, 1994). An unfortunate number of deaths from
tetrachloroethylene have been from sleeping bags that have not been
properly cleaned of the dry cleaning chemical prior to use (Finkel et
al, 1983).
Tetrachloroethylene is active against hookworms ( Ancylostoma and
Necator), its use of was prevalent in the 1920s and 1930s in India
and the Pacific Islands (Ware, 1988). Tetrachloroethylene may still be
used in endemic areas although it has generally been superseded by
drugs that are less toxic and easier to administer (Reynolds, 1993).
It has also been used in the treatment of fasciolopsiasis (Reynolds,
1993).
1.12 Toxicokinetics
1.12.1 Absorption
Pulmonary absorption is the primary route of entry of
tetrachloroethylene under industrial conditions (Baselt and Cravey,
1990).
Human volunteers at rest absorbed about 25% of tetrachloroethylene
administered by inhalation exposure at 72 or 144 ppm over a 4 hour
period. At first the compound was absorbed rapidly, but uptake
decreased as exposure continued. The uptake was influenced more by
(lean) body mass than by respiratory minute volume or adipose tissue
(Monster and Houtkooper, 1979). During work the uptake and minute
volume increased to 3 fold the value at rest. In the post-exposure
period the quotient of the blood concentrations and exhaled air
concentrations of tetrachloroethylene remained at nearly 23. Following
exposure about 80 to 100% of the uptake was excreted unchanged by the
lungs, whereas 70 hours after exposure the amount of trichloroacetyl
chloride (TCA) excreted in urine represented about 1% of the uptake
(Monster et al, 1979; Monster and Houtkooper, 1979; Monster, 1979).
Dermal absorption was rapid in both mice and guinea-pigs, peak
concentrations of tetrachloroethylene in the blood of guinea-pigs
being reached 30 minutes after application. The level of
tetrachloroethylene in the blood of rats reached a maximum 1 hour
after oral ingestion, or immediately after 6 hour inhalation (WHO,
1984; Pegg et al, 1979).
1.12.2 Distribution
The deposition of tetrachloroethylene in man is poorly understood
(Baselt and Cravey, 1990).
Tetrachloroethylene is lipophilic and accumulates in the liver, brain,
kidney, lung and adipose tissue, with gradual redistribution
(Lukaszewski, 1979; Ware, 1988). It crosses the blood-brain barrier
(Ware, 1988).
In human tissue at autopsy, ratios of fat-to-liver concentrations are
greater than 6:1 (McConnell et al, 1975). The fat-to-blood ratio is
about 90:1 and the half-life for saturation of the fat to 50% of its
equilibrium concentration is about 25 hour (Monster, 1979).
Tetrachloroethylene has an estimated volume of distribution of 8.2
L/kg after an oral dose of 400 mg.
A postmortem after a fatal tetrachloroethylene exposure revealed an
eight times greater concentration in the brain compared to the blood
(Lukaszewski, 1979), whereas in another postmortem the liver contained
the highest tetrachloroethylene levels (Levine, 1981).
1.12.3 Metabolism
Less than 4% of the estimated absorbed dose of tetrachloroethylene is
metabolised and excreted as trichloroacetic acid in humans (Fernandez
et al, 1979; Ferroni et al, 1992).
Tetrachloroethylene is stored in the fat and adipose tissue and slowly
metabolised with the loss of chlorine (Gosselin et al, 1984). Once
absorbed, the highest concentrations of tetrachloroethylene are found
in the adipose tissue, reflecting its high lipid solubility (Ware,
1988). The principle site of metabolism is the hepatic microsomal
cytochrome P450 mixed-function oxidase system in a dose-dependent
manner (Gehring et al, 1991; Torkelson, 1994).
Tetrachloroethylene is probably transformed by oxidation to
perchloroethylene oxide and subsequently by rearrangement to
trichloroacetyl chloride and then by hydrolysis to trichloroacetic
acid (TCA) (Lukaszewski, 1979; Yllner, 1961). Metabolism takes place
mainly in the liver. The maximum concentration of TCA is reached at 20
hours after exposure (Monster, 1979).
The major urinary metabolite seems to be trichloroacetic acid, over
half appears as the acid and its conjugate. Much smaller amounts of
oxalic acid, trichloroethanol, dichloroacetic acid and
N-trichloroacetyaminoethanol or its conjugate are excreted (Commission
of the European Communities, 1986; Skender et al, 1991; Torkelson,
1994).
Tetrachloroethylene may give rise to reactive intermediate metabolites
that may impair the tubero-infundibular dopaminergic system (Ferroni
et al, 1992). This mechanism may involve neuroendocrine changes
accounting for gynaecological disturbances eg oligo-menorrhoea and
reduced fertility (Zielhuis et al, 1989) and spontaneous abortion or
perinatal death (Olsen et al, 1990).
1.12.4 Elimination
There seems to be no apparent difference in elimination pathways or
metabolism in animals exposed by oral or inhalation routes. The major
determinant of metabolism and tissue distribution is body burden (Pegg
et al, 1979).
The majority of tetrachloroethylene (about 80%) is eventually excreted
unchanged in expired air; initial elimination is rapid but a
proportion may be retained and excreted slowly (Baselt and Cravey,
1990; Reynolds, 1993; Skender et al, 1991). 15% of an inhaled dose is
eliminated unchanged within 1 hour, 3% is metabolised and excreted via
the urine over a 67 hour period (Baselt and Cravey, 1990; Commission
of the European Communities, 1986; Koppel et al, 1985).
Approximately 25% of an inhaled dose is excreted unchanged in the
breath over 40 hours following exposure (Baselt and Cravey, 1990).
Elimination is then slow due to the release from the fat store,
repeated daily exposures leads to accumulation of tetrachloroethylene
in man (Ellenhorn and Barceloux, 1988).
Alveolar breath concentrations of tetrachloroethylene approach 50% of
the atmospheric concentration of the chemical during constant exposure
(Baselt and Cravey, 1990). In subjects exposed to 100 ppm of the
vapour, breath concentrations averaged 15 ppm during the first hour
after exposure, 8 ppm after 15 hours and 4.5 ppm after 71 hours
(Stewart et al, 1970).
Chlorinated metabolites of tetrachloroethylene generally do not exceed
concentrations of 100mg/L in urine workers exposed to the vapor at air
concentrations of up to 400 ppm (Ikeda et al, 1972).
1.12.5 Half-life
The biological half-life of tetrachloroethylene on inhalation has been
estimated from pulmonary excretion data as between 3 and 72 hours
(Baselt and Cravey, 1990).
Trichloroacetic acid, as a metabolite of tetrachloroethylene, is
eliminated with a half-life of 144 hour via the urine (Ware, 1988).
The biological half-life of tetrachloroethylene appears to be 144
hours following ingestion (Gosselin et al, 1984; Ikeda, 1977; Koppel
et al, 1985; Lukaszewski, 1979).
1.12.6 Special populations
No data.
2 SUMMARY
3 EPIDEMIOLOGY OF POISONING
Tetrachloroethylene was introduced in to the dry cleaning industry in
the late 1930s, but did not replace other synthetic solvents until
shortly after the second world war. By 1977, about 74% of dry cleaning
outlets used tetrachloroethylene (Brown and Kaplan, 1987). At least
1.6 million workers in US are potentially exposed to
tetrachloroethylene annually (Brown and Kaplan, 1987).
4 MECHANISM OF ACTION/TOXICITY
4.1 Mechanism
Systemic toxicity after acute overexposure to tetrachloroethylene
vapour is characterised by central nervous system depression,
hypotension, cardiac arrhythmias, hepatic and renal injury; death may
be due to respiratory failure. The major response to
tetrachloroethylene at high concentrations is CNS depression. It is
not, however, sufficiently effective to be considered a useful
anaesthetic (Torkelson, 1994).
Tetrachloroethylene may sensitise the myocardium to adrenaline and
other catecholamines at high levels of exposure (Hathaway et al, 1991;
Torkelson, 1994).
The vapour and liquid are irritating to the skin and mucous membranes.
There may be nausea and gastrointestinal upset at high concentrations.
Changes in the liver and kidneys may be seen following excessive
exposure; however the effects are not as severe or striking as they
are with other hydrocarbons, e.g. carbon tetrachloride (Ellenhorn and
Barceloux, 1988; Torkelson, 1994).
Dependence may follow habitual inhalation of small quantities of
tetrachloroethylene vapour.
4.2 Toxic dose
Inhalation:
Dose Exposure Symptoms Comments Reference
(ppm) time
50 8 hours No physiological Odour threshold Commision of the
effects (very faint) to European
unacclimatised Communities, 1986
216 45 mins- Respiratory Rowe et al, 1952
2 hours irritation
275 3 hours Coma for 1 hour. Concentration of Hathaway et al, 1991
then then Deranged LFTs tetrachloroethylene
100 30 minutes for 2-3 weeks in expired air,
post-exposure diminished slowly
over 2 weeks
400 2 hours Eye irritation, Odour strong, but Commision of the
slight nasal tolerable European Communities,
irritation, ataxia 1986
600 10 minutes Numb mouth, dizzy, Odour very Commision of the
ataxic for 10 strong but European Communities,
minutes post- tolerable 1986
exposure
1,060 1-2 minutes Not tolerated for Exposed in Rowe et al, 1952
more than 2 minutes chamber
1,500 30 minutes 'Gagging', irritation Odour almost Commision of the
of eyes and intolerable European Communities,
respiratory tract 1986
(almost intolerable),
loss of consiousness
(Continued)
Dose Exposure Symptoms Comments Reference
(ppm) time
5,000 6 minutes Vertigo, nausea and Hathaway et al, 1991
confusion for 10
minutes post-
exposure
Two adults who died shortly after massive exposure of
tetrachloroethylene fumes in dry cleaning establishments were found to
have the following concentrations (mg/L or mg/kg) of
tetrachlorethylene (Baselt and Cravey, 1990):
Patient Blood Brain Lung Liver Kidney
Patient 1 44 360 3 - -
Patient 2 4.5 69 30 240 71
Chronic inhalation:
Twenty dry cleaning workers exposed for an average of 7.5 years to
concentrations of 1-40 ppm had altered electrodiagnostic and
neurological rating scores (Hathaway et al, 1991). Abnormal EEG
readings were found in 4 out of 16 factory employees exposed to
concentrations ranging from 60-450 ppm for 2 to 20 years (WHO, 1984).
Ingestion:
A 6 year old boy ingested 8-10 ml of tetrachloroethylene and became
comatose. He developed a peak blood level of 22 mg/L but survived
(Koppel et al, 1985).
5 FEATURES OF POISONING
5.1 Acute
5.1.1 Ingestion
Ingestion of tetrachloroethylene may cause gastric irritation with
nausea and vomiting. It may cause CNS depression, dizziness,
inebriation, lightheadedness, mental dullness and incoordination
(Hathaway et al, 1991; Stewart et al, 1970). CNS depression may range
form mild narcosis to coma with respiratory depression or death
(Hathaway et al, 1991).
Respiratory effects include coughing, wheezing, pulmonary oedema and
increasing cyanosis. These may occur due to aspiration or following
large inhalation exposure. Full recovery may be seen if exposure is
minimal.
Tetrachloroethylene is thought to sensitise the myocardium to
endogenous catecholamines which may cause arrhythmias and sudden death
after massive acute exposures.
Ingestion of tetrachloroethylene has been associated with the
development of toxic epidermal necrolysis (Potter, 1960).
5.1.2 Inhalation
Tetrachloroethylene vapours are irritant to nasal, ocular and
respiratory mucosa (Rowe et al, 1952). Headache, fatigue, ataxia,
dizziness, nausea, vomiting, hypotension, mental confusion and
temporary blurred vision have been reported after inhalation (Baselt
and Cravey, 1990; Clement International Corporation, 1993; Rowe et al,
1952). Tetrachloroethylene is a CNS depressant and causes drowsiness
that can lead to coma or death.
Tetrachloroethylene is thought to sensitise the myocardium to
endogenous catecholamines which may cause arrhythmias and sudden death
after massive acute exposures.
Short-term exposure tests prove that the visual system is one of the
target organs of acute tetrachloroethylene toxicity.
5.1.3 Dermal
Tetrachloroethylene is irritant to the skin. It may cause dry, scaly
skin, blisters and dermal burns (Baselt and Cravey, 1990; Finkel et
al, 1983). Erythema and a severe burning sensation may occur if
tetrachloroethylene is left on the skin for 40 minutes or longer
(Hathaway et al, 1991). Dermatitis is caused by defatting of the skin
(Torkelson, 1994).
5.1.4 Ocular
Tetrachloroethylene vapours are irritating to eyes at high
concentrations (Ellenhorn and Barceloux, 1988; Grant and Schuman,
1993; Torkelson, 1994). An ocular splash exposure is expected to cause
lacrimation and burning but no permanent damage (Rowe et al, 1952;
Torkelson, 1994).
Spraying rabbits in the eyes with tetrachloroethylene caused immediate
blepharospasm and pain. The corneal epithelium became granular and
optically irregular patches of epithelium were lose, both eyes
recovered completely within 2 days (Grant and Schuman, 1993).
5.1.5 Other routes
Tetrachloroethylene has been found to be weakly nephrotoxic and
hepatotoxic following subcutaneous injection in mice.
Dogs were killed by intravenous doses of 85 mg/kg; the few that
received 75 mg/kg or less survived (Gehring et al, 1991).
5.2 Chronic toxicity
5.2.1 Ingestion
When tetrachloroethylene was administered in drinking water for 90
days to mice, body weight was decreased and there were suggestions of
liver effects but no clear evidence of injury at 1400 mg/kg/day
(Gehring et al, 1991; Torkelson, 1994).
There is no human data available.
5.2.2 Inhalation
Since tetrachloroethylene is minimally metabolised, slowly excreted,
and presumed to be accumulative, chronic exposure to a lower vapour
concentration could conceivably result in human injury or organ
dysfunction (Monster and Houtkooper, 1979; Stewart, 1969; Stewart et
al, 1970).
In a chronic overexposure, post-mortem findings included haemorrhagic
pneumonitis and pulmonary oedema (Trense and Zimmerman, 1969).
Tetrachloroethylene is thought to sensitise the myocardium to
endogenous catecholamines which may cause arrhythmias and sudden death
after massive acute or chronic exposures. Chronic occupational
exposure has been known to produce multiple ventricular premature
beats (Abedin et al, 1980).
Odour tolerance seems to be exhibited in chronically exposed humans.
Sixteen subjects were exposed to 100 ppm over a 7 hour period,
initially 100% were able to detect a faint odour; by the end of
exposure only 40% were still able to detect the odour of the solvent.
Subjects exposed for 5 consecutive days reported that their ability to
perceive the odour progressively diminished during the course of the
week. Although initially the odour was detected on entering the
chamber upon the second day, within two hours only three were able to
smell tetrachloroethylene (Stewart et al, 1970).
Chronic occupational exposure of three years resulted in peripheral
neuropathy, hepatitis, confusion, disorientation, muscle cramps,
fatigue, agitation and damage to liver, kidney and spleen (Baselt and
Cravey, 1990). One case of fatal chronic poisoning showed lobular
necrosis of the liver at postmortem (Trense and Zimmerman, 1989).
Liver enlargement was still present 6 months after cessation of
exposure in one chronic occupational poisoning (Meckler and Phelps,
1966).
A connective tissue disorder characterised by Reynauld's phenomenon,
alopecia, myositis and strongly positive antinuclear antibodies in
patients chronically exposed to tetrachloroethylene has been described
by Sporrow in 1977 (Baselt and Cravey, 1990).
Tetrachloroethylene may give rise to reactive intermediate metabolites
that may impair the tubero-infundibular dopaminergic system (Ferroni
et al, 1992). This mechanism may involve neuroendocrine changes
accounting for gynaecological disturbances eg oligo-menorrhoea and
reduced fertility (Zielhuis et al, 1989) and spontaneous abortion or
perinatal death (Olsen et al, 1990).
Chronic low level exposures of tetrachloroethylene may effect colour
vision although the pathogenesis is unclear (Cavalleri et al, 1994).
The effect does not seem to be rapidly reversible.
Chronic low levels of tetrachloroethylene may significantly impair
performance and affect pituitary function, thus causing increased
levels of the dopaminergic modulation of prolactin (Olsen et al,
1990).
5.2.3 Dermal
Chronic skin exposure may cause reddening and chapping of the skin.
Dry, scaly and fissured dermatitis may also occur from repeated skin
contact.
5.2.4 Ocular
Chronic low level exposures of tetrachloroethylene may affect colour
vision although the pathogenesis is unclear (Cavalleri et al, 1994).
The effect does not seem to be rapidly reversible.
5.2.5 Other routes
No human data available.
5.3 Systematic description of clinical effects
5.3.1 Cardiovascular
Tetrachloroethylene may sensitise the myocardium to adrenaline and
other catecholamines. However, in dogs exposed to highly anaesthetic
levels of tetrachloroethylene (5000 to 10,000 ppm) cardiac arrhythmias
were not detected (Hathaway et al, 1991). The significance of these
findings for humans exposed to allowable concentrations is very
questionable (Torkelson, 1994).
Multiple ventricular premature beats occurred in a worker with chronic
exposure and tetrachloroethylene was detected in the blood. No
arrhythmia was noted one month after the exposure was discontinued
(Abedin et al, 1980).
5.3.2 Respiration
Upper respiratory tract irritation may occur with exposure to high
concentrations of airborne tetrachloroethylene (Clement International
Corporation, 1993; Finkel et al, 1983; Torkelson, 1994). Respiratory
failure may occur in massive overexposure (Rowe et al, 1952).
In a chronic overexposure, postmortem findings included haemorrhagic
pneumonitis and pulmonary oedema (Trense and Zimmerman, 1969).
5.3.3 Neurological
Ingestion or inhalation of tetrachloroethylene causes CNS depression,
dizziness, headache, inebriation, slurred speech, lightheadedness,
mental dullness and incoordination (Hathaway et al, 1991; Stewart,
1969; Stewart et al, 1970). CNS depression may range form mild
narcosis to coma with respiratory depression or death (Hathaway et al,
1991).
A 62 year old man presented with inebriation following exposure to 500
ppm. He recovered within 6 hours (McMullen, 1976).
19 volunteers exposed to tetrachloroethylene vapor concentrations of
20, 100 and 1,500 ppm for 1 month (5 days/week). EEG changes were
recorded in 7 out of 19 subjects during 100 ppm exposure. The EEG
changes were characterised by a reduction in overall wave amplitude
and frequency, most evident in the occipital leads. The altered EEG
pattern was similar to that seen in healthy adults during drowsiness,
light sleep and first stages of anaesthesia (Stewart et al 1981).
In 4 volunteers exposed acutely to 1,000-1,500 ppm dizziness for less
that 2 hours suffered mood changes, ataxia, dizziness and faintness.
Following exposure to 2,000 ppm for 7.5 minutes, subjects experienced
a sensation of impending collapse (Carpenter, 1937). Long exposures
have resulted in collapse, coma and seizures (Hake and Stewart, 1977).
Chronic low levels of tetrachloroethylene affects attention and
executive function, and mood functions thought to be mediated by the
frontal and limbic system of the brain (Echeverria et al, 1995).
Peripheral neuropathy has been described following chronic exposure
(Hathaway et al, 1991).
5.3.4 Gastrointestinal
Nausea and vomiting occur following exposure by inhalation or
ingestion (Baselt and Cravey, 1990; Torkelson, 1994).
5.3.5 Hepatic
Liver damage may result from chronic or severe acute exposure
(Hathaway et al, 1991; Reynolds, 1993; Stewart, 1969; Stewart et al,
1970).
The liver is a target organ in humans, particularly in those
accidentally exposed to high concentrations. Hepatocellular damage was
documented by biopsy in a case study of a women exposed occupationally
to tetrachloroethylene fumes (Meckler and Phelps, 1966). Liver damage
also has been diagnosed by the presence of hepatomegaly, icterus and
elevations of serum biomarkers of liver dysfunctions (Hake and
Stewart, 1977; Meckler and Phelps, 1966).
In a chronic exposure liver enlargement was still present 6 months
after cessation of exposure to tetrachloroethylene (Meckler and
Phelps, 1966).
Chronic occupational exposure has resulted in hepatitis, muscle cramps
and agitation (Baselt and Cravey, 1990).
5.3.6 Urinary
Proteinuria and haematuria has occurred following massive acute
exposure. Proteinuria lasted 20 days in a 60 year old man found lying
in a pool of tetrachloroethylene. Oliguric renal failure has occurred
from inhalation exposure from a self-service dry-cleaning machine
(Hake and Stewart, 1977).
5.3.7 Endocrine and reproductive system
A small scale study on menstral disorders in dry cleaning workers was
carried out by Zielhuis et al (1989). Although there were limitations
upon the study, the results indicated that menstral disorders
(dysmenorrhoea, unusual cycle length, menorrhagia and premenstrual
syndrome) were higher than in the control group.
Several recent case-control studies in dry cleaning workers suggest
that women have an increased risk of spontaneous abortion (Clement
International Corporation, 1993; Kyyrönen et al, 1989).
Eskenazi et al (1991) found that the sperm of male dry cleaning
workers exposed to tetrachloroethylene had more amplitude of lateral
head displacement (ALH) and less linearity in their sperm swimming
paths compared to a control group. Although their semen was considered
to be within normal limits the quality was diminished. As exposure to
tetrachloroethylene increased, men were found to have fewer narrow
sperm but more round sperm. Infertility has been reported in men with
mostly round headed sperm. These sperm lack an acrosome and are unable
to penetrate the ovum. Although proportions of round sperm are
increased and dose-related in tetrachloroethylene exposed men, these
proportions are considerably lower than those noted in a group of
infertile men.
Tetrachloroethylene may give rise to reactive intermediate metabolites
that may impair the tubero-infundibular dopaminergic system (Ferroni
et al, 1992). This mechanism may involve neuroendocrine changes
accounting for gynaecological disturbances eg oligo-menorrhoea and
reduced fertility (Zielhuis et al, 1989) and spontaneous abortion or
perinatal death (Olsen et al, 1990).
A six-week old, breast-fed infant suffered an enlarged liver and
obstructive jaundice under conditions where the mother's milk was
found to contain up to 1 mg tetrachloroethylene per 100 ml caused by
her occupational exposure (Commision of the European Communities,
1986).
Rabbits exposed to 15 mg/L, one hour daily for 15 days developed
gradual increases in the plasma and urine concentrations of
corticosteroids, adrenaline, noradrenaline and
3-methyl-1-hydroxymandelic acid. These effects lasted for 30 days
following cessation of exposure (Maxxa and Brancaccio, 1971). Similar
effects have not been reported in exposed humans.
An increase number of resorption delayed skull, ossifications,
subcutaneous oedema, and sternal malformations were found in the
offspring of rats exposed to 300 ppm tetrachloroethylene for 7 hours
as day on days 6 to 15 of pregnancy (Hathaway et al, 1991).
5.3.8 Dermatological
Tetrachloroethylene is irritant to the skin. It may cause dry, scaly
skin, blisters and dermal burns (Baselt and Cravey, 1990; Finkel et
al, 1983). Erythema and severe burning sensation may occur if
tetrachloroethylene is left on the skin for 40 minutes or longer
(Hathaway et al, 1991). Dermatitis is caused by defatting of the skin
(Torkelson, 1994).
Symptoms of coldness, stiffness, burning pain and discolouration of
hands on exposure reported following tetrachloroethylene exposure
(Rowell, 1977).
Ingestion of tetrachloroethylene was associated with the development
of toxic epidermal necrolysis (Potter, 1960).
5.3.9 Eye, ears, nose and throat
Ocular splash exposure is expected to cause lacrimation and burning,
but no permanent damage (Rowe et al, 1952; Torkelson, 1994).
The vapour is irritating to the eyes, nose and throat at high
concentrations (Ellenhorn and Barceloux, 1988; Grant and Schuman,
1993; Torkelson, 1994).
5.3.10 Haematological
A 13 month old male with sickle cell trait exhibited evidence of
intravascular haemolysis within 24 hours of ingestion and aspiration
of tetrachloroethylene (Algren and Rogers, 1992).
A father and son who were exposed to organic solvents including
tetrachloroethylene was reported to have polycythemia vera, a
proliferative disorder of bone marrow pluripotent stem cells. The son
had 22 years exposure history, including transient exposure above 300
ppm for 5 minutes out of 3 hours (Ratnoff and Gress, 1980). Because
genetic and other environmental factors may predispose a person to
develop polycythemia vera, this condition cannot be related
specifically to tetrachloroethylene exposure.
5.3.11 Immunological
No human data available.
5.3.12 Metabolic
5.3.12.1 Acid-base disturbances
No data.
5.3.12.2 Fluid and electrolyte disturbances
No data.
5.3.12.3 Other
No data available.
5.3.13 Allergic reactions
No human data available.
5.3.14 Other clinical effects
Individuals who live close to dry cleaning facilities using
tetrachloroethylene have been found to have appreciable amounts of
this agent in their exhaled breath (Finkel et al, 1983).
5.4 At risk groups
5.4.1 Elderly
The elderly with declining organ function may be at increased risk
from tetrachloroethylene exposure.
5.4.2 Pregnancy
Exposure to high concentrations of tetrachloroethylene during
pregnancy has been associated with spontaneous abortion in a case
control study of dry cleaner and laundry workers (Kyyrönen et al,
1989).
Tetrachloroethylene is excreted in breast milk and has been associated
with obstructive jaundice in breast fed new born babies (Bagnell and
Ellenberger, 1977).
5.4.3 Children
No data available.
5.4.4 Enzyme deficiencies
No data available.
5.4.5 Enzyme induced
No data available.
5.4.6 Occupations
Most exposures to tetrachloroethylene are occupational, workers most
at risk are those working in the dry cleaning and textile industries.
5.4.7 Others
No data available.
6 MANAGEMENT
6.1 Decontamination
Ingestion
Emesis is not recommended due to the risk of aspiration. Clear fluids
should be encouraged. Gastric lavage with a cuffed endo-tracheal tube,
to ensure the airway is protected as the aspiration risk is high,
should be considered. Data on humans are too limited to predict with
confidence a quantity at which gastric lavage should be carried out.
The use and efficacy of activated charcoal has not been studied
(Ellenhorn and Barceloux, 1988).
Inhalation
Following inhalation patients should be removed from the source with
care so as not to contaminate the rescuers and monitored for signs of
respiratory distress.
Dermal
Exposed skin should be flushed immediately with copious amounts of
water.
Ocular
Eyes should be irrigated for at least 15 minutes with water of normal
saline. The eye should be examined with fluorescein, an
ophthalmological referral may be necessary.
6.2 Supportive care
The most important management principles are decontamination,
monitoring the level of consciousness and respiration, ECG, renal and
liver function. Treatment is symptomatic and supportive.
An emetic must not be given due to the risk of aspiration;
sympathomimetic agents must not be given due to the risk of
sensitisation of the myocardium to catecholamines.
6.3 Monitoring
Monitor liver function, renal function and perform urinalysis for
patients with a significant exposure. Daily urinalysis for proteinuria
and haematuria may be useful after massive exposures (Torkelson,
1994).
Monitor the level of consciousness and respiratory function. Oxygen
should be administered if breathing difficulties occur, ventilate if
necessary. A chest X-ray is advised for patients with persistent
respiratory symptoms due to the risk of pulmonary oedema.
Monitoring the urinary concentrations of chlorinated metabolites of
tetrachloroethylene is of only limited use, because saturation of the
metabolic pathways occurs at air concentrations greater than 50 ppm
and there is no correlation between concentration of urinary
metabolites and exposure at higher air concentrations (Baselt and
Cravey, 1990).
6.4 Antidotes
There are no known antidotes.
6.5 Elimination techniques
Koppel et al (1985) demonstrated in a child who ingested 8-10 ml that
controlled hyperventilation enhanced pulmonary elimination of
tetrachloroethylene. Under this treatment, the clinical condition of
the patient improved considerably. Under hyperventilation the
half-life was reduced to 30 minutes and about 1% of the ingested dose
was excreted via the urine in the first three days with the bulk of
the dose being eliminated via the lungs (Koppel et al, 1985).
This has not been demonstrated elsewhere.
6.6 Investigations
Measured breath tetrachloroethylene concentrations after cessation of
exposure correlate well with the amount absorbed and with the blood
levels (Baselt and Cravey, 1990). This may also be of use in
monitoring workers with chronic exposure (Torkelson, 1994).
Blood tetrachloroethylene concentrations have generally not proved
useful if exposure is known, but may be of use for diagnosis. However,
Skender et al (1991) believes the most reliable indicator of
tetrachloroethylene appears to be in blood.
Tetrachloroethylene is radiopaque in vitro and an X-ray may be of
use in confirming ingestion.
6.7 Management controversies
Following large inhalation or oral exposure the patient must be kept
at complete bed rest, in a quiet environment, on an ECG monitor for at
least 12 hours post-exposure. The use of catecholamines (eg
adrenaline) must be avoided.
Koppel et al (1985) demonstrated that controlled hyperventilation
enhanced pulmonary elimination of tetrachloroethylene. This has not
been demonstrated elsewhere, but may be considered in cases of severe
poisoning.
7 CASE DATA
Ingestion:
1) A 13 month old black male, developed pneumonia and respiratory
failure following the ingestion and aspiration of a dry cleaning fluid
containing tetrachloroethylene. Immediately following the ingestion,
he became unconscious and had a brief generalised convulsion. Upon
arrival at hospital, he was intubated and stabilised with mechanical
ventilation. During the next 24 hours, the serum haemoglobin
concentration fell to 3.5 g/100ml, prompting further investigation to
determine the etiology of the marked decrease in haemoglobin. During
this time, the patient had not experienced any cardiovascular
instability, and his overall condition had improved. The possibility
of occult blood loss was considered but could not be substantiated. A
sickle cell screen was positive. Haemoglobin electrophoresis
subsequently demonstrated haemoglobin AS, consistent with sickle cell
trait. No further haemolysis was observed, and transfusion was not
necessary. The patient was weaned from mechanical ventilation on the
fourth day and recovered without further complications (Algren and
Rodgers, 1992).
2) A 6 year old boy drank 8-10 ml of tetrachloroethylene and one hour
later was admitted to hospital with deterioration of his conscious
state to coma. In order to prevent aspiration, the child was
intubated, and a gastric lavage with paraffin oil was performed. The
initial tetrachloroethylene blood level was 21.5 mg/ml;
hyperventilation therapy was instigated 2 hours after ingestion. The
patient received 6000 U/24 hours of heparin to prevent coagulation
with intravenous infusion therapy. Under this treatment, the clinical
condition of the patient improved considerably. Under hyperventilation
the half-life was reduced to 30 minutes and about 1% of the ingested
dose was excreted via the urine in the first three days with the bulk
of the dose being eliminated via the lungs. Hyperventilation was
terminated on day five. However, extubation was not possible because
of a marked stridor, which necessitated intubation for a further 24
hours. On the ninth day the boy was discharged with no signs of liver
or kidney damage (Koppel et al, 1985).
Inhalation:
3)A 33 year old man was found unconscious after performing work on a
plugged line in a commercial dry cleaning establishment. He had been
left alone to work on the dry-cleaning machine for approximately 20
minutes before being found. He died on the way to hospital. The blood
concentrations of tetrachloroethylene was 44 mg/L, brain tissue levels
were 360 mg/L and in the lungs 3 mg/L was detected. Tests for alcohol
and other drugs proved negative. The lack of metabolites in the urine
was consistent with the short time interval between initial exposure
and death. Absence of tetrachloroethylene in the stomach contents
eliminated ingestion as the route of absorption. The level of
tetrachloroethylene in the lungs, although low in comparison with the
blood, does not indicate the method of absorption since
tetrachloroethylene is both absorbed and excreted via the lungs.
Distribution of tetrachloroethylene was consistent with its lipophilic
properties, being highest in the brain and lowest in the lung tissue
(Lukaszewski, 1979).
4) A 24 year old white male was admitted to hospital with a six month
history of "skipping of heart beats", dizziness and headache. These
symptoms became progressively worse in the two to three months prior
to admission. There was no history of dyspnoea, angina pectoris,
diabetes, blackouts, chest pain, hypertension, Raynaud's phenomenon or
drug abuse. Seven months prior to admission the patient had begun
working in a dry cleaning facility where he was responsible for the
treatment of clothes with tetrachloroethylene. On examination he was
alert, orientated and apyrexial with an irregular pulse of 70/minute,
and a blood pressure within normal limits. On examination nothing
remarkable was found. ECG on admission demonstrated sinus rhythm and
multiple ventricular premature beats (VPB). All other findings were
normal. The VPBs on admission did not respond to lignocaine.
Continuous 24 hour ECG monitoring revealed multiple unifocal VPBs, but
on the second day after admission, without any further treatment, the
VPBs became less frequent. By the fourth day the patient was free from
headache, dizziness and VPBs. On the fifth day he was discharged with
a plasma tetrachloroethylene level of 0.15 ppm. A few days later the
patient returned to work and soon began to become symptomatic again.
Two weeks later he returned to hospital, physical examination was
normal but resting ECG revealed frequent VPB and plasma
tetrachloroethylene levels were 3.8 ppm. The patient was advised to
leave his present employment; one month after exposure stopped the
patient was free from neurological symptoms and cardiac arrhythmias
(Abedin et al, 1980).
Internally extracted data on cases
Of 14 cases of tetrachloroethylene exposure reported, 2 were
asymptomatic and all the other cases recovered within 5 days
post-exposure. Clinical effects that were reported were nausea,
vomiting, slurred speech, ataxia, drowsiness, disorientation,
confusion, euphoria, restlessness, shortness of breath, nystagmus,
hypotonia, tachypnoea and coma.
One adult aged 20 years ingested 20 ml of tetrachloroethylene.
Initially he was unconscious; he then became disorientated and
aggressive and developed oculogyric crisis and a disturbance in his
liver function. He received a gastric lavage, intravenous fluids and
acetylcysteine. The patient was well after 3 days and was discharged.
A 2“ year old boy ingested an unknown quantity of tetrachloroethylene.
He developed ataxia, vomiting, drowsiness and then became unconscious.
He had nystagmus, hypotonia and was tachypnoeic. ECG was normal and
chest X-ray showed mild shadowing. He was discharged well 2 days post-
exposure.
8 ANALYSIS
8.1 Agent/toxin/metabolite
8.2 Sample containers to be used
8.3 Optimum storage conditions
8.4 Transport of samples
8.5 Interpretation of data
The biological tolerance of tetrachloroethylene in blood 16 hours
after exposure (TVL = 50 ppm) is 6.0µmol/L (Skender et al, 1991).
Tetrachloroethylene concentrations averaged 1.2 mg/L in 26 workers
exposed to an average air concentration of 21 ppm for 30 minutes.
Blood concentrations in 6 subjects reached an average peak level of
194 ppm of vapour (Baselt and Cravey, 199o); the compound was rapidly
cleared from the blood when exposure ended and was not detectable (at
sensitivity limit of 1mg/L) after 30 minutes. Blood concentrations
were found to correlate with the atmospheric tetrachloroethylene
concentrations as well as degree of physical activity of an individual
(Monster et al, 1979).
8.6 Conversion factors
1 mg/L = 0.00289 mmol/L (blood)
1 mg/L = 147.4 ppm (air)
1 ppm = 6.78 mg/m3 at 25°C, 760 torr
8.7 Other recommendations
9 OTHER TOXICOLOGICAL DATA
9.1 Carcinogenicity
Increased incidence of hepatocellular carcinomas in mice given
tetrachloroethylene in doses of 500 to 1000 mg/kg for 78 days have
been noted (Baselt and Cravey, 1990; Ellenhorn and Barceloux, 1988;
Hathaway et al, 1991; Pegg et al, 1979). An increase in mononuclear
cell leukaemia in rats inhaling doses of 200 to 400 ppm for 2 years
has also been reported (Hathaway et al, 1991).
Two limited epidemiological studies on the mortality of individuals
with occupational tetrachloroethylene exposure in dry-cleaning and
laundering operations have indicated an increase in liver cancer
(Blair et al, 1979). However, these studies are not satisfactory for
reaching definite conclusions about the potential for
tetrachloroethylene carcinogenicity in humans (Hathaway et al, 1991).
A 1987 cohort mortality study of dry-cleaning workers with exposure to
tetrachloroethylene as well as other petroleum-based solvents detected
an increased incidence of urinary tract cancers (Brown and Kaplen,
1987).
A study in Massachusetts was carried out after tetrachloroethylene was
found to have been in the drinking water for 20 years. There seemed to
be an increase in leukaemia and bladder cancer in the individuals
exposed, which was associated with chronic exposure (Aschengrau et al,
1993).
Other cohort and proportionate mortality studies have variously
reported excesses of leukaemias, lymphosarcomas and cancer of skin,
cervix, oesphagus, kidney, colon, lung, liver and pancreas (Clement
international Corporation, 1993; Hathaway et al, 1991).
However, there have been also been a number of studies (as reviewed in
Clement International Corporation, 1993) that have demonstrated that
there is not enough human data or evidence to connect high
concentrations of tetrachloroethylene to cancer. But this chemical is
suspected as being a human carcinogen and handled as such (Hathaway et
al, 1991).
9.2 Genotoxicity
Assays of clastogenic effects in humans following occupational
exposure to tetrachloroethylene show inconsistent results. Increases
in chromosome aberrations and sister chromatid exchanges were not
detected in lymphocytes from 10 workers exposed to tetrachloroethylene
(Ikeda et al, 1980).
9.3 Mutagenicity
Tetrachloroethylene is a weak mutagen, yielding positive results in
bacterial assays, but baseline responses in mammalian systems did not
find increased sister chromatid exchanges or chromosomal aberrations
in lymphocytes of workers exposed to tetrachloroethylene (Ikeda et al,
1980).
9.4 Reprotoxicity
Pregnant rats exposed to 300 ppm tetrachloroethylene for 7 hours a
day, on days 6 through 15 of gestation had 4 to 5% reduced in body
weight and twice the number of per implantation compared with controls
(Ware, 1988).
9.5 Teratogenicity
An increased number of resorption delayed skull, ossifications,
subcutaneous oedema, and sternal malformations were found in the
offspring of rats exposed to 300 ppm tetrachloroethylene for 7 hours a
day on days 6 to 15 of pregnancy (Hathaway et al, 1991).
No reports of teratogenicity associated with tetrachloroethylene were
found in humans.
9.6 ADI
9.7 MRL
0.6 ppm (Clement International Corporation, 1993).
9.8 AOEL
9.9 TLV
50 ppm (COSHH, 1995; Ferroni et al, 1992).
9.10 Relevant animal data
Experimental rats were unconscious in minutes following exposure to
concentrations of 6,000 ppm or more, several hours at 3,000 ppm but
not at 2,000 ppm (Rowe et al, 1952).
In rats exposed via inhalation, tetrachloroethylene levels rise more
or less continuously with duration of exposure in brain, lungs, and
fat, but they tend to level off in blood and liver after a 3 hour
exposure. Brain cerebrum concentrations of tetrachloroethylene exceed
blood levels by about four-fold and brain cerebellum levels by
three-fold, independent of the duration of exposure (Savolainen et al,
1977).
Rats were exposed to tetrachloroethylene vapour levels of 70, 230 and
470 ppm for 7 months. Occasionally the rats were exposed to higher
concentrations (averaging 7,000 ppm) and became slightly ataxic which
disappeared within a few minutes post-exposure. It is thought that
they developed tolerance to high concentrations. All concentrations
above 2,750 ppm produce anaesthesia during acute exposure. However,
after 6 exposures to concentrations of 2,750 ppm it was found that the
rats did not become anaethetised even above a concentration of 10,000
ppm (Carpenter, 1937).
When fed to laboratory mice, an LD50 of 8850 mg/kg was determined.
Dogs and cats have survived doses of 4000 mg/kg and rabbits 5000
mg/kg. However, dogs were killed by intravenous doses of 85 mg/kg; the
few that received 75 mg/kg or less survived (Gehring et al, 1991).
Single oral doses of [36Cl] tetrachloroethylene were absorbed
completely when administered to rats at 189 mg/kg (Daniel, 1963), as
were doses of [14C] tetrachloroethylene dissolved in corn oil
administered to mice at 500 mg/L (Schumann et al, 1980).
Several mutagenicity studies have been performed on
tetrachloroethylene which employ the Ames Salmonella/microsomes test
or modifications of this test. Most tests reveal little or no evidence
of mutagenic activity, except at concentrations that resulted in
greater than 90% bacterial toxicity (Ware, 1988).
9.11 Relevant in vitro data
No data
10 ENVIRONMENTAL DATA
10.1 Ecotoxicological data
Solubility in water
Municipal drinking-water in the UK contains an average of 1.3 mg/L of
tetrachloroethylene and the total daily food intake is about 160 mg
per day (WHO, 1984).
WHO drinking water guidance level based on a carcinogenic endpoint in
10µ/L (Clement International Corporation, 1993).
In ground water where volatilisation does not occur,
tetrachloroethylene remains for months or years.
In 1988, in the US, it was estimasted that 23,000 pounds of
tetrachloroethylene was released to water from manufacturing and
processing facilities.
Volatilisation
Volatilisation seems to be the major way in which tetrachloroethylene
is lost from water.
Other
Tetrachloroethylene is ubiquitous in air, with levels in the ppt to
ppb range.
Tetrachloroethylene has been detected in dairy products (milk, cheese
and butter) at 0.3-13 µg/kg, meat at 0.9-1.0 µg/kg, oils and fats at
0.01-7 µg/kg, beverages at 2-3 µg/kg, fruits and vegetables at 0.7-2
µg/kg and fresh bread at 1 µg/kg (Clement International Corporation,
1993).
The log octanol/water partition coefficient is 2.86.
10.2 Behaviour
Adsorption onto soil
Contamination of soil can occur via leachate from landfill sites. It
is very mobile in soil and readily migrates to ground water.
10.3 Biodegradation
Environmental fate
About 85% of tetrachloroethylene used annually in the USA is lost to
the atmosphere, and the world-wide emission of tetrachloroethylene has
been estimated to be about 450 kilotonnes per year (WHO, 1984). In the
United Kingdom, estimates for air samples range from 1-9 ppt from over
the Atlantic Ocean near Lands End, 8-57 ppt on Exmoor, and 15-40 ppb
at a Northern England industrial area (Commision of the European
Communities, 1986).
Atmospheric emissions occur from metal degreasing uses, production of
fluorocarbons and other chemicals, textile industry uses, and
miscellaneous solvent-associated applications. Annual mean levels of 6
ppb and 10 ppb were detected downwind of a chemical laundry and a
rubber factory, respectively, in Hamburg, Germany (Bruckmann et al,
1987). Emissions also occur at landfill sites containing the chemical.
Levels of 0.7 ppb and 0.9 ppb were detected 1.5 and 0.5 metres above
landfill soil near the city of Bielefeld, Germany (Clement
International Corporation, 1993).
In 1988 it was estimated that a total of 32.3 million pounds of
tetrachloroethylene was released to the air from manufacturing and
processing facilities in the US (Clement International Corporation,
1993).
Releases of tetrachloroethylene to surface water appear to be minor in
comparison to atmospheric releases (Clement International Corporation,
1993). Release to water through aqueous waste account for 1% or less
of the total releases of tetrachloroethylene to the environment
(Clement International Corporation, 1993). Aeration processes at waste
treatment facilities strip much of the tetrachloroethylene from the
water and release it into the atmosphere as a result of the high
volatility of this chemical.
There are many processes of recycling tetrachloroethylene, which
generate tetrachloroethylene-containing sludges and dirty filters that
have been landfilled in the past. Contamination of soil can occur
through leaching of tetrachloroethylene from these disposal sites. In
1988, 106,000 pounds of tetrachloroethylene was thought to be released
to land from manufacturing and processing facilites in the US (Clement
International Corporation, 1993).
Aerobic/anaerobic
Tetrachloroethylene can be transformed by reduction dehalogenation to
trichloroethylene, dichloroethylene and vinyl chloride under anaerobic
conditions. It has also been suggested that there is a potential that
tetrachloroethylene completely mineralises to carbon monoxide in soil
and aquifer systems and in biological treatment processes (Vogel and
McCarty, 1985).
Microbial
Photolysis
Benignus et al (1985) (as cited in Commission of the European
Commmunities, 1986) state that tetrachloroethylene undergoes
photochemical degredation in the troposphere. Trichloroacetyl chloride
is described as a major degredation product and phosgene a lesser one.
tetrachloroethylene exists in the troposphere for one year or less.
Hydrolysis
Tetrachloroethylene in the atmosphere is hydrolysed to trichloroacetic
acid and then decomposes to carbon dioxide and chloride ions (Pearson
and McConnell, 1975).
Half-life in water, soil and vegetation
Zoeteman et al (1980) estimated the half-life of tetrachloroethylene
to be 3-30 days for river water and 30-300 days for lake- and ground-
water.
10.4 Environmentally important metabolites
Tetrachloroethylene in the atmosphere is hydrolysed to trichloroacetic
acid and then decomposes to carbon dioxide and chloride ions (Pearson
and McConnell, 1975). Under certain conditions, tetrachloroethylene in
ground water has been reported to degrade to and then to
dichloroethylene and vinyl chloride.
10.5 Hazard warnings
10.5.1 Aquatic life
Concentrations of tetrachloroethylene detected in fish in the Irish
Sea ranged from below detection limits to 43 ng/g (dry weight), which
was only 2-25 times greater thatn levels found in seawater. Levels of
0.3-43 µg/g (wet weight) were found in 15 species of fish collected
off the coast of Great Britain (Clement International Corporation,
1993).
10.5.2 Bees
10.5.3 Birds
10.5.4 Mammals
10.5.5 Plants
10.5.6 Protected species
10.6 Waste disposal data
One method of disposal involves absorption by vermiculite, dry sand,
earth, or a similar material and then burial in a secured sanitary
landfill. A second method involves incineration after mixing with
another combustible fuel. With the latter method, combustion must be
complete to prevent the formation of phosgene, and an acid scrubber
must be used to remove the haloacids produced (Clement International
Corporation, 1993).
Author
Henrietta Wheeler
National Poisons Information Service (London Centre)
Medical Toxicology Unit
Guy's & St Thomas' Hospital Trust
Avonley Road
London
SE14 5ER
UK
This monograph was produced by the staff of the London Centre of the
National Poisons Information Service in the United Kingdom. The work
was commissioned and funded by the UK Departments of Health, and was
designed as a source of detailed information for use by poisons
information centres.
Peer review was undertaken by the Directors of the UK National Poisons
Information Service.
March 1996
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