INFORMATION REGARDING TRICHLOROETHYLENE
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~WTAIw6:1
TRICHLOROETHYLENE
CASRN: 79-01-6
Human Health Effects:
Evidence for Carcinogenicity:
There is limited evidence in humans for the
carcinogenicity of trichloroethylene. There is
sufficient evidence in experimental animals for the carcinogenicity of trichloroethylene.
OVERALL EVALUATION: Trichloroethylene is probably
carcinogenic to humans Group 2A. In making the overall evaluation, the working
group considered the following evidence: (1) Although the hypothesis linking the
formation of mouse liver tumors with peroxisome proliferation is plausible, trichloroethylene
also induced tumors at other sites in mice and rats.
A5. A5= Not suspected as a human carcinogen.
(1993) ... The substance has been demonstrated by well-controlled
epidemiological studies not to be associated with any increased risk of cancer
in exposed humans.
Human Toxicity Excerpts:
IN ACUTE INHALATION EXPOSURES RAPID COMA MAY
ENSUE WITH EVENTUAL DEATH FROM HEPATIC OR RENAL FAILURE. AN OCCASIONAL SUDDEN
DEATH SUGGESTS VENTRICULAR FIBRILLATION. SEQUELAE, WHICH MAY BE MORE COMMON
AFTER INHALATION THAN AFTER INGESTION, INCLUDE LIVER AND KIDNEY LESIONS,
REVERSIBLE TRIGEMINAL (OR OTHER NERVE) DEGENERATION AND PSYCHIC DISTURBANCES.
... Workers exposed @ concn avg about 10 ppm
... complained of headache, dizziness and sleepiness. ... An epidemiology study
on the hepatic tumor incidence in subjects working with trichloroethylene
... failed to show a correlation between liver /cancer/ and occupational
exposure. ... Another ... study looked at the mortality of 2117 workers exposed
to trichloroethylene ... found no correlation between
cancer and occupational exposure.
Trichloroethylene is
only mildly irritating to the skin if allowed to evaporate. From continued use
of the material in contact with the skin, defatting can take place.
Fatal hepatic failure has been observed
following the use of trichloroethylene as an
anesthetic. This effect has occurred in patients with complicating conditions
such as malnutrition, toxemias, burns, or those who have received transfusions.
Prolonged occupational exposure to trichloroethylene
has been associated with impairment of peripheral nervous system function,
persistent neuritis and temporary loss of tactile sense and paralysis of the
fingers after direct contact with the solvent.
A case of severe liver necrosis following a
prolonged (4-1/2 hour) use of trichloroethylene as an
anesthetic has been reported.
Following chronic and acute overexposure to trichloroethylene
during operation of a dry cleaning unit, symptoms included symmetrical bilateral
VIIIth cranial nerve deafness as well as cerebral cortical dysrhythmia and
alterations in the electroencephalogram. The patient recovered after the
exposure stopped.
Acute overexposure to trichloroethylene
resulted in chronic involvement of the bulbar cranial nerves and esophageal and
pharyngeal motility impairment.
Autopsy findings in a 16 yr old boy who died
while sniffing plastic cement containing TCE indicated severe heart failure. ...
Liver failure is not the usual cause of death among solvent sniffers, but liver
biopsies often reveal toxic centrilobular necrosis.
The behavioral effects of exposure to trichloroethylene
/indicate that/ laboratory /and work-place/ exposure to 540 or 1080 mg/cu m for
70 min, has no effect on reaction time or short-term memory.
Chromosome analyses of cultured lymphocytes
from 28 workers aged 23-67 who had been employed on degreasing unit using trichloroethylene
for 1-21 years showed high rates of hypodiploid cells (9 of 28).
Evoked trigeminal potentials were studied in
104 subjects occupationally exposed to trichloroethylene.
Subjects had an average exposure time of 8.23 yr and an average daily exposure
of 7 hr (exposure levels were not given). Controls were 52 healthy nonexposed
subjects. Symptoms suffered by 49 of the exposed subjects included dizziness,
headache, asthenia, insommnia, mood perturbation, and sexual problems. Eighteen
subjects had trigeminal nerve symptoms. These subjects were significantly older
(p< 0.001) than asymptomatic subjects. Forty subjects had a pathological
trigeminal somatosensory evoked potential. Of these, 28 had a normal trigeminal
examination and 12 an abnormal one. For those with trigeminal symptoms, an
abnormal trigeminal somatosensory evoked potential was observed in subjects who
had the longest and most intense exposure periods.
Estimated human lifetime carcinogenic risk:
3.77X10-7 for male and 6.84X10-8 for female /From table, assuming a daily
consumption of 1 liter of water containing trichloroethylene
in a concn of 1 ug/l/
... Eye irritation: 160 ppm; supportable
during 30 min: 379-372 ppm; full /SRP: CNS depression/: 2,500-6,000 ppm; severe
toxic effects: 2,000 ppm= 10,940 mg/cu m, 60 min; symptoms of illness: 800 ppm=
4,376 mg/cu m; unsatisfactory /exposure level/: > 400 ppm= 2,188 mg/cu m
... The estimated fatal oral dose in humans is
3-5 ml/kg. The lowest concn produce unconsciousness in adult humans is 16 mg/l
(3,000 ppm); the equivalent oral dose is 40-150 ml.
77 of 104 trichloroethylene
workers showed abnormal electrocardiographic tracings, which may precede
permanent heart damage.
Adverse psychological and behavioral
abnormalities have been reported in industrial overexposures and include
symptoms of headache, fatigue, lightheadedness, depression, insomnia,
irritability, and confusion. Cranial and peripheral neuropathies have been
associated with industrial and medical use. Selective trigeminal neuralgia has
been diagnosed in one study in 20% of trichloroethylene
workers by demonstrating electrophysiological abnormalities.
Skin: defatting action /of trichloroethylene/
can cause dermatitis.
In anesthetic concn, trichloroethylene
causes little or no irritation to the respiratory tract. Trichloroethylene
causes increased respiratory rate (tachypnea) but decreased alveolar ventilatory
amplitude, which is associated with decreased blood oxygen tension and increased
carbon dioxide tension.
... In almost all cases where a xenobiotic /incl
trichloroethylene/ has a terminal carbon with two
halides attached, side-chain oxidation mediated by cytochrome p450 will produce
a toxic, reactive intermediate.
Eight men inhaled trichloroethylene
at concentrations of 0, 100, 300, and 1000 ppm for 2 hr. Each man received the
different concentrations in random order. Five tests of visualmotor performance
were administered to each volunteer three times during each 2 hr session, and
one additional test was administered immediately before and immediately after
exposure. At a concentration of 1000 ppm, the compound adversely affected
performance in tests of depth perception, steadiness, and manual skill but had
no statistically significant effect on performance in three other standard
tests. The small increase in errors associated with 100 and 300 ppm were not
statistically significant.
Six naive volunteers were exposed to trichloroethylene
aerosol and vapor for 8 hr in one day (two 4 hr exposures separated by a 1.5 hr
interval); the concentration varied from 90 to 130 ppm. A slight sense of
dizziness and transient eye irritation occurred during maximal fractuations in
concentration. Although there was no objective disturbance of motor function,
coordination, equilibrium, or behavior, there was a statistically significant
decrement in performance of standard tests of perception, memory, complex
reaction time, and manual dexterity. Similar results were obtained when the
study was repeated with six workers who were accustomed to the odor of the
compound.
Three volunteers each placed one thumb in trichloroethylene
for 30 min. They experienced a burning sensation on the dorsum of their thumbs
within 3-18 min, and this burning became moderately severe within 5 min after
onset in two persons but remained mild in one. The pain became more intense for
several minutes just after the thumbs were removed from the solvent, and
tingling persisted for 30 min. Erythema subsided within 2 hr. The compound was
measurable in the breath of some volunteers within 10 min after exposure started
and in all within 20 min. The mean peak breath concentration was 0.5 ppm.
Vapors of trichloroethylene
are only slightly irritating to the respiratory tract. Premedication with
atropine or scopolamine hydrobromide is recommended to eliminate possible mucus
secretions. The anesthetic typically accelerates respiratory rate. As the
tachypnea progresses, respiratory activity becomes more rapid and shallower.
Sudden bursts of tachypnea are sometimes associated directly with surgical
stimulation.
A retrospective cohort study of 14,457 workers
at an aircraft maintenance facility was undertaken to evaluate mortality
associated with exposures in their workplace. The purpose was to determine
whether working with solvents, particularly trichloroethylene,
posed any excess risk of mortality. The study group consisted of all civilian
employees who worked for at least one year at Hill Air Force Base, Utah, between
1 January 1952 and 31 December 1956. Work histories were obtained from /official
records/ ... and the cohort was followed up for ascertainment of vital state
until 31 December 1982. Observed deaths among white people were compared with
the expected numbers of deaths, based on the Utah white population, and adjusted
for age, sex and calendar period. Significant deficits occurred for mortality
from all causes (SMR 92, 95% CI 90-95), all malignant neoplasms (SMR 90, CI
83-97), ischemic heart disease (SMR 93, 95% CI 88-98), nonmalignant respiratory
disease (SMR 87, 95% CI 76-98) and accidents (SMR 61, 95% CI 52-70). Mortality
was raised for multiple myeloma in white women (SMR 236, 95% CI 87-514),
non-Hodgkin's lymphoma in white women (SMR 212, 95% CI 102-390), and cancer of
the biliary passages and liver of white men dying after 1980 (SMR 358, 95% CI
116-836). Detailed analysis of 6929 employees occupationally exposed to trichloroethylene,
the most widely used solvent at the base during the 1950s and 1960s, did not
show any significant or persuasive association between several measures of
exposure to trichloroethylene and any excess of cancer.
Women employed in departments in which fabric cleaning and parachute repair
operations were performed had more deaths than expected from multiple myeloma
and non-Hodgkin's lymphoma. The inconsistent mortality patterns by sex, multiple
and overlapping exposures, and small numbers made it difficult to ascribe these
excesses to any particular substance. ...
Human subjects with high repeated, but
non-occupational, exposure may exhibit toxic effects on the liver (e.g.,
elevated aspartate & alanine aminotransferase), renal insufficiency, &
abnormal EEG patterns.
Acute effects on the CNS are characterized by
two sequential phases (i.e., excitation & depression), & are usually
reversible. ... In the early phase of excitation, euphoria & inebriation are
present. The subsequent phase of CNS depression is characterized by various
degrees of narcosis culminating in coma. Muscular hypotomy, muscular spasms,
reduced tendon reflexes, & loss of coordination may occur.
Childhood leukemia in a community in
Massachusetts, USA, where water from two wells was contaminated with trichloroethylene
/was studied/. Measurements made in 1979 showed a concentration of 267 ppb (ug/l)
trichloroethylene in the well water. Twenty cases of
childhood leukemia were diagnosed in the community in 1964-83, and these were
associated with a significantly higher estimated cumulative exposure to water
from the two contaminated wells than a random sample of children from the
community (observed cumulative exposure, 21.1; expected cumulative exposure,
10.6; p= 0.03).
A study conducted in New Jersey, USA, during
1979-87 included 75 towns, of which 27 were included in a /previous/ study. Trichloroethylene
concentrations were measured during 1984-85, and an average level was assigned
to each town. The highest level assigned was 67 ug/l. The water supply of six
towns contained > 5 ug/l trichloroethylene (average,
23.4 ug/l). Women in these towns had a significantly higher total incidence of
leukemia than the inhabitants of towns were the concentration of trichloroethylene
in drinking water was < 0.1 ug/l (relative risk, 1.4; 95% CI, 1.1-1.9); no
such effect was seen for men (1.1, 0.84-1.4). The risk among women was
particularly elevated for acute lymphocytic leukemia, chronic lymphocytic
leukemia in childhood was also significantly increased, in girls but not in
boys. Increased risks for non-Hodgkin's lymphoma were apparent in towns in the
highest category of trichloroethylene contamination
(0.2; 0.94-1.5 for men and 1.4; 1.1-1.7 for women) and was particularly elevated
for high-grade lymphomas.
Trichloroethylene
(Tri) caused modest cytotoxicity in freshly isolated human proximal tubular (hPT)
cells, as assessed by significant decreases in lactate dehydrogenase (LDH)
activity after 1 hr of exposure to 500 muM Tri. Oxidative metabolism of Tri by
cytochrome p450 to form chloral hydrate (CH) was only detectable in kidney
microsomes from one patient out of four tested & was not detected in hPT
cells. In contrast, GSH conjugation of Tri was detected in cells from every
patient tested. The kinetics of Tri metab to its GSH conjugate
S-(1,2-dichlorovinyl)glutathione (DCVG) followed biphasic kinetics, with
apparent Km & Vmax values of 0.51 & 24.9 mM & 0.10 & 1.0 nmol/min/mg
protein, respectively. S-(1,2-dichlorovinyl)-L-cysteine (DCVC), the cysteine
conjugate metabolite of Tri that is considered the penultimate nephrotoxic
species, caused both time- & concn-dependent increases in LDH release in
freshly isolated hPT cells. Preincubation of hPT cells with 0.1 mM
aminooxyacetic acid did not protect hPT cells from DCVC-induced cellular injury,
suggesting that another enzyme besides the cysteine conjugate beta-lyase may be
important in DCVC bioactivation. ... These data indicate that the pathway
involved in the cytotoxicity & metab of Tri in hPT cells is the GSH
conjugation pathway & that the cytochrome p450-dependent pathway has little
direct role in renal Tri metabolism in humans.
Trichloroethylene (TCE)
is both acutely toxic & carcinogenic to the mouse lung following exposure by
inhalation. In contrast, it is not carcinogenic in the rat lung & is
markedly less toxic following acute exposure. Toxicity to the mouse lung is
confined almost exclusively to the nonciliated Clara cell & is characterized
by vacuolation & incr in cell replication. Chloral, a metabolite of TCE that
accumulates in Clara cells and has been shown to be the cause of the toxicity,
also causes aneuploidy in some test systems. Cytotoxicity, increased cell
division, & aneuploidy are known risk factors in the development of cancer
& provide a plausible mode of action for TCE as a mouse lung carcinogen. All
acute & chronic effects of TCE on the mouse lung are believed to be a direct
consequence of high cytochrome P450 activity & impaired metab of chloral in
Clara cells. Comparisons between species suggest that the ability of the human
lung to metabolize TCE is approx 600-fold < that in the mouse. In addtn, the
human lung differs markedly from the mouse lung in the number & morphology
of its Clara cells. Thus, the large quantitative differences between the
metabolic capacity of the mouse lung & the human lung, together with the
species differences in the number & morphology of lung Clara cells, suggest
that the risks to humans are minimal & that other tumor sites should take
precedent over the lung when assessing the potential risks to humans exposed to
TCE.
An ecological epidemiological study was
conducted with data obtained from an environmental dose-reconstruction study
& the Arizona Birth Information Tapes. Before 1981, a portion of the city of
Tucson water-distribution system was contaminated with trichloroethylene
(i.e., <5 ug/l of water to 107 ug/l of water). Target & comparison
populations were selected with a Geographic Information System.
Logistical-regression analysis revealed an association between maternal exposure
to trichloroethylene via drinking water &
very-low-birth-weight babies (i.e., < 1,501 grams) (odds ratio = 3.3; 95%
confidence interval = 0.5, 20.6; & Wald chi-square p value = 0.2). No
association was found between maternal exposure to trichloroethylene
via drinking water & low birth weight or full-term low-birth-weight infants
(gestational period > 35 wk & <46 wk).
... Changes in EKG waves have been observed
among persons with exposure to trichloroethylene.
Human Toxicity Values:
Estimated fatal oral dose 3 to 5 mg/kg
Skin, Eye and Respiratory Irritations:
Exposure to trichloroethylene
vapor may cause irritation of the eyes, nose, and throat.
Liquid: irritating to skin and eyes.
Drug Warnings:
TRICHLOROETHYLENE HAS
BEEN REPORTED TO CAUSE CONVULSIONS IN CHILDREN; THEREFORE, IT SHOULD NOT BE USED
IN PATIENTS WITH CONVULSIVE DISORDERS.
Patients exposed to trichloroethylene
should be warned of the potential adverse effects of ethanol ingestion.
Isopropanol and acetone ... cause enhanced
hepatotoxicity with ... trichloroethylene.
...Its anesthetic action is weak. Its low
volatility appears in part to be responsible for this effect. ... Apparatus that
employs bubbling oxygen assists in accelarating the volatility of the anesthetic
to increase its potency. Because of its inherent weakness as an anesthetic,
induction of anesthesia is slow. Cardiac arrhythmias produced by the anesthetic
are unfavorable. Trichloroethylene cannot be used in a
closed circuit with soda lime because of formation of a toxic product.
Relaxation of abdominal musculature is poor
during trichloroethylene anesthesia.This effect is
similar to other agents (eg, ketamine, alpha-chloralose) that do not induce
Stage III anesthesia. Trichloroethylene is considered
unsatisfactory for this type of surgery unless it is used in conjunction with a
skeletal muscle relaxant. It has very little if any effect upon uterine
function. It readly crosses the placenta to reach the fetal circulation of
sheep, goats, and probably other species.
Medical Surveillance:
Preplacement and periodic exam should incl the
skin, resp, cardiac, central, and peripheral nervous systems, as well as liver
and kidney function. Alcohol intake should be evaluated.
Effective medical supervision requires an
adequate assessment of the level of exposure. This should be achieved by
environmental monitoring ... as well as by biological monitoring.
/Protect/ from exposure those individuals with
diseases of central nervous system, lung, liver, and kidneys.
PRECAUTIONS FOR "CARCINOGENS":
Whenever medical surveillance is indicated, in particular when exposure to a
carcinogen has occurred, ad hoc decisions should be taken concerning ... /cytogenetic
and/or other/ tests that might become useful or mandatory. /Chemical
Carcinogens/
... Changes in EKG waves have been observed
among persons with exposure to trichloroethylene.
The assessment of trichloroethylene
exposure can be accomplished through measurement of either trichloroethylene
or the metabolite, trichloroethanol. The most reliable biological monitoring
test appears to be measurement of trichloroethanol, which has been found to
correlate with exposure levels. ... Whole Blood Reference Ranges: Normal - none
detected (trichloroethylene, trichloroethanol); Exposed
- BEI (sampling time is end of shift at end of workweek, measured as free
trichloroethanol) 4.0 mg/l, BAT (sampling time is end of exposure or end of
shift, or for long-term exposure sampling time is after several shifts: both
measured as the metabolite, trichloroethanol) 5 mg/l; Toxic - levels greater
than 1500 ug/l have been associated with onset of coma.
The assessment of trichloroethylene
exposure can be accomplished through measurement of either trichloroacetic acid
or trichloroethanol. These levels have been found to correlate well with
exposure levels. ... Urine Reference Ranges: Normal - none detected (trichloroacetic
acid or trichloroethanol); Exposed - BEI (sampling time is end of workweek,
measured as the metabolite, trichloroacetic acid) 100 mg/g creatinine, BEI
(sampling time is end of workweek, measured as the metabolites trichloroacetic
acid and trichloroethanol) 300 mg/g creatinine, BAT (sampling time is end of
exposure or end of shift, or for long-term exposures sampling time is after
several shifts: both measured as the metabolite, trichloroacetic acid) 100 mg/l;
Toxic - not established.
Liver Function Tests: ... Biochemical tests -
Enzymes that reflect cholestasis: alkaline phosphatase (AP), 5'-nucleotidase
(5'-NT) /and/ leucine aminopeptidase (LAP); ... Enzymes that detect direct
hepatic damage: aspartate aminotransferase (AST) /and/ alanine aminotransferase
(ALT). ... Clearance tests - indocyanine green ... antipyrine test ... /and/
serum bile acids.
Probable Routes of Human Exposure:
TRICHLOROETHYLENE
WHEN PRESENT IN AIR NEAR OPEN ARC WELDING MAY BE DECOMP TO LEVELS OF PHOSGENE
DANGEROUS TO HEALTH, WHEREAS THE HCL AND CL2 FORMED SIMULTANEOUSLY MAY NOT
ALWAYS PROVIDE AN ADEQUATE WARNING AGAINST THE PRESENCE OF PHOSGENE.
Many industrial workers, operating room
personnel and dentists are regularly exposed to TCE, some to large doses. The
general public encounters trichloroethylene in cleaning
fluids, some decaffeinated coffees and spice extracts.
NIOSH (NOES Survey 1981-1983) has
statistically estimated that 392,805 workers (169,851 of these are female) are
potentially exposed to trichloroethylene in the US(1).
Occupational exposure to trichloroethylene may occur
through inhalation and dermal contact with this compound at workplaces where trichloroethylene
is produced or used(SRC). Extensive monitoring data indicate that the general
population may be exposed to trichloroethylene via
inhalation of ambient air, ingestion of food and drinking water, and dermal
contact with this compound and other products containing trichloroethylene(SRC).
An open-top and an enclosed conveyor-loaded
production trichloroethylene vapor degreasers had
average emission factors of 2.6 g TCE/min and 0.67 g TCE/min, respectively(1).
Waste gases from aluminum plasma-etching processes (using chlorine containing
etchants) during semiconductor production contained trichloroethylene
at an average concn of 315.70 ng /l(2). The number of US workers exposed to TCE
is estimated to be 283,000(3). Operating room levels range from 0.3-103 ppm,
with an estimated 5000 medical, dental and hospital personnel being routinely
exposed(1). Air levels at a dial assembly workshop in Japan measured 25-100 ppm;
degreasing room levels, 150-250 ppm(3). Trichloroethylene
was detected in 6% of 7705 solvent air samples reported from different
industries in Norway and stored in the EXPO occupational exposure database(4).
23-41% of trichloroethylene
in feed water to showers was lost with a water temperature of 23 to 40 deg C(1).
Trichloroethylene was detected in chlorinated swimming
pool water from a pool in Gdansk, Poland at concns of not detected (detection
limit, on average, 0.01 ug/cu dm) to 13.3 ug/cu dm for 4 different dates in
1991(2).
Body Burden:
Therapeutic or normal blood level 0.1-9 mg%
PERSONAL AIR: The exhaled breath of 73% of 26
smokers and 81% of 43 nonsmokers contained trichloroethylene
at unreported concns(1). Breath of 12.5% of 50 individuals living in the Los
Angeles area contained trichloroethylene(2). 51.2% of
personal air samples collected from these 50 individuals contained trichloroethylene(2).
Increased personal air exposures were reported following solvent use, household
cleaning, furniture stripping, visiting a dry cleaning shop, photo developing
and using paint remover of up to 220 ug/cu m from a baseline of <2 ug/cu
m(3). Personal air samples of Los Angeles and Contra Costa residents contained trichloroethylene
at concns of 7.8 (n=110, Los Angeles residents, February 1984), 6.4(n=50, Los
Angeles residents, May 1984) and 3.8 (n=67, Contra Costa residents, June
1984)(4).
Blood samples from 179 of 277 people from the
general population contained trichloroethylene at a
mean concn of 458 ng/l; a mean blood concn of 763 ng/l was reported from 63 of
113 urban workers as compared to 180 ng/l from 82 of 127 workers(1). Blood
samples collected from workers exposed to trichloroethylene
in 4 dry-cleaning shops (air concns ranged from 25-40 ppm) contained this
compound (median=3.39 umol /l after work (range=0.46-12.71), 0.38 umol /l before
work (range=0.15-3.58)(2). Urine samples from the same workers contained the trichloroethylene
metabolite, trichloroethanol (median=54.89 umol/mol creatinine,
range=5.30-177.67 after work; median=9.70 umol/mol creatinine, range=0.38-35.65
before work)(2). Kidney (n=9), lung (n=13), and muscle (n=16) tissues collected
from humans in Turku, Finland in 1987 contained trichloroethylene
at 0.7, 0.02, and 0.2 ug/kg, respectively(3). 20% of composite adipose tissue
samples collected in FY82 (n=46 composite samples) contained trichloroethylene(4).
Breathing air samples from 30 residents of Tokyo, Japan had a mean concn of 2.0
ug/cu m trichloroethylene with a calculated daily
intake due to breathing ambient air of 40 ug/person (men 24.9 ug/person; women
51.5 ug/person)(5). Breath samples of Los Angeles and Contra Costa residents
contained trichloroethylene at concns of 1.6 (n=110,
Los Angeles residents, February 1984), 1.0 (n=50, Los Angeles residents, May
1984) and 0.6 (n=67, Contra Costa residents, June 1984)(6).
Trichloroethylene was
detected in mother's milk samples from 4 US urban areas, with 8 of 8 samples
testing pos(1). Concns in post-mortem wet tissue samples were 1-32 ppb(2).
Breath samples Love Canal residents, Niagara Falls, NY contained a trace of trichloroethylene
with 4 of 9 samples pos; blood - 0.09.50 ppb, 6 of 9 samples pos; and urine -
40-550 parts/trillion, 9 of 9 samples pos(3). Concns in whole blood specimens
from 250 subjects ranged from not detected to 1.5 ppb, with a 0.4 ppb avg(4).
Trichloroethylene was
detected in the blood of 13 of 677 samples taken from non-occupationally exposed
Americans (detection limit= 0.010 ppb(1). Trichloroethylene
was measured in blood samples collected from 79 humans at concns ranging from
<0.015 to 0.090 ug/l(2). Exhaled breath from humans following both inhalation
and dermal exposures during showering or dermal exposure following bathing using
normal tap water contained trichloroethylene at concns
up to 0.32 ug/cu m/ug/l(3).
Animal Toxicity Studies:
Evidence for Carcinogenicity:
There is limited evidence in humans for the
carcinogenicity of trichloroethylene. There is
sufficient evidence in experimental animals for the carcinogenicity of trichloroethylene.
OVERALL EVALUATION: Trichloroethylene is probably
carcinogenic to humans Group 2A. In making the overall evaluation, the working
group considered the following evidence: (1) Although the hypothesis linking the
formation of mouse liver tumors with peroxisome proliferation is plausible, trichloroethylene
also induced tumors at other sites in mice and rats.
A5. A5= Not suspected as a human carcinogen.
(1993) ... The substance has been demonstrated by well-controlled
epidemiological studies not to be associated with any increased risk of cancer
in exposed humans.
Non-Human Toxicity Excerpts:
MUTAGENICITY: MUTATION RESEARCH 86: 355
(1981). MOUSE IN VIVO SOMATIC MUTATION ASSAY (SPOT TEST) - COAT COLOR MUTANTS:
POSITIVE.
... REPORTED SYMPTOMS OF CHRONIC INTOXICATION
IN DOGS IN 3-8 WEEKS AFTER INHALATION OF 500 TO 750 PPM FOR 4-8 HOURS DAILY, 5-6
DAYS PER WEEK. THE SYMPTOMS CONSISTED OF LETHARGY, ANOREXIA, NAUSEA, VOMITING
AND LOSS OF WEIGHT. LIVER DYSFUNCTION WAS ALSO SHOWN IN THESE DOGS.
... REPEATED EXPOSURE TO 3000 PPM (27
EXPOSURES DURING 36 DAYS) ... CAUSED DISTURBANCES OF EQUILIBRIUM AND
COORDINATION ... AFTER ... 1ST WEEK SALIVATION, RESTLESSNESS AND
HYPEREXCITABILITY, THEY RECOVERED ... ONLY HISTOLOGICAL ABNORMALITY ... FAT
VACUOLES IN ... LIVER OF FEMALE RATS.
WHEN SOYA-BEAN MEAL IS EXTRACTED WITH TRICHLOROETHYLENE
IT WAS TOXIC TO CATTLE ... THE SYNDROME IN CATTLE IS KNOWN VARIOUSLY AS STOCKMAN
DISEASE, DUREN DISEASE AND BARBANT DISEASE.
CATS AND GUINEA PIGS EXPOSED TO 1000 PPM DAILY
FOR 1 1/2 HR ... FROM 10 DAYS TO 10 MONTHS ... IN THOSE WHICH SURVIVED SEVERAL
MONTHS, CIRRHOSIS AND BILIARY HYPERPLASIA ... LATTER PROGRESSING IN SOME ANIMALS
TO PROLIFERATIVE 'BILIARY ADENOMATOSIS'.
GASTRIC INTUBATION OF 2.4 OR 1.2 G/KG BODY WT TRICHLOROETHYLENE
5 TIMES WEEKLY IN MALE B6C3F1 MICE (AGE NOT SPECIFIED) & OF 1.8 OR 0.9 G/KG
BODY WT IN FEMALES INDUCED HEPATOCELLULAR CARCINOMAS IN 30/98 MICE GIVEN LOW
DOSE & IN 41/95 (43.2%) MICE GIVEN HIGHER DOSE. HEPATOCELLULAR CARCINOMAS
... IN 1/40 (2.5%) CONTROL MICE.
FEMALE RATS EXPOSED TO VAPORS OF 200 TO 1800
PPM FOR 2 WK SHOWED NO EFFECTS INDICATIVE OF TREATMENT-RELATED MATERNAL
TOXICITY, EMBRYOTOXICITY, ... TERATOGENICITY OR BEHAVIORAL DEFECTS. ... /SRP:
EVIDENCE OF DEVELOPMENTAL DELAY WAS SEEN/.
PURE TRICHLOROETHYLENE
STABILIZED BY AMINE BASE, ADMIN BY INHALATION @ 0, 100 & 500 PPM FOR 6
HR/DAY, 5 DAY/WK FOR 18 MO TO /NMRI/ MICE, RATS & SYRIAN HAMSTERS. ONLY
FEMALE MICE SHOWED INCR IN MALIGNANT LYMPHOMAS.
EXPOSURE OF MALE MICE TO TRICHLOROETHYLENE
VAPORS DURING 24 HR @ LEVELS OF 50, 202 & 450 PPM DID NOT REVEAL MUTAGENIC
EFFECTS IN DOMINANT LETHAL ASSAY.
TRICHLOROETHYLENE WAS
AMONG HALOGENATED HYDROCARBONS TESTED FOR CARCINOGENICITY BY CHRONIC ADMIN BY 1
OR MORE ROUTES IN HA:ICR SWISS MICE. TCE INACTIVE BY CRITERIA USED.
... 50 MALE & 50 FEMALE B6C3F1 HYBRID
MICE, 5 WK OLD, WERE ADMIN 99% PURE TRICHLOROETHYLENE,
CONTAINING 0.19% 1,2-EPOXYBUTANE & 0.09% EPICHLOROHYDRIN IN CORN OIL BY
GAVAGE ON 5 DAYS A WK FOR 78 WK. HIGH DOSE MALES RECEIVED 2000-2400 MG/KG BODY
WT/DAY, & FEMALE 1400-1800 MG/KG BODY WT/DAY; LOW DOSE MALE & FEMALES
RECEIVED 1000-1200 MG/KG BODY WT/DAY & 700-900 MG/KG BODY WT. ALL SURVIVING
ANIMALS WERE OBSERVED UNTIL ... 95 WK OF AGE. ... HEPATOCELLULAR CARCINOMA
OCCURRED IN 1/20 CONTROL MALES AND 0/20 CONTROL FEMALES, IN 26/50 LOW DOSE MALES
& 4/50 LOW DOSE FEMALES, & IN 31/48 HIGH DOSE MALES, 11/47 HIGH DOSE
FEMALES. METASTASES OF THE LIVER CELL TUMORS TO THE LUNG WAS FOUND IN 7/98
TREATED MALES & IN 1 CONTROL MALE. LUNG TUMORS OCCURRED IN TREATED ANIMALS
OF BOTH SEXES ... ONLY ONE LUNG ADENOMA IN FEMALE.
A single 1000 mg/kg body wt dose ... in corn
oil was admin by gavage to 50 mice of each sex, and doses of 1000 and 500 mg/kg
body wt were given in the same manner to 50 rats of each sex 5 days/wk for 2 yr.
For each group of test animals there were corresponding groups of controls
composed of 50 animals of each sex. The trichloroethylene
was stabilized with an amine antioxidant (diisopropylamine) and contained no
detectable traces of 1,2-epoxybutane or epichlorohydrin. ... The results
observed in the mice support the previous NCI (1976) findings that trichloroethylene
significantly incr the incidence of hepatocellular carcinomas in B6C3F1 mice of
both sexes.
IN VIVO AND IN VITRO METHODOLOGIES THAT HAVE
EMPLOYED THE YEAST SCHIZOSACCHAROMYCES POMBE AS GENETIC INDICATOR HAVE BEEN
UTILIZED TO INVESTIGATE THE MUTAGENICITY OF TWO TRICHLOROETHYLENE
(TCE) SAMPLES OF PURE AND TECHNICAL GRADE. BOTH TCE SAMPLES GAVE NEGATIVE
RESULTS FOR IN VIVO AND IN VITRO ASSAYS, WHEREAS THE 2 CONTAMINANTS WERE FOUND
MUTAGENIC ONLY IN VITRO.
No liver lesions or hepatomas were found in
NLC mice which had received oral doses of 0.1 ml of a 40% solution of trichloroethylene
in oil twice weekly for an unspecified period.
Trichloroethylene
(3.3 mM) in the presence of a metabolic activating microsomal system induced
reverse mutations in Escherichia coli strain K12. It has also been shown to
induce frame-shift as well as base substitution mutations in Saccharomyces
cerevisiae strain XV185-14C in the presence of mouse liver homogenate.
In rabbits, blood levels of greater than 30
mg/l (following continuous iv infusion of 1-5 mg/kg/min, trichloroethylene)
induced positional nystagmus /SRP: rapid movement of the eyeball when the head
is held in various positions/.
ACS purity trichloroethylene
induced both point mutation and gene conversion at the ilv and trp loci of the
D7 strains of Saccharomyces cerevisiae in the presence of a mouse liver 10,000 g
supernatant metabolizing system. A dose response was observed in both instances
over the range of 10-40 mM.
Application of 0.1 ml of trichloroethylene
directly applied to the eye of a rabbit produced a mild-moderate conjunctivitis
with some epithelial abrasions being noted on examination with fluorescein.
Microscopic examination on day 7 indicated epithelial keratosis in the process
of healing. The eye returned to normal in two weeks.
Concentration of 1 mM trichloroethylene
induced transformation of rat embryo cells (Fischer rat embryo cell system
F1706) in vitro which appeared as a progressively growing foci of cells lacking
contact inhibition and by the growth of macroscopic foci when inoculated in
semi-solid agar. The transformed cells grew as undifferentiated fibrosarcomas at
the site of inoculation in 100% of newborn Fischer rats between 27 and 68 days
post-inoculation.
Chronic administration /by gavage/ of 2400
mg/kg per day of trichloroethylene to male B6C3F1 mice,
induced localized cell necrosis, enhanced DNA synthesis, and centrilobular
hepatocellular swelling. Prolonged exposure (3 weeks), the primary response was
dose-related centrilobular hepatocellular swelling and the occurrence of
mineralized (calcified) cells.
Trichloroethylene was
non-mutagenic in the Ames Salmonella assay when tested with TA100 in a 10 liter
desicator. Exposure levels were as high as 20% in air (v/v) for up to 16 hr. The
assay was performed in the presence and absence of a phenobarbital-induced liver
S9 fraction from male mice. Chloral hydrate, a metabolite of trichloroethylene,
was found to be mutagenic in strain TA100 in the Salmonella standard plate
incorporation assay in doses ranging from 0.5 to 10.0 mg/plate. The mutagenic
activity was enhanced in the presence of rat liver S9 mix.
Sperm exam from mice exposed to 0.3% for 4 hr
daily for 5 days revealed incr abnormalities after 28 days.
Rats exposed to 37,000, 42,000, and 56,000
mg/cu m of trichloroethylene vapor for two hours
exhibited elevated activities of serum glutamic pyruvic transaminase, glutamic
oxaloacetic transaminase, and isocitrate dehydrogenase. Hepatotoxicity
(indicated by the increased levels of these hepatic enzymes in the serum) was
greatly enhanced by pretreatment with 3-methylcholanthrene.
Trichloroethylene was
neither embryotoxic nor teratogenic in Sprague-Dawley rats and Swiss Webster
mice inhaling trichloroethylene. These results have
been confirmed in two other studies in female rats exposed in one case to 500
ppm and in other to 1800 ppm. Trichloroethylene was
found to be weakly mutagenic in Escherichia coli in the presence of a
metabolizing system ... or in extensive studies in Drosophila. Positive effects
in some studies may be due to epoxy stabilizers sometimes present in trichloroethylene.
Female Sprague-Dawley rats were given trichloroethylene
(TCE) in distilled drinking water at concentrations of 312, 625, and 1250 mg/l.
Dams received TCE from 14 days prior to breeding, throughout gestation, and
until the pups were weaned at 21 days of age. Control dams received untreated
distilled water. Male offspring of experimental and control dams were used to
study exploratory behavior either 28, 60, or 90 days of age. Wheel-running,
feeding, and drinking behavior tests in rat pups were conducted for 24 hr/day
from 55-60 days of age. At 28 days of age, no difference in exploratory activity
was seen among treatment groups. At 60 and 90 days of age, rat pups exposed to /SRP:
even the lowest concentrations/ of TCE exibited increased levels of exploration.
Rats exposed to 1250 mg/l TCE were more active on the wheel than controls or
those exposed to 625 mg/l TCE. No significant differences were detected among
treatment groups for the levels or timing of feeding or drinking activities.
Trichloroethylene was
evaluated for mutagenicity in the Salmonella/microsome preincubation assay using
the standard protocol approved by the National Toxicology Program. Trichloroethylene
was tested doses at doses of 0.01, 0.033, 0.10, 0.333, and 1.0 mg/plate in as
many as 5 Salmonella typhimurium strains (TA1535, TA1537, TA97, TA98, and TA100)
in the presence and absence of rat or hamster liver S-9. Trichloroethylene
was negative in these tests and the highest ineffective dose tested in any S
typhimurium strain was 1.0 mg/plate. Slight clearing of the background bacterial
lawn occurred in all cultures at the high dose.
Affected fathead minnows, 31 days old, in
toxicant concentrations ranging from 8.43-77.3 mg/l, lost schooling behavior,
swam in a corkscrew/spiral pattern near the surface, were hyperactive &
hemorrhaging. Equilibrium loss was not observed prior to death. No effect data
were recorded. Individual lengths & weights were not recorded; however, the
measured mean weight was 0.109 g. Spike recovery data were not available, but
the mean recovery was likely >90%.
Trichloroethylene
/0.5 ml/ (purity 99.5%) applied to the shaved non-abraded skin of rabbits for 24
hours under an occlusive dressing, produced severe skin irritation.
Trichloroethylene
(1.0 ml) /purity not specified/ was applied, occluded in a skin depot, to the
clipped skin of a guinea pig. Histological examinations performed at 15 minutes,
1, 4, and 16 hour /indicated/ degenerative changes (pyknotic nuclei) were
observed in the epidermis after 15 minutes, and were progressive (pyknosis,
karyolysis, junctional separation of the epidermis) up to the end of the study.
Groups of 49-50 female ICR mice 4 weeks of age
... exposed by inhalation to trichloroethylene (purity
= 99.8%, with 0.128% carbon tetrachloride, 0.019% benzene, 0.019%
epichlorohydrin, and 0.01% 1,1,2-trichlorethane) at 0.270, 810, or 2430 mg/cu m
7 hr/day for 5 days/wk, for 104 weeks. The surviving animals were /sacrificed/
107 weeks after the start of the study. Mortality was similar in control and
treated groups. Lung adenomas were found in 5, 2, 5, and 4 mice in the control,
low-dose, mid-dose and high-dose groups, respectively. Adenocarcinomas occurred
in 1/49, 3/50, 8/50, and 7/46 mice in the control, low-dose, mid-dose and
high-dose groups, respectively; increased incidences in the mid- and high-dose
groups were statistically significant compared with controls.
A pure sample of trichloroethylene,
stabilized with thymol /concentration not specified/ did not induce forward
mutations at the HGPRT locus of a Chinese hamster V-79 cell line treated in
vitro, with or without S9 mix metabolic activation.
Gelatinsorbitol microcapsules containing 44.1%
trichloroethylene (TCE) were prepared and mixed in
NIH-07 rodent meal diet and provided at microcapsule concentrations of 0
(untreated control group), 1.25, 2.5, 5.0, or 10% (equivalent to 0, 0.55, 1.10,
2.21, or 4.41% TCE in the diet, respectively) to groups of 10 male F344 rats for
14 days. An additional control group received diets containing 5% empty
capsules. For comparisions, TCE dissolved in corn oil was administered by gavage
to different groups of 10 male rats for 14 consecutive days at dose levels
adjusted to correspond to those in the feed study. Treatment-related deaths
occurred only in the highest dose group of the gavage study. Body weight gain
and feed consumption were reduced in high-dose groups of both the feed and
gavage studies. ... Dose-related increases in organ (liver and kidney)
weight/body weight ratios, individual cell necrosis in the liver, and hepatic
microsomal NADPH cytochrome-c reductase and peroxisomal palmitoyl-CoA oxidase
and catalase activities were found in both the dosed-feed and gavage groups.
Induction of cytochrome p450 occurred only in the dosed-feed study.
... MAJOR CONSIDERATION MUST BE GIVEN TO
CUMULATIVE EFFECTS OF THIS COMPOUND. ... IN LONG-TERM FEEDING STUDIES CARRIED
OUT BY THE NATIONAL CANCER INSTITUTE (1976b), ... MICE (BOTH SEXES, AT BOTH LOW
AND HIGH DOSE LEVELS) EXPERIENCED A HIGHLY SIGNIFICANT INCREASE IN
HEPATOCELLULAR CARCINOMAS. ... MIKISKOVA AND MIKISKA (1966) DEMONSTRATED THAT
TRICHLOROETHANOL HAD A PRONOUNCED DEPRESSANT EFFECT ON THE CENTRAL NERVOUS
SYSTEM.
When fed in drinking water to mice for 4 to 6
months at concentrations of 0, 0.1, 1.0, and 2.5, and 5.0 mg/ml of water,
"There was a decreased body weight gain at the highest dose, which could be
attributed to a decrease in fluid consumption. The most significant effects
attributable to TCE were an increase in liver weight in both sexes accompanied
by increased nonprotein sulfhydryl levels in the males, and an increase in
kidney weight in both sexes accompanied by increases in protein and ketones in
the urine. ... The 6 months average daily doses were 0, 144, 217, 393, and 660
mg/kg body weight for the male mice. Female mice averaged 0, 18, 193, 437, and
793 mg/kg/day.
... Several species of animals /were exposed/
7 hr/day, 5 days/week for approximately 6 months. At 3000 ppm by volume in air,
rats and rabbits both showed an increase in liver and kidney weight. At 400 ppm
rats showed an increase in liver and kidney weights and the male rats also
showed significantly less growth. Guinea pigs had increased liver weights and
the growth of the exposed males was less than the controls. Rabbits showed a
slight increase in liver weight. An exposed monkey showed no response at 400 ppm.
At 200 ppm, the only effect was depressed growth in guinea pigs. Rats, rabbits,
and monkeys showed no response. At a concentration of 100 ppm, none of the
species showed any significant response. The maximum concentrations tolerated
without adverse effect for the 6 month period were as follows: monkeys, 400 ppm;
rats and rabbits, 200 ppm; and guinea pigs, 100 ppm.
... Rats, guinea pigs, dogs, rabbits, and
monkeys /were exposed/ 24 hr/day for 90 days to 35 ppm with no effect except
slight growth depression. Repeated 8 hr daily exposures to 700 ppm for 90 days
were also without effect.
Pregnant /rats and mice and their offsprings/
were exposed for 7 hr to 300 ppm on days 6 to 15 of pregnancy with no evidence
of adverse effect on the dams, on reproduction, or on the offspring by any of
the usual criteria of a teratogenic study.
In a teratology reproduction study, the NTP
fed microencapsulated trichloroethylene to rats and
mice at doses as high as 300 mg/kg/day to rats and 750 mg/kg/day to mice with
little effect. Sperm motility was reduced 45% in F0, males and 18% in F1, male
mice. There is no ready explanation for less response in the F1-generation male
mice.
When fed to B6D2F1 mice by gavage on days 1 to
5, 6 to 10, or 10 to 15 (day 1, vaginal plug) trichloroethylene
in corn oil cause no reproductive, maternal, or foal effects. Daily dosages were
0, 1/10, or 1/100 of the oral LD50 (2402 mg/kg used as LD50 value). Weanlings
were kept for 21 days or 42 days. Trichloroethylene
also had no effect on in vitro fertilization.
Apart from two reports in which trichloroethylene
weakly induced mutation in Salmonella typhimurium TA1535, purified trichloroethylene
did not induce gene mutation in various strains of Salmonella in the absence of
metabolic activation; however, trichloroethylene
containing directly mutagenic epoxide stabilizers did.
Previous epidemiological studies with humans
& laboratory studies with chickens & rats linked trichloroethylene
(TCE) exposure to cardiac defects. Although the cardiac defects in humans &
laboratory animals produced by TCE are diverse, a majority of them involves
valvular & septal structures. Progenitors of the valves & septa are
formed by an epithelial-mesenchymal cell transformation of endothelial cells in
the atrioventricular (AV) canal & outflow tract areas of the heart. Based on
these studies, we hypothesized that TCE might cause cardiac valve & septa
defects by specifically perturbing epithelial-mesenchymal cell transformation.
We tested this hypothesis using an in vitro chick-AV canal culture model. This
study shows that TCE affected several elements of epithelial-mesenchymal cell
transformation. In particular, TCE blocked the endothelial cell-cell separation
process that is associated with endothelial activation. Moreover, TCE inhibited
mesenchymal cell formation throughout the concn range tested (50-250 ppm). In
contrast, TCE had no effect on the cell migration rate of the fully formed
mesenchymal cells. Finally, the expression of 3 proteins (selected as molecular
markers of epithelial-mesenchymal cell transformation) was analyzed in untreated
& TCE-treated cultures. TCE inhibited the expression of the transcription
factor Mox-1 & extracellular matrix (ECM) protein fibrillin 2. In contrast,
TCE had no effect on the expression of alpha-smooth muscle actin. These data
suggest that TCE may cause cardiac valvular & septal malformations by
inhibiting endothelial separation & early events of mesenchymal cell
formation in the heart.
Strategies are needed for assessing the risks
of exposures to airborne toxicants that vary over concns & durations. The
goal of this project was to describe the relationship between the concn &
duration of exposure to inhaled trichloroethylene (TCE),
a representative volatile organic chemical, tissue dose as predicted by a
physiologically based pharmacokinetic model, & neurotoxicity. Three measures
of neurotoxicity were studied: hearing loss, signal detection behavior, &
visual function. The null hypothesis was that exposure scenarios having an
equivalent product of concn & duration would produce equal toxic effects,
according to the classic linear form of Haber's Rule ... . All experiments used
adult male, Long-Evans rats. Acute & repeated exposure to TCE increased
hearing thresholds, & acute exposure to TCE impaired signal detection
behavior & visual function. Examination of all three measures of
neurotoxicity showed that if Haber's Rule were used to predict outcomes across
exposure durations, the risk would be overestimated when extrapolating from
shorter to longer duration exposures, & underestimated when extrapolating
from longer to shorter duration exposures. For the acute effects of TCE on
behavior & visual function, the estimated concn of TCE in blood at the time
of testing correlated well with outcomes, whereas cumulative exposure, measured
as the area under the blood TCE concn curve, did not. ... Models incorporating
dosimetry can account for differing exposure scenarios & will therefore
improve risk assessments over models considering only parameters of external
exposure.
Trichloroethylene (TCE)
induces liver cancer in mice but not in rats. Three metabolites of TCE may
contribute chloral hydrate (CH), dichloroacetate (DCA), & trichloroacetate (TCA).
CH & TCA appear capable of only inducing liver tumors in mice, but DCA is
active in rats as well. The concns of TCA in blood required to induce liver
cancer approach the mM range. Concns of DCA in blood associated with
carcinogenesis are in the sub-muM range. The carcinogenic activity of CH is
largely dependent on its conversion to TCA &/or DCA. TCA is a peroxisome
proliferator in the same dose range that induces liver cancer. Mice with
targeted disruptions of the peroxisome proliferator-activated receptor alpha (PPARalpha)
are insensitive to the liver cancer-inducing properties of other peroxisome
proliferators. Human cells do not display the responses associated with
PPARalpha that are observed in rodents. This may be attributed to lower levels
of expressed PPARalpha in human liver. DCA treatment produces liver tumors with
a different phenotype than TCA. Its tumorigenic effects are closely associated
with differential effects on cell replication rates in tumors, normal
hepatocytes, & suppression of apoptosis. Growth of DCA-induced tumors has
been shown to arrest after cessation of treatment. The DCA & TCA adequately
account for the hepatocarcinogenic responses to TCE. Low-level exposure to TCE
is not likely to induce liver cancer in humans. Higher exposures to TCE could
affect sensitive populations. Sensitivity could be based on different metabolic
capacities for TCE or its metabolites or result from certain chronic diseases
that have a genetic basis.
The possibility that the acute neurotoxic
effects of organic solvents change with repeated exposure will affect risk
assessment of these pollutants. ... Rats inhaling trichloroethylene
(TCE) showed a progressive attenuation of impairment of signal detection
behavior across several wk of intermittent exposure, suggesting the development
of tolerance. Here, we explored the development of tolerance to TCE during 2 wk
of daily exposures, & the degree to which learned behavioral modifications
("behavioral tolerance") could account for the effect. Adult
Long-Evans rats were trained to perform a visual signal detection task (SDT) in
which a press on one lever yielded food if a visual stimulus (a
"signal") had occurred on that trial, & a press on a second lever
produced food if no signal had been presented. In two experiments, with 2000
& 2400 ppm of TCE res pectively, trained rats were divided into two groups
(n = 8/group) with equivalent accuracy & then exposed to TCE in two-phase
studies. In Phase 1, one group of rats received daily SDT tests paired with
70-min TCE exposures, followed by 70-min exposures to clean air after testing.
The other group received daily SDT tests in clean air, followed by 70-min
exposures to TCE (unpaired exposure & testing). All rats thus received the
same number & daily sequence of exposures to TCE that differed only in the
pairing with SDT testing. Both concns of TCE disrupted performance of the paired
groups & this disruption abated over the 9 days of exposure. In Phase 2, the
pairing of exposure & test conditions were reversed for the two groups. The
groups that were shifted from unpaired to paired exposures (Unpaired-Paired
groups) showed qualitatively similar patterns of deficit & recovery as did
the rats whose tests were initially paired with TCE (Paired-Unpaired groups),
indicating that task-specific learning was involved in the development of
tolerance. Quantitative differences in the magnitude & duration of the
effects of TCE in the two groups indicated that other factors, not specific to
the SDT, also contributed to the development tolerance to TCE.
Exposure of rats to trichloroethylene
induces a sustained excretion of large amounts of formic acid in urine. Both of
the major metabolites, trichloroethanol & trichloroacetic acid, were found
to induce this response, but not the minor metabolite S-(1, 2-dichlorovinyl)
cysteine. Other polychlorinated solvents, including carbon tetrachloride &
chloroform, also increased urinary formate excretion. Addition of folic acid
either to diet or drinking water modulated the response indicating that these
rats were folate deficient. Two markers of vitamin B(12) deficiency,
methylmalonic acid & 5-methyltetrahydrofolate, were also markedly incr in
urine & plasma respectively. The incr in 5-methyltetrahydrofolate is
consistent with a folate deficiency caused by an inhibition of the vitamin B(12)
dependent methionine salvage pathway. Since both vitamin B(12) & chemicals
containing polychlorinated carbon atoms readily form free radicals, it is
suggested that trichloroacetic acid & trichloroethanol interact with vitamin
B(12) through a free radical mechanism inducing a B(12) deficiency &, as a
consequence, a folate deficiency. As a result of the folate deficiency, excess
formic acid, which is normally utilised through this pathway, is excreted in
urine.
... There is increasing evidence relating
exposure to trichloroethylene /(1,1,2-trichloroethene)/
with autoimmunity. To investigate potential mechanisms, we treated the
autoimmune-prone MRL + / + mice with trichloroethylene
in the drinking water at 0, 2.5 or 5.0 mg/ml ... . As early as 4 wk of
treatment. Western blot analysis showed a dose-dependent incr in the level of trichloroethylene-modified
proteins, indicating that a reactive metabolite of trichloroethylene
was formed. Significant increases in antinuclear antibodies (ANA) & total
serum immunoglobulins were found following 4-8 wk of trichloroethylene
treatment, indicating that trichloroethylene was
accelerating an autoimmune response. Investigation into possible mechanisms of
this autoimmune response revealed that trichloroethylene
tre atment dramatically increased the expression of the activation marker CD44
on splenic CD4+ T cells at 4 wk. In addtn, splenic T cells from mice treated for
4 wk with trichloroethylene secreted more IFN-gamma
& less IL-4 than control T cells, consistent of a T-helper type 1 (Th1) type
immune or inflammatory response. A specific immune response directed against
dichloroacetylated proteins was found at 22 wk of trichloroethylene
treatment. ... The results suggest that trichloroethylene
treatment accelerated an autoimmune response characteristic of MRL + / + mice in
association with nonspecific activation of Th1 cells. In addtn, long-term
treatment with trichloroethylene led to the initiation
of a trichloroethylene-specific immune response.
The mechanism of trichloroethylene-induced
liver peroxisome proliferation & the sex difference in response was
investigated using wild-type Sv/129 & peroxisome proliferator-activated
receptor alpha (PPARalpha)-null mice. Trichloroethylene
treatment (0.75 g/kg for 2 wk by gavage) resulted in liver peroxisome
proliferation in wild-type mice, but not in PPARalpha-null mice, suggesting that
trichloroethylene-induced peroxisome proliferation is
primarily mediated by PPARalpha. No remarkable sex difference was observed in
induction of peroxisome proliferation, as measured morphologically, but a
markedly higher induction of several enzymes & PPARalpha protein & mRNA
was found in males. On the other hand, trichloroethylene
induced liver cytochrome P450 2E1, the principal enzyme responsible for
metabolizing trichloroethylene to chloral hydrate, only
in males, which resulted in similar expression levels in both sexes after the
treatment. Trichloroethylene influenced neither the
level of catalase, an enzyme involved in the reduction of oxidative stress, nor
aldehyde dehydrogenase, the main enzyme catalyzing the conversion to
trichloroacetic acid. These results suggest that trichloroethylene
treatment causes a male-specific PPARalpha-dependent increase in cellular
oxidative stress.
Trichloroethylene (TCE),
dichloroacetic acid (DCA), & trichloroacetic acid (TCA) are environmental
contaminants that are carcinogenic in mouse liver. 5-Methylcytosine (5-MeC) in
DNA is a mechanism that controls the transcription of mRNA, including the
protooncogenes, c-jun & c-myc. ... TCE decreased methylation of the c-jun
& c-myc genes & increased the level of their mRNAs. Decreased
methylation of the protooncogenes could be a result of a deficiency in S-adenosylmethionine
(SAM), so that methionine, by increasing the level of SAM, would prevent
hypomethylation of the genes. For 5 days, female B6C3F1 mice were admin, daily
by oral gavage, either 1000 mg/kg bw of TCE or 500 mg/kg DCA or TCA. At 30 min
after each dose of carcinogen, the mice received, by ip injection, 0, 30, 100,
or 450 mg/kg methionine. Mice were euthanized at 100 min after the last dose of
DCA, TCA, or TCE. Decreased methylation in the promoter regions of the c-jun
& c-myc genes & increased levels of their mRNA & proteins were found
in livers of mice exposed to TCE, DCA, & TCA. Methionine prevented both the
decreased methylation & the increased levels of the mRNA & proteins of
the two protooncogenes. The prevention by methionine of DCA- TCA-, & TCE-induced
DNA hypomethylation supports the hypothesis that these carcinogenes act by
depleting the availability of SAM. Hence, methionine would prevent DNA
hypomethylation by maintaining the level of SAM. Furthermore, the results
suggest that the dose of DCA, TCA, or TCE must be sufficient to decrease the
level of SAM in order for these carcinogens to be active.
National Toxicology Program Studies:
Toxicology and carcinogenesis studies of trichloroethylene
(more than 99% pure, stabilized with 8 ppm diisopropylamine) were conducted by
administering the chemical in corn oil by gavage at doses of 0, 500, or 1000
mg/kg/day 5 days/wk for 103 wk to groups of 50 male and 50 female ACI, August,
Marshall, and Osborne-Mendel rats. ... Under the conditions of these two yr
gavage studies of trichloroethylene in male and female
ACI, August, Marshall, and Osborne-Mendel rats, trichloroethylene
administration caused renal tubular cytomegaly and toxic nephropathy in both
sexes of the four strains. However, these are considered to be inadequate
studies of carcinogenic activity because of chemically induced toxicity, reduced
survival, and deficiencies in the conduct of these studies. Despite these
limitations, tubular cell neoplasms of the kidney were observed in rats exposed
to trichloroethylene and interstitial cell neoplasms of
the testis were observed in Marshall rats exposed to trichloroethylene.
/Trichloroethylene stabilized with 8 ppm
diisopropylamine/
Carcinogenesis studies of epichlorohydrin-free
trichloroethylene (TCE) was conducted by administering
the test chemical in corn oil by gavage to groups of 50 male and 50 female
F344/N rats and B6C3F1 mice. Dosage levels were 500 and 1,000 mg/kg for rats and
1,000 mg/kg for mice. Trichloroethylene was
administered five times per week for 103 weeks, and surviving animals were
killed between weeks 103 and 107. Groups of 50 rats and 50 mice of each sex
received corn oil by gavage on the same schedule and served as vehicle controls.
Groups of 50 male and 50 female rats were used as untreated controls.
Epichlorohydrin-free trichloroethylene caused renal
tubular-cell neoplasms in male F344/N rats, produced toxic nephrosis in both
sexes, and shortened the survival time of males. This experiment in male F344/N
rats was considered to be inadequate to evaluate the presence or absence of a
carcinogenic response to trichloroethylene. For female
F344/N rats receiving trichloroethylene, containing no
epichlorohydrin, there was no evidence of carcinogenicity. Trichloroethylene
(without epichlorohydrin) was carcinogenic for B6C3F1 mice, causing increased
incidences of hepatocellular carcinomas in males and females and of
hepatocellular adenomas in females.
Trichloroethylene (TCE),
a common industrial solvent & dry cleaning agent, was tested for its effects
on reproduction & fertility in Fisher 344 rats using the RACB protocol. TCE
was microencapsulated in a gelatin/sorbitol shell, & added to the diet. Data
from a 2 wk dose-range-finding study (Task 1) were used to set exposure concns
for the Task 2 continuous cohabitation study at 0.15, 0.30, & 0.60% w/w.
Based on the results of the analysis of feed formulations & measures of feed
consumption, the daily TCE dosages were nearly equal to 76, 156, & 289
mg/kg/day. In the F0 animals, there were no clinical signs of toxicity, & no
animals died during the Task 2 phase. Dam postpartum body weights were reduced
at all dose levels during Task 2: from 4-6% at the low dose to nearly equal to
8% at the high dose. There was a monotonic trend to fewer litters/pair (from 3.5
in controls to 2.9 in the high dose group), & the middle & high dose
groups had 9% & 16% fewer pups/litter than the controls. Pup weight &
viability were unchanged at any dose level. The last litter was reared by the
dam. During this 21 day nursing period, viability was not affected by TCE
exposure, but body weights were depressed for pups from all treated groups. The
decr was not dose-related, & ranged from 9%-20% compared to controls. At 21
& 45 days post-partum, the F1 rats from all groups were tested for
behavioral alterations in an open-field test. At 21 days there were no
differences across groups, while at 45 days, mice at the high dose crossed the
field fewer times, each trip was quicker than controls, & there were fewer
rearing episodes, & more time spent grooming. The changes in fertility &
pup number seen in Task 2 prompted the conduct of a Task 3 crossover to
determine the affected sex using the control & top dose groups. While 100%
of the control x control pairs mated, only 75% of the groups containing a
treated animal did. There were no differences across groups in terms of the
number of pups/litter, or the viability or weight of those pups. An affected sex
could not be determined for this compound. After the delivery & assessment
of the Task 3 litters, the control & high dose F0 adults were killed &
necropsied. The body weight of high-dose treated males was reduced by nearly
equal to 4%, while relative liver weight & kidney weight was increased by
nearly equal to 24% & 12%, respectively, compared to controls. There were no
changes in sperm indices. For females, body weight was reduced by nearly equal
to 10%, while relative liver weight was increased by nearly equal to 19% &
kidney weight was increased by nearly equal to 7%. The fertility of the second
generation was evaluated for all dose groups. There was no treatment-related
effect on the proportion of pairs mating or delivering litters, nor were there
any differences between the groups in terms of number of pups/litter, or pup
viability or weight. After delivery & evaluation of the F2 pups, the F1
adults were killed & necropsied. Male body weights were reduced by 5%, 7%,
& 9% (low to high dose groups, respectively). Absolute testis weight was
also reduced, by 6-8% in all dosed groups. Adjusted liver weights were increased
by 6%, 9%, & 16%, respectively. Seminal vesicle weight was increased by
nearly equal to 18% at the middle dose only. Treated female body weights were
reduced by 4%, 3%, & 11%, respectively, from low to high dose groups, while
adjusted liver weight was increased by 10% at both the middle & high dose
levels. Abnormal sperm forms were more numerous at the low dose, approx doubled
from 0.54% to 1.13%. No other sperm changes were noted. No vaginal cyclicity
data were collected. In sum, these data indicate that TCE produced some general
toxicity (reduced body weight gain, increased relative liver & kidney
weights) at all doses, while reducing reproductive indices only in the F1 rats
at the middle & high dose levels. Thus, TCE was not found to be a selective
reproductive toxicant in rats.
Trichloroethylene (TCE),
a common industrial solvent & dry cleaning agent, was tested for its effects
on reproduction & fertility in Swiss CD-1 mice using the RACB protocol. TCE
was microencapsulated in a gelatin/sorbitol shell, & added to the diet. Data
from a 2 wk dose-range-finding study (Task 1) were used to set exposure concns
for the Task 2 continuous cohabitation study at 0.15, 0.30, & 0.60% w/w.
Based on the results of the analysis of feed formulations & an avg daily
feed consumption of nearly equal to 5.0g, the daily TCE dosages were nearly
equal to 100, 300, & 700 mg/kg/day. TCE exposure was associated with no
adverse clinical signs, & post-partum dam weights during the Task 2
cohabitation phase were not reduced by TCE. The only adverse reproductive change
noted during Task 2 was a 4% reduction in pup weight adjusted for litter size at
the high dose. The last litter from the control & high dose groups was
reared to weaning, for subsequent evaluation of second generation fertility.
Maternal TCE exposure during lactation was associated with a significant incr in
perinatal mortality: the 28% mortality rate in control litters is significantly
less than the 61% mortality rats in the high dose TCE group. After weaning,
mortality rates were comparable between the two groups. After the F1 pups were
weaned, the F0 control & high dose mice were killed & necropsied. Male
body weight was not changed, while absolute testis weight was reduced by 4%,
adjusted liver weight was increased by nearly equal to 34%, & adjusted
prostate weight was reduced by nearly equal to 16%. Sperm motility was reduced
by nearly equal to 45% in the high dose TCE treated animals; no other sperm or
reproductive changes were noted. In females, body weight was unchanged while
adjusted liver weight was increased by nearly equal to 30%. No histologically-visible
changes in vaginal epithelium were noted. Treated mice had a greater incidence
of centrilobular hypertrophy, & renal tubular degeneration &
corticomedullary epithelial karyomegaly. Males were generally more affected than
females. The second generation mice from the control & high dose groups were
cohabited at nearly equal to /postnatal day/ 74. No reproductive endpoint was
altered by TCE exposure. After evaluation of the F2 pups, the F1 adults were
killed & necropsied. Male body weight was unchanged, but adjusted liver
weight was increased by nearly equal to 60%, adjusted kidney weight was
increased by nearly equal to 9%, & adjusted epididymis weight increased by
nearly equal to 9%. The % motile sperm was reduced by nearly equal to 20%, while
the proportion of abnormal sperm was increased from a control value of 8%, to
10% in the treated mice. TCE-treated female body weights were not different from
controls, while adjusted liver weight & kidney weight were increased by
nearly equal to 30% & 16%, respectively. Hepatic & renal microscopic
lesions were similar to those noted for the F0 mice. Histologic evaluation of
the vaginal epithelium indicated cycling in both groups, but cycles were not
assessed in vivo. In summary, TCE exposure to mice via the diet produced
significant hepatic & renal toxicity (increased weights & microscopic
lesions), reduced sperm motility in both generations, & produced greater
lactational mortality in the high dose group. These data suggest that the
hepatic/renal/lactational toxicities were more severe than the relatively
moderate reductions in sperm motility.
... The purpose of this time course study was
to determine the potential effects of trichloroethylene
to induce autoimmunity in the Brown Norway Rat model and to determine the time
of maximum effect. The studies were conducted in female Brown Norway Rat. The
animals were administered trichloroethylene (500 mg/kg)
five days a week for an 8-week period by oral gavage. Trichloroethylene
was prepared weekly in a 10% Alkamus-deionized water solution. Additional groups
of vehicle- and trichloroethylene-exposed animals also
received mercuric chloride (1 mg/kg) three times per week by subcutaneous
injection for 2 additional weeks. Various parameters of autoimmunity were
evaluated weekly, at the time of sacrifice following trichloroethylene
treatment, and at time of sacrifice following challenge with mercuric chloride.
... The results of the time course study demonstrate that female Brown Norway
rats have a strong aversion to being exposed to trichloroethylene
by oral gavage. Furthermore, during the study 3 deaths directly related to
chemical exposure were observed in the trichloroethylene
exposure group which consisted of 15 animals. Animals exposed to trichloroethylene
had decreased body weights compared to the vehicle control animals during the
first two weeks of the study and a decrease in body weight gain over the course
of the study period. While no effect was observed on spleen, lungs, thymus or
adrenal weights, increases were observed in relative kidney (8%) and liver (14%)
weights compared to the vehicle controls. When parameters indicative of
autoimmune responses were evaluated, no effect was observed on serum IgE levels
evaluated weekly, at the time of sacrifice or following challenge with mercuric
chloride. No effect was observed on total serum IgG levels at the time of
sacrifice; however, a decreased total IgG response was observed in the trichloroethylene-exposed
animals following challenge with mercuric chloride. No effect was observed on
serum IgG antibody titers to dinitrophenol-human serum albumin (DNP-HSA)
evaluated weekly or at the time of sacrifice. Decreased serum IgG antibody
titers to DNP-HSA response were observed in the trichloroethylene-exposed
animals following challenge with mercuric chloride. While no effect was observed
on serum IgG antibody titers to sheep erythrocytes at the time of sacrifice, a
decrease in serum IgG antibody titers to sheep erythrocytes was observed in the trichloroethylene-exposed
animals following challenge with mercuric chloride. When parameters related to
autoimmune disease were evaluated, no effects were observed in blood urea
nitrogen (BUN) levels at the time of sacrifice or following challenge with
mercuric chloride. No effect was observed on urinalysis parameters which
included glucose, protein, pH, and blood in the urine as measured using
Hema-Combistix. No effect was observed on serum IgG antibody titers to laminin
evaluated weekly or at the time of sacrifice. A decrease in serum IgG antibody
titers to laminin was observed in the trichloroethylene-exposed
animals following challenge with mercuric chloride; however, the decrease did
not reach the level of statistical significance. No effects were observed in
serum IgG antibody titers to double stranded DNA (dsDNA) at the time of
sacrifice or following challenge with mercuric chloride. In conclusion, this
time course study demonstrates that exposure to trichloroethylene
at a dose level of 500 mg/kg for eight weeks results in significant changes in
parameters of autoimmunity and that the time of maximum effect on IgG responses
occurred 6 weeks after initiation of trichloroethylene
exposure. Although no effects were observed on IgE responses, significant
changes were observed in IgG antibody-mediated parameters following mercuric
chloride challenge. Trichloroethylene, at a dose level
of 500 mg/kg, produced no significant effect on any of the indicators of
autoimmune disease. Due to the exposure-related loss of animals at the 500 mg/kg
dose level, future studies using the Brown Norway rat should be conducted at
lower doses.
... Trichloroethylene
... had previously been shown to suppress immune function. Trichloroethylene
was selected for study with the intent of performing an interaction study with
ethanol with the immune system being the target system. Previous studies were
performed by the investigators showing that trichloroethylene,
administered in the drinking water to CD-mice for 120 days, suppressed selected
parameters of the immune system. The purpose of this range-finding study was to
select doses for use in the interaction study. In order for the study to be
performed within the confines of an interaction study, the period of exposure
was set at 14 days and higher doses than were previously reported were used. The
route of administration was by gavage. Corn oil was selected as the vehicle ...
. Toxicological parameters assessed were body weight, selected organ weights and
selected hematological indicators. The two immunological assays used to assess
immune status were the IgM spleen antibody-forming cell (AFC) response to sheep
erythrocytes (sRBC) and the cytotoxic T lymphocyte (CTL) response.
Tricloroethylene, in doses between and including 50 and 800 mg/kg administered
for 14 days, did not alter body weight or body weight gain or change the
hematological parameters examined. Trichlorethylene, in doses including and
between 100 and 800 mg/kg, caused a dose-related increase in liver weight but no
changes in kidney, spleen or thymus weight. Tricloroethylene, in doses between
and including 50 and 800 mg/kg administered for 14 days, did not affect the
spleen IgM antibody-forming cell response to sheep erythrocytes.
Trichlorethylene, in doses including and between 100 and 800 mg/kg, did not
affect the cytotoxic T lymphocyte response. ...
Non-Human Toxicity Values:
LC50 Rat inhalation 26,000 ppm/1 hr.
LC50 Rat inhalation 12,000 ppm/4 hr.
LC50 Mouse inhalation 8450 ppm/4 hr.
LD50 Rabbit percutaneous 29 g/kg.
LD10 Female CD-1 Mouse gavage 1161 mg/kg; male
CD-1 mouse gavage 1347 mg/kg.
LD50 Female CD-1 Mouse gavage 2443 mg/kg; male
CD-1 mouse gavage 2402 mg/kg
LD90 Female CD-1 Mouse gavage 2443 mg/kg; male
CD-1 mouse gavage 4253 mg/kg.
LD100 Female CD-1 Mouse gavage 5500 mg/kg;
male CD-1 mouse gavage 6000 mg/kg.
LD50 Mouse inhalation 49,000 ppm/30 min
Rat inhalation 100 ppm/8 hr, no effect.
Rabbit inhalation 1,200 ppm/473 hr, no effect.
Rabbit, ape, rat, guinea pig inhalation 730
ppm/8 hr/day, 6 weeks, no effects.
LD50 Mouse inhalation 5,500 ppm/10 hr
LD50 Dog oral 5680 mg/kg
LD50 Dog ip 2,800 mg/kg
LD50 Rabbit dermal 20 ml/kg
LD50 Rat oral 4920 mg/kg
LD50 Mouse (female) oral 2443 mg/kg
LD50 Mice (male) oral 2402 mg/kg
LD50 Mouse ip 3222 mg/kg
LD50 Dog ip 2783 mg/kg
Ecotoxicity Values:
LC50 Sheepshead minnow 20 mg/l/96 hr.
/Conditions of bioassay not specified/
LC50 Bluegill sunfish 44,700 ug/l/96 hr.
/Static bioassay/
LC50 Grass shrimp 2 mg/l/96 hr. /Conditions of
bioassay not specified/
Toxicity Threshold (Cell Multiplication
Inhibition Test) Entosiphon sulcatum (protozoa) 1200 mg/l /Time not specified,
conditions of bioassay not specified/
Toxicity Threshold (Cell Multiplication
Inhibition Test) Uronema parduczi Chatton-Lwoff (protozoa) >960 mg/l /Time
not specified, conditions of bioassay not specified/
Toxicity Threshold (Cell Multiplication
Inhibition Test) Scenedesmus quadricauda(green algae) >1000 mg/l /Time not
specified, conditions of bioassay not specified/
Toxicity Threshold (Cell Multiplication
Inhibition Test) Microcystis aeruginosa (algae) 63 mg/l /Time not specified,
conditions of bioassay not specified/
LC50 Mexican axolotl (3-4 wk after hatching)
48 mg/l/48 hr /Conditions of bioassay not specified/
LC50 Clawed toad (3-4 wk after hatching) 45
mg/l/48 hr /Conditions of bioassay not specified/
LC50 Pimephales promelas (fathead minnow) 40.7
mg/l/96 hr (95% confidence limits 31.4-71.8 mg/l) /Flow-through test/
LC50 Pimephales promelas (fathead minnow) 66.8
mg/l/96 hr (95% confidence limits 59.6-74.7 mg/l) /Static test/
EC10 Pimephales promelas (fathead minnow) 15.2
mg/l/24 hr; 16.9 mg/l/48 hr; 15.5 mg/l/72 hr; 13.7 mg/l/96 hr; Toxic effect for
all concentrations specified: loss of equilibrium. /Flow-through bioassay/
EC50 Pimephales promelas (fathead minnow) 23.0
mg/l/24 hr; 22.7 mg/l/48 hr; 22.2 mg/l/72 hr; 21.9 mg/l/96 hr; Toxic effect for
all concentrations specified: loss of equilibrium. /Flow-through bioassay/
EC90 Pimephales promelas (fathead minnow) 36.2
mg/l/24 hr; 30.6 mg/l/48 hr; 31.8 mg/l/72 hr; 34.9 mg/l/96 hr; Toxic effect for
all concentrations specified: loss of equilibrium. /Flow-through bioassay/
Toxicity Threshold (Cell Multiplication
Inhibition Test) Pseudomonas putida (bacteria) 65 mg/l
TSCA Test Submissions:
The ability of trichloroethylene
to induce morphological transformation in the BALB/3T3 mouse cell line (Cell
Transformation Assay) was evaluated. Based on preliminary toxicity
determinations (exposure time=1 day), trichloroethylene
was tested at 0, 4, 20, 100 and 250 ug/ml, with cell survival ranging from 125%
to 96% relative to untreated controls. The test compound did not produce
significantly greater transformation frequencies than untreated controls.
The effects of trichloroethylene
were examined in the mouse hepatocyte primary culture DNA repair assay. Based on
preliminary toxicity tests, trichloroethylene was
tested at concentrations of 1, 0.1, 0.01, 0.001, 1x10(-4), 1x10(-5) and
1x10(-6)% in DMSO solvent vehicle. The highest two concentrations were too
cytotoxic to evaluate in the assay. The lower levels were not cytotoxic but the
0.01 and 0.001% levels caused a significant increase in the unscheduled DNA
synthesis over the solvent control (DMSO).
The effects of trichloroethylene
were examined in the rat hepatocyte primary culture DNA repair assay. Based on
preliminary toxicity tests, trichloroethylene was
tested at concentrations of 1, 0.1, 0.01, 0.001, 1x10(-4) and 1x10(-5)% in DMSO
solvent vehicle. The higher two levels were too cytotoxic to be evaluated in the
assay. The concentrations at 0.01% or lower were not cytotoxic and did not cause
a significant increase in the unscheduled DNA synthesis over the solvent
control.
The mutagenicity of trichloroethane was
evaluated in Salmonella tester strains TA98, TA100, TA1535 and TA1537 (Ames
Test), both in the presence and absence of added metabolic activation by Aroclor-induced
rat liver S9 fraction. Trichloroethylene caused a
positive response in strains TA100 and TA1535, both with and without added
metabolic activation. Trichloroethylene did not cause a
positive response in strains TA98 or TA1537 in any of the test. Trichloroethylene
was evaluated using a protocol in which the test article was usually tested over
a minimum of 6 dose levels, the highest nontoxic dose level being 10 mg/plate
unless solubility, mutagenicity or toxicity dictated a lower limit.
The pharmacokinetics of 1,1,2-trichloroethylene
(TRI) was evaluated in male B6C3F1 mice (4/exposure) and male Osborne-Mendel
rats (4/exposure) receiving nominal concentrations of 14C-TRI at 10ppm or 600ppm
for 6 hours in a dynamic airflow chamber. Mice and rats were placed in Roth-type
metabolism cages for collection of feces, urine and expired air for 50 hours
post exposure. Within 50 hours, 98-99% of the total radioactivity observed in
all exposed male mice was metabolized. The primary route of elimination
(approximately, 75% of total body burden) for all mice was via the urine.
Approximately 9% of 14C-TRI body burden in mice was biotransformed to the
14C-carbon dioxide. No indication of saturation of 14C-TRI metabolites in the
high dose mice was observed. In contrast, rats metabolism of 14C-TRI appeared to
show characteristics of saturation at the high dose level. Total metabolism of
14C-TRI in rats at the high dose level (79% of absorbed dose) was decreased
relative to the low dose rats (98% of the absorbed dose). Also, exhalation of
14C-TRI increased 10-fold with increased exposure in rats. The primary route of
elimination of 14C-TRI in the rat was via the urine which accounted for
approximately 62% and 55% of the 14C-TRI body burden in low and high doses,
respectively. Mice metabolized 2.2 fold and 3.6 fold more TRI on a per kg body
weight basis than rats at 10ppm and 600ppm, respectively.
The ability of 1,1,2-trichloroethylene
to alkylate hepatic DNA was evaluated in four male B6C3F1 mice receiving a
carcinogenic dose (1200mg/kg) of 14C-TRI orally by gavage. Mice were sacrificed
5 hours post exposure, and liver were excised. 1,1,2-Trichloroethylene
alkylated hepatic DNA in mice to a very small degree, with the maximum estimate
average DNA alkylation of 0.62 (+/-0.42) alkylations/10(6) nucleotides for three
mice and no 14C-associated bases were detected in the fourth mouse.
The ability of trichloroethylene
(TCE) to cause unscheduled DNA synthesis was evaluated in 3 sets of male B6C3F1
mice (10-12/group) exposed by gavage using 3 regimes: Set 1, 0 or 2400 mg/kg/day
for 3 days; Set 2, 0 or 2400 mg/kg/day for 5 days/week for 3 weeks; and Set 3, 0
, 250, 500, 1200 or 2400 mg/kg/day for 5 days/week for 3 weeks. Mice were
injected subcutaneously with radiolabelled thymidine, Set 1 daily, and Sets 2
and 3 on the last 5 and 4 days of TCE treatment, respectively. The animals were
sacrificed upon termination of treatment and the kidneys (Set 1 only) and livers
examined. There were statistically significant differences noted between treated
and control mice in the following: Sets 1 and 2 (p < 0.01, Dunnett's or
Student's t-test), increased liver/body weight ratio and hepatic DNA synthesis,
and decreased ug DNA/g tissue; Set 3, dose-related increase in liver/body weight
ratio (500 mg/kg/day and above, p < 0.01), and a dose-related decrease in
hepatic DNA synthesis (500 mg/kg/day and above, p < 0.01). No significant
differences were observed between the kidneys of treated and control mice of Set
2. Histopathological changes in hepatic tissue were observed in all treated
animals (dose-related in Set 3 animals). Five mice treated with 1200 mg
radiolabelled TCE/kg by gavage and sacrificed 3 hrs later indicated that TCE
alkylated hepatic DNA only to a small degree.
The ability of trichloroethylene
(TCE) to cause unscheduled DNA synthesis was evaluated in 2 sets of male
Osborne-Mendel rats (4/group) exposed by gavage using 2 regimes: Set 1, 0 or
1100 mg/kg/day for 3 days, and Set 2, 0 or 1100 mg/kg/day for 5 days/week for 3
weeks. The rats were injected subcutaneously with radiolabelled thymidine, Set 1
daily, and Set 2 on the last 5 days of TCE treatment. The animals were
sacrificed upon termination of treatment and the kidneys (Set 1 only) and livers
examined. There were statistically significant differences noted between treated
and control rats in the following: Set 2 (p < 0.01, Dunnett's or Student's
t-test), increased liver/body weight ratio and hepatic DNA synthesis. No
significant differences were observed between the kidneys of treated and control
rats of Set 2 or the livers of treated and control rats of Set 1. No significant
histopathological changes in hepatic tissue were observed in any of the groups
of animals.
The macromolecular binding of 1,1,2-trichloroethylene
(TRI) was evaluated in male B6C3F1 mice (12/exposure) and male Osborne-Mendel
rats (12/exposure) receiving nominal concentrations of 14C-TRI at 10ppm or
600ppm for 6 hours in a dynamic air flow chamber. Four rats and four mice were
sacrificed at 0, 6 and 24 hours post exposure, and liver and kidneys were
excised. Additional mice and rats were sacrificed at 50 hour post exposure from
a previous study under the same conditions. The mice had greater binding of
radiolabel from TRI than the rat after exposure to 10 or 600ppm of 14C-TRI.
Macromolecular binding as measured by pmole Eq C14-TRI per ug protein was three
to four times greater in both hepatic and renal tissue in mice following 600ppm
exposure than rats. Only a modest increase was observed in hepatic tissue of the
mouse following 10ppm exposure relative to the rat. Maximum binding in the liver
for both species was observed immediately following exposure (3 hours for the
kidneys) and decreased steadily over the next 48 hours.
Metabolism/Pharmacokinetics:
Metabolism/Metabolites:
RATS EXCRETE 5-7 TIMES MORE TRICHLOROETHANOL
THAN TRICHLOROACETIC ACID AFTER EXPOSURE TO TRICHLOROETHYLENE.
EXCRETION OF METABOLITES HAS BEEN STATED TO
AMT TO 56% OF TRICHLOROETHYLENE INHALED-7-27%
TRICHLOROACETIC ACID, 22.2-22.5% TRICHLOROETHANOL, FREE OR CONJUGATED,
22.5-45.5% UROCHLORALIC ACID AND SMALL AMT ... OF MONOCHLOROACETIC ACID AND
CHLOROFORM. ...
METAB OF TCE PROCEEDED THROUGH FORMATION OF A
COMPLEX WITH OXYGENATED CYTOCHROME P450 WHICH, BY REARRANGEMENT, CAN LEAD TO:
(A) SUICIDAL HEME DESTRUCTION; (B) FORMATION OF CHLORAL, WHICH COULD BE REDUCED
TO TRICHLOROETHANOL AND CONJUGATED TO FORM A GLUCURONIDE OR OXIDIZED TO
TRICHLOROACETIC ACID; (C) FORMATION OF TCE OXIDE, WHICH DECOMP TO CO AND
GLYOXYLIC ACID; AND (D) METABOLITES WHICH BIND IRREVERSIBLY TO PROTEIN, DNA, AND
RNA.
Hepatic microsomes from rats fed for 3 weeks
on an isocaloric diet deficient in carbohydrate (sucrose) had an increased
capacity (2-1/2-fold) to metabolize trichloroethylene.
IN VITRO ADDITION OF TCE TO INCUBATION MIXTURE
DECR METAB OF ETHYLMORPHINE & HEXOBARBITAL BY HEPATIC MICROSOMES IN RATS.
INHIBITION OF HEXOBARBITAL METAB WAS COMPETITIVE. REPEATED ADMIN TO RATS DECR
MICROSOMAL CYTOCHROME P450; INCR LIVER/BODY WT RATIO, MICROSOMAL PROTEINS,
NADPH-CYTOCHROME C REDUCTASE ACTIVITY, ANILINE HYDROXYLASE ACTIVITY.
The metabolism of TCE in rats involves
oxidation by the liver /SRP: post-mitochondrial supernatant/ mixed function
oxidase system to an epoxide intermediate, which binds covalantly to proteins
and causes centrilobular damage in the liver. ...
Rats and mice metabolize trichloroethylene
in a qualitatively similar fashion; however, the greater rate of metabolism in
mice resulted in (a) a 4-fold greater burden of metabolized trichloroethylene
per kilogram of body weight (600 ppm/hr and 2000 mg/kg oral dose) and (b) 4- and
7-fold higher blood concentrations of trichloroethanol and trichloroacetic acid
in mice versus rats (1000 mg/kg oral dose), respectively. Humans metabolize trichloroethylene
to trichloroethanol and trichloroacetic acid, but more slowly than either mice
or rats, which is thought to have important implications with respect to the
greater sensitivity of the mouse to toxic effects of trichloroethylene.
Trichloroethylene is metabolized by the cytochrome p450
mixed-function oxidase system to chloral (trichloroacetaldehyde), which is
subsequently oxidized to trichloroacetic acid or reduced to trichloroethanol
(free and conjugated).
Trichloroethylene is
converted to trichloroethanol, free and conjugated with glucuronic acid. The
initial conversion of the solvent is to chloral hydrate. Trichloroacetic and the
monochloroacetic acid and trichloroethanol are found in the urine. Urinary
metabolites can be used for assessment of exposure.
The toxicity & metab of trichloroethylene
(TRI) were studied in renal proximal tubular (PT) & distal tubular (DT)
cells from male Fischer 344 rats. TRI was slightly toxic to both PT and DT
cells, & inhibition of cytochrome P450 (P450; substrate, reduced-flavoprotein:oxygen
oxidoreductase (RH-hydroxylating or -epoxidizing); EC 1.14.14.1) increased TRI
toxicity only in DT cells. In untreated cells, glutathione (GSH) conjugation of
TRI to form S-(1,2-dichlorovinyl)glutathione (DCVG) was detected only in PT
cells. Inhibition of P450 transiently increased DCVG formation in PT cells &
resulted in detection of DCVG formation in DT cells. Formation of DCVG in PT
cells was described by a two-component model (apparent Vmax values of 0.65 &
0.47 nmol/min per mg protein & Km values of 2.91 & 0.46 mM). Cytosol
isolated from rat renal cortical, PT, & DT cells expressed high levels of
GSH S-transferase (GST; RX:glutathione R-transferase; EC 2.5.1.18) alpha (GSTalpha)
but not GSTpi. Low levels of GSTmu were detected in cortical & DT cells.
Purified rat GSTalpha2-2 exhibited markedly higher affinity for TRI than did
GSTalpha1-1 or GSTalpha1-2, but each isoform exhibited similar Vmax values.
Triethyltinbromide (TETB) (9 muM) inhibited DCVG formation by purified
GSTalpha1-1 & GSTalpha2-2, but not GSTalpha1-2. Bromosulfophthalein (BSP) (4
muM) only inhibited DCVG formation by GSTalpha2-2. TETB & BSP inhibited
approximately 90% of DCVG formation in PT cytosol but had no effect in DT
cytosol. This suggests that GSTalpha1-1 is the primary isoform in rat renal PT
cells responsible for GSH conjugation of TRI. These data ... describe the metab
of TRI by individual GST isoforms & suggest that DCVG feedback inhibits TRI
metab by GSTs.
A major focus in the study of metab &
disposition of trichloroethylene (TCE) is to identify
metabolites that can be used reliably to assess flux through the various
pathways of TCE metab & to identify those metabolites that are causally
associated with toxic responses. ... Sex- & species-dependent differences in
biotransformation pathways ... can play an important role in the utility of
laboratory animal data for understanding the pharmacokinetics &
pharmacodynamics of TCE in humans. Sex-, species-, & strain-dependent
differences in absorption & distribution of TCE may play some role in
explaining differences in metab & susceptibility to toxicity from TCE
exposure. The majority of differences in susceptibility, however, are likely due
to sex-, species-, & strain-dependent differences in activities of the
various enzymes that can metabolize TCE & its subsequent metabolites. An
addtl factor that plays a role in human health risk assessment for TCE is the
high degree of variability in the activity of certain enzymes. TCE undergoes
metab by two major pathways, cytochrome P450 (P450)-dependent oxidation &
conjugation with glutathione (GSH). Key P450-derived metabolites of TCE that
have been associated with specific target organs, such as the liver & lungs,
include chloral hydrate, trichloroacetate, & dichloroacetate. Metabolites
derived from the GSH conjugate of TCE, in contrast, have been associated with
the kidney as a target organ. Specifically, metab of the cysteine conjugate of
TCE by the cysteine conjugate beta-lyase generates a reactive metabolite that is
nephrotoxic & may be nephrocarcinogenic. Although the P450 pathway is a
higher activity & higher affinity pathway than the GSH conjugation pathway,
one should not automatically conclude that the latter pathway is only important
at very high doses.
Metabolites of toluene (hippuric acid) & trichloroethylene
(total trichloro cmpds) have been estimated in labotratory rats after microsomal
induction by phenobarbital. Phenobarbital pretreatment accelerated the removal
of total trichloro cmpds, however, excretion of hippuric acid was moderately
diminished. Results on cytochrome P450 suggest that microsomal induction by
phenobarbital was higher in trichloroethylene treated
rats than toluene treated rats. It is concluded that in addition to distinct
substrate specificity of CYP450 isozymes several other factors like Vmax/Km
& QH determine the metab of organic solvents.
A ... study investigated the possible
differences in metabolism and pharmacokinetics between mice and rats exposed to trichloroethylene.
A comparison of metabolized trichloroethylene on a wt
basis indicates that the mouse metabolizes 2.2 times more than the rat at 10 ppm
and 3.6 times at 600 ppm. Hepatic macromolecular binding was greater in the
mouse than in the rat. The binding data suggest that tumor formation in the
mouse exposed to trichloroethylene occurred via a
nongenetic mechanism and tumors are not expected if liver injury does not occur.
Absorption, Distribution & Excretion:
... It can penetrate intact human skin.
PLACENTAL TRANSMISSION DATA: TIME TO APPEAR IN
FETUS--2 MIN; TIME TO FETAL/MATERNAL CONCN EQUILIBRIUM--6 MIN; FETAL/MATERNAL
CONCENTRATION RATIO--1.0 /FROM TABLE/
... A DAILY EXPOSURE LEVEL OF APPROXIMATELY
100 PPM, ONLY ONE-THIRD OF THE RETAINED TRICHLOROETHYLENE
(CALCULATED) IS EXCRETED AS METABOLITES IN THE URINE DURING THE WORK DAY.
BINDING OF TCE TO LIVER MICROSOMAL PROTEINS OF
MALE B6C3 HYBRID MICE WAS 46% HIGHER THAN /BINDING OF/ (14)C-TCE TO MICROSOMAL
PROTEINS FROM MALE OSBORNE-MENDEL RATS.
10 VOLUNTEER STUDENTS WERE EXPOSED TO 250-380
PPM OF TRICHLOROETHYLENE FOR 160 MIN. RETENTION
AMOUNTED TO 36%. 16% OF THE RETAINED AMT WAS ELIMINATED THROUGH RESPIRATION
AFTER EXPOSURE. TRICHLOROACETIC ACID EXCRETION IN FEMALES WAS 2-3 TIMES MORE
THAN THAT IN MALES FOR THE 1ST 24 HR AFTER EXPOSURE. TWICE AS MUCH
TRICHLOROETHANOL WAS EXCRETED IN MALES THAN IN FEMALES FOR THE 1ST 12 HR. THESE
FINDINGS SUGGEST A SEX DIFFERENCE IN HUMAN METABOLISM OF TRICHLOROETHYLENE.
The blood concn of trichloroethylene
during inhalation and elimination /in humans/ closely parallels alveolar gas
concn. Trichloroethylene most rapidly attains
equilibrium by passive diffusion into the vessel rich group of tissues (VRG)
(brain, heart, kidneys, liver, endocrine and digestive systems), more slowly
with lean mass (MG) (muscle and skin) and lastly with adipose tissue (FG). As
determined from elimination kinetics following exposure, trichloroethylene
distributes from blood into these 3 major compartments at approx rate constants
of VRG: 17 hr(-1) (half-life, 2.4 min), MG: 1.7 hr(-1) (t/2, 25 min) and FG: 0.2
hr(-1) (half-life, 3.5 hr). While MG is 50% of the body vol versus 20% for FG,
saturation and desaturation proceeds more rapidly from the MG compartment than
the FG compartment because of the considerably greater solubility of trichloroethylene
in lipids. Thus, variations in trichloroethylene uptake
between individuals is influenced first by lean body mass and second by adipose
tissue mass.
Careful balance studies using GC methodology
show, that after single or repeated daily exposures to trichloroethylene
concentrations between 50 and 380 ppm, an average of 11% of /absorbed/ trichloroethylene
is eliminated unchanged by the lung (half-life= 5 hr), 2% of the dose is
eliminated as trichloroethanol by the lung (half-life 10 to 12 hr) and 58% is
eliminated as urinary metabolites. The remaining 30% of the dose has been
postulated to be metabolized by additional pathways or routes of elimination of
one or more unknown metabolites.
The ratio between trichloroethylene
exposure and urinary trichloroacetic acid excretion appears to decrease with
age.
Pure trichloroethylene
is absorbed through mouse abdominal skin at a rate of 55 nmol/sq cm/min.
When (14)C-trichloroethylene
was administered by im injection at a dose of 50 mg/kg, the radioactivity
excreted in the urine and feces ranged from 40-60% of the dose in chimpanzees,
11-28% in baboons, and 7-40% in rhesus monkeys.
When 18 mg/kg of trichloroethylene
in 5 ml of water or corn oil was intragastrically administered to fasting rats
(400 g), the peak blood concn (5.6 minutes for aqueous solution) averaged 15
times higher for water than for corn oil solution (14.7 vs <1.0 ug/ml). The
peak blood concn was reached faster for water than for oil solution, which
exhibited a second delayed peak 80 minutes post-absorption.
In humans, the blood/air partition coefficient
ranges from 9 to 15. Daily body uptake has been estimated to be approximately 6
mg/kg body weight, for an exposure of 4 hr at 378 mg/cu m and /is not
influenced/ by the quantity of adipose tissue.
Trichloroethylene
retention varies according to physical activity. Under laboratory conditions,
human volunteers at rest exposed to concentrations of 540 or 1080 mg/cu m for 30
minutes, 50% of the quantity inhaled was retained. The percentage retained
decreased from 50% to 25% when activity rose from rest to a 150 watt workload,
but, because of increased ventilation, the absolute amount absorbed still
increased.
Trichlororethylene is expired from the lungs
for 2 days after exposure, & traces may be present on the 3rd day. About 8%
of the retained material is excreted as metabolites in the feces, but most is
excreted in the urine. /It was/ found that an average of 73% of the trichloroethylene
retained by men & women after inhalation could be recovered in the urine as
follows: monochloroacetic acid, 4%; trichloroacetic acid, 19%; &
trichloroethanol, 50%. In humans, excretion of the metabolites of trichloroethylene
is fastest for monochloroacetic acid, intermediate for trichloroethanol, &
slowest for trichloroacetic acid. Following the use of trichloroethylene
as an anesthetic, trichloroacetic acid may be detected in the urine for 5-12
days. Following accidental ingestion of trichloroethylene,
trichloroacetic acid was found in the serum & urine for 27 days.
Trichloroethylene
& its metabolites appear to cross the placenta readily in many species. In
mice, inhalation of trichloroethylene resulted in
accumulation of its metabolite, trichloroacetic acid, in amniotic fluid.
A physiologically based pharmacokinetic (PBPK)
model was developed that provides a comprehensive description of the kinetics of
trichloroethylene (TCE) & its metabolites,
trichloroethanol (TCOH), trichloroacetic acid (TCA), & dichloroacetic acid (DCA),
in the mouse, rat, & human for both oral & inhalation exposure. The
model includes descriptions of the three principal target tissues for cancer
identified in animal bioassays: liver, lung, & kidney. Cancer dose metrics
provided in the model include the area under the concn curve (AUC) for TCA &
DCA in the plasma, the peak concn & AUC for chloral in the tracheobronchial
region of the lung, & the production of a thioacetylating intermediate from
dichlorovinylcysteine in the kidney. Addtl dose metrics provided for noncancer
risk assessment include the peak concns & AUCs for TCE & TCOH in the
blood, as well as the total metab of TCE divided by the body weight. Sensitivity
& uncertainty analyses were performed on the model to evaluate its
suitability for use in a pharmacokinetic risk assessment for TCE. Model
predictions of TCE, TCA, DCA, & TCOH concns in rodents & humans are in
good agreement with a variety of experimental data, suggesting that the model
should provide a useful basis for evaluating cross-species differences in
pharmacokinetics for these chemicals. In the case of the lung & kidney
target tissues, however, only limited data are available for establishing
cross-species pharmacokinetics. As a result, PBPK model calculations of target
tissue dose for lung & kidney should be used with caution.
Trichloroethylene (TCE)
pharmacokinetics have been studied in experimental animals & humans for over
30 yr. Compartmental & physiologically based pharmacokinetic (PBPK) models
have been developed for the uptake, distribution, & metab of TCE & the
production, distribution, metab, & elimination of P450-mediated metabolites
of TCE. TCE is readily taken up into systemic circulation by oral &
inhalation routes of exposure & is rapidly metabolized by the hepatic P450
system and to a much lesser degree, by direct conjugation with glutathione.
Recent PBPK models for TCE & its metabolites have focused on the major
metabolic pathway for metab of TCE (P450-mediated metabolic pathway). This
article briefly reviews selected published compartmental & PBPK models for
TCE. Trichloroacetic acid (TCA) is considered a principal metabolite responsible
for TCE-induced live r cancer in mice. Liver cancer in mice was considered a
critical effect by the U.S. EPA for deriving the current maximum contaminant
level for TCE in water. In the literature both whole blood & plasma
measurements of TCA are reported in mice & humans. To reduce confusion about
disparately measured & model-predicted levels of TCA in plasma & whole
blood, model-predicted outcomes are compared for first-generation (plasma) &
second-generation (whole blood) PBPK models published by Fisher &
colleagues. Qualitatively, animals & humans metabolize TCE in a similar
fashion, producing the same metabolites. Quantitatively, PBPK models for TCE
& its metabolites are important tools for providing dosimetry comparisons
between experimental animals & humans. TCE PBPK models can be used today to
aid in crafting scientifically sound public health decisions for TCE.
Trichloroethylene (TCE)
... is oxidized by high-affinity, low-capacity cytochrome P450 isozymes &
subsequently converted to metabolites, some of which are carcinogenic in mice
& rats. Although the initial oxidation step is known to be rate-limiting
& saturable, the oral dosage-range over which saturation materializes is
unclear. One objective of this study was to characterize the dose-dependency of
GI absorption of TCE & its kinetics over a wide range of oral bolus doses. A
related objective was to investigate cause(s) of the apparent saturation
kinetics observed. ... /TCE was/ given in doses of 2 to 1200 mg/kg bw via the
stomach tube. ... The rate of GI absorption of TCE diminished as the dosage
increased. Pharmacokinetic analysis indicated that TCE was eliminated by
capacity-limited hepatic metab, with incursion into nonlinear kinetics with
bolus doses :8 to 16 mg/kg. Effects of p-nitrophenol, a competitive metabolic
inhibitor, were manifest at a high, but not at a low TCE dose. Gavage bolus
doses as high as 1200 mg/kg did not cause rapid elevation of serum enzyme
levels, typical of the solvation of hepatocellular membranes observed after
portal vein admin of TCE ... . No evidence of cytochrome P4502E1 (CYP2E1)
destruction was seen with oral doses up to 1000 mg/kg. Instead, CYP2E1 activity
was induced as early as 1 h postdosing. Induction was maximal at 12 hr, then
returned toward controls during the next 12 h. Pretreatment with cycloheximide
did not reduce CYP2E1 activity in rats given 432 or 1000 mg TCE/kg, suggesting
that binding of TCE to CYP2E1 may stabilize the isozyme. Metabolic saturation,
in concert with relatively slow GI absorption, are responsible for the prolonged
elevation of blood TCE levels in rats given high TCE doses, while suicidal
inactivation of CYP2E1 & hepatocellular injury apparently play little role.
... To assess the dermal bioavailability of trichloroethylene
(TCE), exhaled breath was monitored ... using an ion trap mass spectrometer
(MS/MS) to track the uptake & elimination of TCE from dermal exposures in
rats & humans. A physiologically based pharmacokinetic (PBPK) model was used
to estimate total bioavailability. Male F344 rats were exposed to TCE in water
or soil under occluded or nonoccluded conditions by applying a patch to a
clipper-shaved area of the back. Rats were placed in off-gassing chambers &
chamber air TCE concn was quantified for 3-5 h post-dosing using the MS/MS.
Human volunteers were exposed either by whole-hand immersion or by attaching
patches containing TCE in soil or water on each forearm. Volunteers were
provided breathing air via a face mask to eliminate inhalation exposure, &
exhaled breath was analyzed using the MS/MS. The total TCE absorbed & the
dermal permeability coefficient (KP) were estimated for each individual by
optimization of the PBPK model to the exhaled breath data & the changing
media &/or dermal patch concns. Rat skin was significantly more permeable
than human skin. Estimates for KP in a water matrix were 0.31 : 0.01 cm/h &
0.015 : 0.003 cm/hr in rats & humans, respectively. KP estimates were more
than three times higher from water than soil matrices in both species. KP values
calculated using the standard Fick's Law equation were strongly affected by
exposure length & volatilization of TCE. In comparison, KP values estimated
using noninvasive real-time breath analysis coupled with the PBPK model were
consistent, regardless of volatilization, exposure concentration, or duration.
In lifetime bioassays, trichloroethylene
(TCE, CAS No. 79-01-6) causes liver tumors in mice following gavage, liver &
lung tumors in mice following inhalation, & kidney tumors in rats following
gavage or inhalation. Recently developed pharmacokinetic models provide
estimates of internal, target-organ doses of the TCE metabolites thought
responsible for these tumor responses. Dose-response analyses following recently
proposed methods for carcinogen risk assessment from the U.S. EPA are conducted
on the animal tumor data using the pharmacokinetic dosimeters to derive a series
of alternative projections of the potential carcinogenic potency of TCE in
humans exposed to low environmental concns. Although mechanistic considerations
suggest action of possibly nonlinear processes, dose-response shapes in the
observable range of tumor incidence evince little sign of such patterns. Results
depend on which of several alternative pharmacokinetic analyses are used to
define target-organ doses. Human potency projections under the U.S. EPA linear
method based on mouse liver tumors & internal dosimetry equal or somewhat
exceed calculations based on admin dose, & projections based on mouse liver
tumors exceed those from mouse lung or rat kidney tumors. Estimates of the
carcinogenic potency of the two primary oxidative metabolites of
TCE--trichloroacetic acid & dichloroacetic acid, which are mouse liver
carcinogens in their own right--are also made, but it is not clear whether the
carcinogenic potency of TCE can be quantitatively ascribed to metabolic
generation of these metabolites.
Regulatory agencies are challenged to conduct
risk assessments on chemical mixtures without full information on toxicological
interactions that may occur at real-world, low-dose exposure levels. The present
study was undertaken to investigate the pharmacokinetic impact of low-dose
coexposures to toluene & trichloroethylene in vivo
in male F344 rats using a real-time breath analysis system coupled with
physiologically based pharmacokinetic (PBPK) modeling. Rats were exposed to
compounds alone or as a binary mixture, at low (5 to 25 mg/kg) or high (240 to
800 mg/kg) dose levels. Exhaled breath from the exposed animals was monitored
for the parent cmpds & a PBPK model was used to analyze the data. At low
doses, exhaled breath kinetics from the binary mixture exposure compared with
those obtained during single exposures, thus indicating that no metabolic
interaction occurred with the se low doses. In contract, at higher doses the
binary PBPK model simulating independent metab was found to under predict the
exhaled breath concn, suggesting an inhibition of metab. Therefore the binary
mixture PBPK model was used to compare the measured exhaled breath levels from
high- & low-dose exposures with the predicted levels under various metabolic
interaction simulations (competitive, noncompetitive, or uncompetitive
inhibition). Of these simulations, the optimized competitive metabolic
interaction description yielded a Ki value closest to the Km of the inhibitor
solvent, indicating that competitive inhibition is the most plausible type of
metabolic interaction between these two solvents.
Biological Half-Life:
THE BIOL HALF-LIVES OF THE URINARY METABOLITES
OF HUMANS OCCUPATIONALLY EXPOSED TO TRICHLOROETHYLENE
WAS APPROX 41 HR.
The half-life of trichloroethylene
in exhaled air & in the blood depends on the length of exposure & on the
time of sampling after exposure. ... Maximum concn /of trichloroethanol/ in
blood & urine /is reached/ almost directly after exposure. ... concn decr
with a half-life of about 10-15 hr. ... Concn of trichloroacetic acid in both
the blood & urine incr for up to 20-40 hr after /a single/ exposure. ...
concn decr with a half-life of about 70-100 hr.
Mechanism of Action:
TCE WAS INCUBATED WITH RAT LIVER MICROSOME,
NADPH AND RNA (FROM YEAST). THE METABOLITES WERE IRREVERSIBLY BOUND TO
MICROSOMAL PROTEINS. HYDROLYSIS OF RNA & SEPARATION OF NUCLEOSIDES SHOWED
DIFFERENT ALKYLATION PRODUCTS ARISING FROM TCE & VINYL CHLORIDE. ... NEWBORN
RATS WERE EXPOSED FOR 10 WEEKS TO 2000 PPM VINYL CHLORIDE OR TRICHLOROETHYLENE
(8H/DAY; 5 DAYS/WEEK). AFTER THIS PERIOD LIVERS OF THE ANIMALS WERE STAINED FOR
NUCLEOSIDE-5-TRIPHOSPHATASE. WHEREAS THE VINYL CHLORIDE EXPOSED RATS SHOWED
FOCAL HEPATOCELLULAR DEFICIENCIES IN THIS ENZYME, WHICH ARE SUPPOSED TO
REPRESENT AN EARLY SIGN OF MALIGNANCY, NO SUCH CHANGES WERE INDUCED BY TRICHLOROETHYLENE
EXPOSURE.
BINDING CONSTANTS (KS) FOR INTERACTION WITH
RAT LIVER MICROSOMAL P450 FOR ITS METAB TO CHLORAL HYDRATE WERE NOT ALTERED BY
INDUCTION WITH PHENOBARBITAL, 3-METHYLCHOLANTHRENE OR SPIRONOLACTONE. TCE
APPEARED TO BE ACTIVATED BY CYTOCHROME TO ACTIVELY ALTER HEME MOIETY OF THE
CYTOCHROME P450.
Interactions:
DISULFIRAM IS SAID TO INHIBIT THE OXIDATION
/OF TRICHLOROETHYLENE/ IN MAN TO THE MORE TOXIC
TRICHLOROETHANOL (AND THENCE TO TRICHLOROACETIC ACID) ...
IN VITRO, ADDITION OF TCE DECR METAB OF
ETHYLMORPHINE & HEXOBARBITAL BY RAT HEPATIC MICROSOMES. IN VIVO, TCE
INHIBITED HEXOBARBITAL METABOLISM IN RATS.
BIOCHEM & TOXICOLOGICAL EFFECTS OF
COMBINED EXPOSURE TO 1,1,1-TRICHLOROETHANE (500 PPM) & TCE (200 PPM) FOR 4
DAYS 6 HR DAILY CAUSED ACCUM OF 1,1,1-TRICHLOROETHANE IN PERIRENAL FAT. FURTHER
EXPOSURE ON DAY 5 CAUSED RAPID INCR IN VARIOUS ORGAN CONTENTS OF BOTH SOLVENTS
WITH DEPRESSION OF BRAIN RNA.
Rabbits were given 10 mg/kg doses of caffeine
30 minutes prior to exposure to 6000 ppm (32,280 mg/cu m) of trichloroethylene
under dynamic airflow conditions. Epinephrine was infused until arrhythmias
occurred after 7.5, 15, 30, 45, and 60 minutes of exposure and 15 and 30 minutes
post-exposure. An increase in epinephrine-induced arrhythmias in trichloroethylene-exposed
rabbits was observed when the animals were treated with caffeine and challenged
with doses of epinephrine as low as 0.5 ug/kg.
Phenobarbital administration to rats or
hamsters in vivo increases the oxidation of trichloroethylene.
This results in an incr in the conversion of trichloroethylene
to trichloroacetaldehyde.
Compared to chloral hydrate alone, ingestion
of ethanol 30 minutes after chloral hydrate resulted in higher and more
prolonged concentrations of plasma trichloroethanol and in lower plasma
trichloroacetic acid levels and in urinary trichloroethanol glucuronide. ...
Disulfiram (1.35 mmol/kg) was administered
perorally to rabbits 24 and 6 hr prior to a 1 hr exposure (6000 ppm 32,280 mg/cu
m) of trichloroethylene. When challenged with 0.5-3.0
ug/kg epinephrine, disulfiram prevented epinephrine-induced arrhythmias.
Isopropanol and acetone ... cause enhanced
hepatotoxicity with ... trichloroethylene.
Studies /conducted/ with rats /indicate/ that
the effects of trichloroethylene were more pronounced
in the animals that were fed a high carbohydrate diet than those on a high
protein diet. /Concentration of trichloroethylene not
specified/
Rats exposed to 37,000, 42,000, and 56,000
mg/cu m of trichloroethylene vapor for two hours
exhibited elevated activities of serum glutamic pyruvic transaminase, glutamic
oxaloacetic transaminase, and isocitrate dehydrogenase. Hepatotoxicity
(indicated by the increased levels of these hepatic enzymes in the serum) was
greatly enhanced by pretreatment with 3-methylcholanthrene.
To elicit the "degreaser's flush,"
ethanol was administered to seven male volunteers who were repeatedly exposed to
trichloroethylene (TCE) vapor. In six exposed subjects,
transient vasodilatation of superficial skin vessels occured after the ingestion
of small amounts of ethanol (<0.5 ml/kg body weight). The dermal response
reached maximum intensity 30 minutes after its onset and then faded completely
within 60 minutes. Two factors appear necessary before the dermal response can
be elicited: (1) repeated exposures to TCE and (2) ingestion of alcohol.
... The induction of the hepatic microsomal
mixed-function oxidase system by drugs, taken for therapeutic reasons, or by
exposure to certain environmental chemicals (e.g., phenobarbital, toluene, PCBs)
can bring about an incr rate of trichloroethylene
metabolism.
Elimination of trichloroacetic acid &
trichloroethanol was studied in rats exposed to trichloroethylene
alone, or in combination with xylene, at 4.5 mmol/cu m air for five consecutive
days. Prior to each inhalation, the rats were pretreated per os with ethyl
alcohol at 1366 mg/kg bw or 2732 mg/kg bw. Both xylene & ethanol given
separately, dependent on the dose, decreased urine elimination of
trichloroacetic acid & trichloroethanol by about 34% (1366 mg/kg) & 45%
(2732 mg/kg), respectively. Under conditions of the combined ethanol/xylene
exposure, the xenobiotics reduced the elimination of trichloroethylene
& trichloroethanol by about 80% & 20% respectively.
Neonatal male B6C3F1 (CRL, MI) mice were
injected ip at 15 days of age with either 2.5 or 10 ug/g body weight
ethylnitrosourea (ENU) (26-33/group) or 2 ul/g body weight of 0.1M sodium
acetate (32/group) as the solvent control. At 28 days of age, the mice were
placed on drinking water containing 3 or 40 mg/l trichloroethylene
and they were killed after 61 weeks exposure to trichloroethylene.
Controls (22-23/group) were given 0, 2.5, or 10 ug/g body weight
ethylnitrosourea + sodium chloride (2 g/l). Trichloroethylene
resulted in a significant increase in liver weight (p< 0.001) when given at
40 mg/l to mice pretreated with 2.5 ug/g body weight of ethylnitrosourea. Trichloroethylene
alone, however, did not increase the incidence of adenomas or hepatocellular
carcinomas above control levels.
Pharmacology:
Therapeutic Uses:
Anesthetics, Inhalation; Solvents
Trichloroethylene ...
is no longer used /as anesthetic agent/.
MEDICATION (VET): INHALATION ANESTHETIC
Dental anesthetic. /Former use in USA/
INHALATION ANALGESIC. /Former use in USA/
Drug Warnings:
TRICHLOROETHYLENE HAS
BEEN REPORTED TO CAUSE CONVULSIONS IN CHILDREN; THEREFORE, IT SHOULD NOT BE USED
IN PATIENTS WITH CONVULSIVE DISORDERS.
Patients exposed to trichloroethylene
should be warned of the potential adverse effects of ethanol ingestion.
Isopropanol and acetone ... cause enhanced
hepatotoxicity with ... trichloroethylene.
...Its anesthetic action is weak. Its low
volatility appears in part to be responsible for this effect. ... Apparatus that
employs bubbling oxygen assists in accelarating the volatility of the anesthetic
to increase its potency. Because of its inherent weakness as an anesthetic,
induction of anesthesia is slow. Cardiac arrhythmias produced by the anesthetic
are unfavorable. Trichloroethylene cannot be used in a
closed circuit with soda lime because of formation of a toxic product.
Relaxation of abdominal musculature is poor
during trichloroethylene anesthesia.This effect is
similar to other agents (eg, ketamine, alpha-chloralose) that do not induce
Stage III anesthesia. Trichloroethylene is considered
unsatisfactory for this type of surgery unless it is used in conjunction with a
skeletal muscle relaxant. It has very little if any effect upon uterine
function. It readly crosses the placenta to reach the fetal circulation of
sheep, goats, and probably other species.
Interactions:
DISULFIRAM IS SAID TO INHIBIT THE OXIDATION
/OF TRICHLOROETHYLENE/ IN MAN TO THE MORE TOXIC
TRICHLOROETHANOL (AND THENCE TO TRICHLOROACETIC ACID) ...
IN VITRO, ADDITION OF TCE DECR METAB OF
ETHYLMORPHINE & HEXOBARBITAL BY RAT HEPATIC MICROSOMES. IN VIVO, TCE
INHIBITED HEXOBARBITAL METABOLISM IN RATS.
BIOCHEM & TOXICOLOGICAL EFFECTS OF
COMBINED EXPOSURE TO 1,1,1-TRICHLOROETHANE (500 PPM) & TCE (200 PPM) FOR 4
DAYS 6 HR DAILY CAUSED ACCUM OF 1,1,1-TRICHLOROETHANE IN PERIRENAL FAT. FURTHER
EXPOSURE ON DAY 5 CAUSED RAPID INCR IN VARIOUS ORGAN CONTENTS OF BOTH SOLVENTS
WITH DEPRESSION OF BRAIN RNA.
Rabbits were given 10 mg/kg doses of caffeine
30 minutes prior to exposure to 6000 ppm (32,280 mg/cu m) of trichloroethylene
under dynamic airflow conditions. Epinephrine was infused until arrhythmias
occurred after 7.5, 15, 30, 45, and 60 minutes of exposure and 15 and 30 minutes
post-exposure. An increase in epinephrine-induced arrhythmias in trichloroethylene-exposed
rabbits was observed when the animals were treated with caffeine and challenged
with doses of epinephrine as low as 0.5 ug/kg.
Phenobarbital administration to rats or
hamsters in vivo increases the oxidation of trichloroethylene.
This results in an incr in the conversion of trichloroethylene
to trichloroacetaldehyde.
Compared to chloral hydrate alone, ingestion
of ethanol 30 minutes after chloral hydrate resulted in higher and more
prolonged concentrations of plasma trichloroethanol and in lower plasma
trichloroacetic acid levels and in urinary trichloroethanol glucuronide. ...
Disulfiram (1.35 mmol/kg) was administered
perorally to rabbits 24 and 6 hr prior to a 1 hr exposure (6000 ppm 32,280 mg/cu
m) of trichloroethylene. When challenged with 0.5-3.0
ug/kg epinephrine, disulfiram prevented epinephrine-induced arrhythmias.
Isopropanol and acetone ... cause enhanced
hepatotoxicity with ... trichloroethylene.
Studies /conducted/ with rats /indicate/ that
the effects of trichloroethylene were more pronounced
in the animals that were fed a high carbohydrate diet than those on a high
protein diet. /Concentration of trichloroethylene not
specified/
Rats exposed to 37,000, 42,000, and 56,000
mg/cu m of trichloroethylene vapor for two hours
exhibited elevated activities of serum glutamic pyruvic transaminase, glutamic
oxaloacetic transaminase, and isocitrate dehydrogenase. Hepatotoxicity
(indicated by the increased levels of these hepatic enzymes in the serum) was
greatly enhanced by pretreatment with 3-methylcholanthrene.
To elicit the "degreaser's flush,"
ethanol was administered to seven male volunteers who were repeatedly exposed to
trichloroethylene (TCE) vapor. In six exposed subjects,
transient vasodilatation of superficial skin vessels occured after the ingestion
of small amounts of ethanol (<0.5 ml/kg body weight). The dermal response
reached maximum intensity 30 minutes after its onset and then faded completely
within 60 minutes. Two factors appear necessary before the dermal response can
be elicited: (1) repeated exposures to TCE and (2) ingestion of alcohol.
... The induction of the hepatic microsomal
mixed-function oxidase system by drugs, taken for therapeutic reasons, or by
exposure to certain environmental chemicals (e.g., phenobarbital, toluene, PCBs)
can bring about an incr rate of trichloroethylene
metabolism.
Elimination of trichloroacetic acid &
trichloroethanol was studied in rats exposed to trichloroethylene
alone, or in combination with xylene, at 4.5 mmol/cu m air for five consecutive
days. Prior to each inhalation, the rats were pretreated per os with ethyl
alcohol at 1366 mg/kg bw or 2732 mg/kg bw. Both xylene & ethanol given
separately, dependent on the dose, decreased urine elimination of
trichloroacetic acid & trichloroethanol by about 34% (1366 mg/kg) & 45%
(2732 mg/kg), respectively. Under conditions of the combined ethanol/xylene
exposure, the xenobiotics reduced the elimination of trichloroethylene
& trichloroethanol by about 80% & 20% respectively.
Neonatal male B6C3F1 (CRL, MI) mice were
injected ip at 15 days of age with either 2.5 or 10 ug/g body weight
ethylnitrosourea (ENU) (26-33/group) or 2 ul/g body weight of 0.1M sodium
acetate (32/group) as the solvent control. At 28 days of age, the mice were
placed on drinking water containing 3 or 40 mg/l trichloroethylene
and they were killed after 61 weeks exposure to trichloroethylene.
Controls (22-23/group) were given 0, 2.5, or 10 ug/g body weight
ethylnitrosourea + sodium chloride (2 g/l). Trichloroethylene
resulted in a significant increase in liver weight (p< 0.001) when given at
40 mg/l to mice pretreated with 2.5 ug/g body weight of ethylnitrosourea. Trichloroethylene
alone, however, did not increase the incidence of adenomas or hepatocellular
carcinomas above control levels.
Environmental Fate & Exposure:
Environmental Fate/Exposure Summary:
Trichloroethylene's
production and use in degreasing operations as well as in plastics, appliances,
jewellery, automobile, plumbing fixtures, textiles, paper, glass and printing
industries may result in its release to the environment through various waste
streams. If released to air, a vapor pressure of 69 mm Hg at 25 deg C indicates trichloroethylene
will exist solely as a vapor in the ambient atmosphere. Vapor-phase trichloroethylene
will be degraded in the atmosphere by reaction with photochemically-produced
hydroxyl radicals; the half-life for this reaction in air is estimated to be 7
hours. If released to soil, trichloroethylene is
expected to have high mobility based upon an average Koc of 101, measured in 32
soils. Volatilization from moist soil surfaces is expected to be an important
fate process based upon a Henry's Law constant of 9.85X10-3 atm-cu m/mole. Trichloroethylene
is expected to volatilize from dry soil surfaces based upon its vapor pressure.
Cometabolic biodegradation of trichloroethylene has
been reported under aerobic conditions where additional nutrients have been
added. Under anaerobic conditions, as might be seen in flooded soils, sediments
or aquifer environments, trichloroethylene is slowly
biodegraded via reductive dechlorination; the extent and rate of degradation is
dependent upon the strength of the reducing environment. Trichloroethylene
half-lives in the field for aquifer studies range from 35 days to over 6 years.
If released into water, trichloroethylene is not
expected to adsorb to suspended solids and sediment based on an average Koc
value of 101. Volatilization from water surfaces will be an important fate
process based upon this compound's Henry's Law constant. Estimated
volatilization half-lives for a model river and model lake are 3.5 hours and 5
days, respectively. Volatilization half-lives in an experimental field mesocosm
ranged from 10.7 to 28 days. BCF values in fish ranging from 4 to 39 suggest
bioconcentration in aquatic organisms is moderate to low. Occupational exposure
to trichloroethylene has been shown to occur through
inhalation and dermal contact with this compound at workplaces where trichloroethylene
is produced or used. Extensive monitoring data indicate that the general
population may be exposed to trichloroethylene via
inhalation of ambient air, ingestion of food and drinking water, and dermal
contact with this compound and other consumer products containing trichloroethylene.
Trichloroethylene is widely detected in groundwater. (SRC)
Probable Routes of Human Exposure:
TRICHLOROETHYLENE
WHEN PRESENT IN AIR NEAR OPEN ARC WELDING MAY BE DECOMP TO LEVELS OF PHOSGENE
DANGEROUS TO HEALTH, WHEREAS THE HCL AND CL2 FORMED SIMULTANEOUSLY MAY NOT
ALWAYS PROVIDE AN ADEQUATE WARNING AGAINST THE PRESENCE OF PHOSGENE.
Many industrial workers, operating room
personnel and dentists are regularly exposed to TCE, some to large doses. The
general public encounters trichloroethylene in cleaning
fluids, some decaffeinated coffees and spice extracts.
NIOSH (NOES Survey 1981-1983) has
statistically estimated that 392,805 workers (169,851 of these are female) are
potentially exposed to trichloroethylene in the US(1).
Occupational exposure to trichloroethylene may occur
through inhalation and dermal contact with this compound at workplaces where trichloroethylene
is produced or used(SRC). Extensive monitoring data indicate that the general
population may be exposed to trichloroethylene via
inhalation of ambient air, ingestion of food and drinking water, and dermal
contact with this compound and other products containing trichloroethylene(SRC).
An open-top and an enclosed conveyor-loaded
production trichloroethylene vapor degreasers had
average emission factors of 2.6 g TCE/min and 0.67 g TCE/min, respectively(1).
Waste gases from aluminum plasma-etching processes (using chlorine containing
etchants) during semiconductor production contained trichloroethylene
at an average concn of 315.70 ng /l(2). The number of US workers exposed to TCE
is estimated to be 283,000(3). Operating room levels range from 0.3-103 ppm,
with an estimated 5000 medical, dental and hospital personnel being routinely
exposed(1). Air levels at a dial assembly workshop in Japan measured 25-100 ppm;
degreasing room levels, 150-250 ppm(3). Trichloroethylene
was detected in 6% of 7705 solvent air samples reported from different
industries in Norway and stored in the EXPO occupational exposure database(4).
23-41% of trichloroethylene
in feed water to showers was lost with a water temperature of 23 to 40 deg C(1).
Trichloroethylene was detected in chlorinated swimming
pool water from a pool in Gdansk, Poland at concns of not detected (detection
limit, on average, 0.01 ug/cu dm) to 13.3 ug/cu dm for 4 different dates in
1991(2).
Body Burden:
Therapeutic or normal blood level 0.1-9 mg%
PERSONAL AIR: The exhaled breath of 73% of 26
smokers and 81% of 43 nonsmokers contained trichloroethylene
at unreported concns(1). Breath of 12.5% of 50 individuals living in the Los
Angeles area contained trichloroethylene(2). 51.2% of
personal air samples collected from these 50 individuals contained trichloroethylene(2).
Increased personal air exposures were reported following solvent use, household
cleaning, furniture stripping, visiting a dry cleaning shop, photo developing
and using paint remover of up to 220 ug/cu m from a baseline of <2 ug/cu
m(3). Personal air samples of Los Angeles and Contra Costa residents contained trichloroethylene
at concns of 7.8 (n=110, Los Angeles residents, February 1984), 6.4(n=50, Los
Angeles residents, May 1984) and 3.8 (n=67, Contra Costa residents, June
1984)(4).
Blood samples from 179 of 277 people from the
general population contained trichloroethylene at a
mean concn of 458 ng/l; a mean blood concn of 763 ng/l was reported from 63 of
113 urban workers as compared to 180 ng/l from 82 of 127 workers(1). Blood
samples collected from workers exposed to trichloroethylene
in 4 dry-cleaning shops (air concns ranged from 25-40 ppm) contained this
compound (median=3.39 umol /l after work (range=0.46-12.71), 0.38 umol /l before
work (range=0.15-3.58)(2). Urine samples from the same workers contained the trichloroethylene
metabolite, trichloroethanol (median=54.89 umol/mol creatinine,
range=5.30-177.67 after work; median=9.70 umol/mol creatinine, range=0.38-35.65
before work)(2). Kidney (n=9), lung (n=13), and muscle (n=16) tissues collected
from humans in Turku, Finland in 1987 contained trichloroethylene
at 0.7, 0.02, and 0.2 ug/kg, respectively(3). 20% of composite adipose tissue
samples collected in FY82 (n=46 composite samples) contained trichloroethylene(4).
Breathing air samples from 30 residents of Tokyo, Japan had a mean concn of 2.0
ug/cu m trichloroethylene with a calculated daily
intake due to breathing ambient air of 40 ug/person (men 24.9 ug/person; women
51.5 ug/person)(5). Breath samples of Los Angeles and Contra Costa residents
contained trichloroethylene at concns of 1.6 (n=110,
Los Angeles residents, February 1984), 1.0 (n=50, Los Angeles residents, May
1984) and 0.6 (n=67, Contra Costa residents, June 1984)(6).
Trichloroethylene was
detected in mother's milk samples from 4 US urban areas, with 8 of 8 samples
testing pos(1). Concns in post-mortem wet tissue samples were 1-32 ppb(2).
Breath samples Love Canal residents, Niagara Falls, NY contained a trace of trichloroethylene
with 4 of 9 samples pos; blood - 0.09.50 ppb, 6 of 9 samples pos; and urine -
40-550 parts/trillion, 9 of 9 samples pos(3). Concns in whole blood specimens
from 250 subjects ranged from not detected to 1.5 ppb, with a 0.4 ppb avg(4).
Trichloroethylene was
detected in the blood of 13 of 677 samples taken from non-occupationally exposed
Americans (detection limit= 0.010 ppb(1). Trichloroethylene
was measured in blood samples collected from 79 humans at concns ranging from
<0.015 to 0.090 ug/l(2). Exhaled breath from humans following both inhalation
and dermal exposures during showering or dermal exposure following bathing using
normal tap water contained trichloroethylene at concns
up to 0.32 ug/cu m/ug/l(3).
Natural Pollution Sources:
Trichloroethylene is
not known to occur as a natural product.
Artificial Pollution Sources:
Trichloroethylene's
production and use in degreasing operations in five main industrial groups
(furniture and fixtures, fabricated metal products, electric and electronic
equipment, transport equipment and miscellaneous manufacturing industries)(1)
may result in its release to the environment through various waste streams(SRC).
It is also used in plastics, appliances, jewellery, automobile, plumbing
fixtures, textiles, paper, glass and printing industries(1). Air emissions from
metal degreasing plants contain trichloroethylene(2);
it has also been reported in wastewater from metal finishing, paint and ink
formulation, electrical/electronic components, and rubber processing
industries(3).
Environmental Fate:
TERRESTRIAL FATE: Based on a classification
scheme(1), an average Koc value of 101, based on measurements in 32 soils(2),
indicates that trichloroethylene is expected to have
high mobility in soil(SRC). Volatilization of trichloroethylene
from moist soil surfaces is expected to be an important fate process(SRC) given
a Henry's Law constant of 9.85X10-3 atm-cu m/mole(3). The potential for
volatilization of trichloroethylene from dry soil
surfaces may exist(SRC) based upon a vapor pressure of 69 mm Hg(4). The initial
percentage of trichloroethylene in the gas (24, 52,
57%), liquid (5, 3, 4%) and adsorbed (71, 45, 39%) phases was determined in
three soils, respectively (Rindge, 11.2% organic matter, 35.4% moisture; Yolo,
2.2% organic matter, 11.7% moisture; Reiff, 1.4% organic matter, 13.9%
moisture)(5). Trichloroethylene is resistant to aerobic
biodegradation although biodegradation may proceed cometabolically(5,6). Under
anaerobic conditions, as might be seen in soil microsites, flooded soils or
aquifer sites, trichloroethylene is slowly biodegraded
via reductive dechlorination; the extent and rate of degradation is dependent
upon the strength of the reducing environment(7).
AQUATIC FATE: Based on a classification
scheme(1), an average Koc value of 101, based on measurements in 32 soils(2),
indicates that trichloroethylene is not expected to
adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces
is expected to be a major fate process for this compound in water(3) based upon
a Henry's Law constant of 9.85X10-3 atm-cu m/mole(4). Using this Henry's Law
constant and an estimation method(3), volatilization half-lives for a model
river and model lake are 3.5 hours and 5 days, respectively(SRC). Trichloroethylene
volatilization half-lives from a mesocosm field experiment in Narragansett Bay
ranged from 10.7 to 28 days(5). Trichloroethylene is
not degraded under aerobic conditions although cometabolic biodegradation has
been reported under conditions where additional nutrients have been added(6-8).
Under anaerobic conditions, as might be seen in sediments or groundwater, trichloroethylene
is slowly biodegraded via reductive dechlorination; the extent and rate of
degradation is dependent upon the strength of the reducing environment(9).
According to a classification scheme(10), BCF values ranging from 4.0 in
carp(11) to 39 in rainbow trout(12), suggests the potential for bioconcentration
in aquatic organisms is low to moderate.
ATMOSPHERIC FATE: According to a model of
gas/particle partitioning of semivolatile organic compounds in the
atmosphere(1), trichloroethylene, which has a vapor
pressure of 69 mm Hg at 25 deg C(2), is expected to exist solely as a vapor in
the ambient atmosphere. Vapor-phase trichloroethylene
is degraded in the atmosphere by reaction with photochemically-produced hydroxyl
radicals(SRC); the half-life for this reaction in air is estimated to be 7
days(SRC), calculated from its rate constant of 2.36X10-12 cu cm/molecule-sec at
25 deg C(3). Phosgene, dichloroacetyl chloride, chloroform and formyl chloride
are formed from the reaction of trichloroethylene with
hydroxyl radicals(4-6).
Environmental Biodegradation:
AEROBIC: Under aerobic conditions, trichloroethylene
is biodegraded only in the presence of another compound that can support
microbial growth in a process called cometabolism; biodegradation is generally
complete and vinyl chloride is not produced(2). Indigenous sources of carbon
associated with soil organic matter did not support cometabolic degradation of trichloroethylene
in a soil study(3). Trichloroethylene was aerobically
degraded in a column composed of aquifer sediments by 9 and 87% during the first
6.5 months and the following 3.5 months, respectively; the initial loss of 9%
may have been due to abiotic losses such as adsorption or volatilization(1).
cis-1,2-Dichloroethylene was reported as the major product of trichloroethylene
degradation in this experiment(1). Trichloroethylene
was mineralized by up to 30% in microcosms containing soil and vegetation from a
former trichloroethylene-contaminated site (4).
Microcosms which were either non-vegetated or sterile showed mineralization of trichloroethylene,
measured as CO2 production, of 10 to 15% and 5 to 10%, respectively(4).
AEROBIC: In a municipal activated sludge
plant, 47.3, 47.8, and 0.0% of the influent trichloroethylene
concn (at 40.7 ug/l) was biodegraded, stripped and found in the waste sludge,
respectively (effluent concn of 2.0 ug/l)(1). Two laboratory scale activated
sludge reactors (AS-L, AS-H) and 2 biological aerated filter reactors (BAF-L,
BAF-H) under high- and low-loaded conditions were used to study the removal of trichloroethylene
during wastewater treatment(2). The average influent concn was 32.1 ug /l;
effluent concns for AS-L, AS-H, BAF-L, and BAF-H were 5.3, 6.1, 2.3, and 9.7 ug/l,
respectively(2). Loss due to biodegradation was 0, 0, 58, and 3% influent
loadings, respectively, while loss due to stripping was 66, 85, 34, and 67%
influent loadings, respectively(2).
ANAEROBIC: 90% of trichloroethylene
initially added to contaminated bed sediments from a freshwater lake and
incubated under methanogenic conditions for 60 days was degraded; ethene (46%),
methane(9%) and carbon dioxide (12%) were produced during its degradation(1).
Biodegradation rates for trichloroethylene in anaerobic
groundwater field studies were reported as follows: Dover Air Force Base, DE
(half-life of 2.8 years; methanogenic, redox>50 mV)(2); Vejen Landfill,
Denmark (4 in situ microcosms, methanogenic, no biodegradation over 180 days(5),
Grindsted Landfill, Denmark (methanogenic/iron- and sulfate-reducing conditions,
924 day monitoring period, half-lives=533-2310 days)(6), Plattsburgh Air Force
Base, NY (3 transects, half-lives of 0.56 years, 1.82 years, and no
degradation)(7), Tibbetts Road Superfund site, NH (3 transects, half-lives=1.17
to 1.69 years)(8), St. Joseph, MI (half-lives of 1.82, 0.53, 0.745, 0.495
years)(9,10), St. Joseph, MI (half-lives of 113, 124, and 433 days for 3
different transects)(3), Picatinny Arsenal, NJ (half- life of 0.578 years(10);
half-life of 2.2 years(11)), Sacramento, CA (half-life of 0.63 years)(10), Necco
Park, NY (half-life of 1 year)(10), Plattsburgh Air Force Base, NY (half-lives
of 0.53 years, 3.01 years and no biodegradation)(10), San Francisco, CA
(half-life of 0.16 years)(10), Cecil Field, FL (half-lives of 0.095 to 0.21
years)(10), Eielson Air Force Base, Alaska (half-life of 3.8 years), and Cape
Canaveral Air Station, Florida (half-life of 2.4 years)(12). Trichloroethylene
was degraded under methanogenic and sulfate-reducing conditions in a fractured
bedrock aquifer to ethene(4).
Biodegradation rates for trichloroethylene
in anaerobic aquifer microcosm studies were reported as follows: Wilder's Grove,
NC landfill (methanogenic, lag phase of <41 to >300 days; degradation
complete within 40 to 110 days once started)(1), Dover Air Force Base,
DE(methanogenic, half-lives of 57 and 267 days for 2 locations at site)(2),
Picatinny Arsenal, NJ (first-order rate constant of 0.001 to 0.02 per week)(3),
Picatinny Arsenal, NJ (half-lives of 1.1, 1.65, and 3.3 years)(6), Picatinny
Arsenal, NJ (first-order rate constant of 0.004 to 0.035 per week)(7), Vejen
Landfill, Denmark(4 microcosms, methanogenic, no degradation over 140-180
days)(4), Tibbetts Road Superfund site, NH (half-lives of 0.188 years(5), 0.144
years(6)), St. Joseph, MI (half-lives of 0.385 and 0.58 years), and Traverse
City, MI (half-life of 0.385 years)(6). In situ microcosm studies were conducted
in both polluted aerobic and anaerobic and in unpolluted aerobic aquifer
conditions in the Vejen City landfill; trichloroethylene
was not degraded under either oxygen condition over a 90-day period(9). Trichloroethylene
is reductively dechlorinated forming cis-1,2-dichloroethylene initially, then
vinyl chloride and possibly ethene and ethane depending on the strength of the
reducing environment(8). Under iron or sulfate-reducing conditions,
cis-1,2-dichloroethylene is the major metabolite of trichloroethylene
biodegradation while ethene is the major metabolite under methanogenic
conditions(10).
ANAEROBIC: Mass balance analysis of the loss
of trichloroethylene from an aquifer beneath Picatinny
Arsenal showed that 78, 11, and 11% of the trichloroethylene
annually removed was due to biodegradation, advective transport to a local water
body, and advection-driven volatilization, respectively(1).
Environmental Abiotic Degradation:
The rate constant for the vapor-phase reaction
of trichloroethylene with photochemically-produced
hydroxyl radicals has been measured as 2.36X10-12 cu cm/molecule-sec at 25 deg
C(1). This corresponds to an atmospheric half-life of about 7 days at an
atmospheric concn of 5X10+5 hydroxyl radicals per cu cm(1). Atmospheric
residence time based upon reaction with hydroxyl radical is 5 to 6 days(2-4)
with the production of phosgene, dichloroacetyl chloride, chloroform and formyl
chloride(3,6,7). The rate constant for the vapor-phase reaction of trichloroethylene
with nitrate radicals has been measured as 2.93X10-16 cu cm/molecule-sec at 25
deg C(13). This corresponds to an atmospheric half-life of about 114 days at an
atmospheric concn of 2.4X10+8 nitrate radicals per cu cm(14). Ozone depletion
potential values for trichloroethylene range from 0.083
to 0.13 relative to CFC-11(8). The mean value for the gas scavenging ratio for trichloroethylene
is 3.7 at 8 deg C(9). Trichloroethylene is relatively
reactive under smog conditions(12) with 60% degradation in 140 min(6) and 50%
degradation in 1 to 3.5 hours(11) reported. Trichloroethylene
is not hydrolyzed by water under normal conditions(10). Trichloroethylene
absorbs light greater than 290 nm weakly; therefore, direct photolysis is not
expected to be an important fate prcoess(10). However, slow photooxidation in
water has been noted (half-life of l0.7 months)(11).
Two pilot-scale activated sludge systems (flow
rate 35 gpm; hydraulic retention time 7.5 hours; SRT of 4 days) fed municipal
wastewater were spiked with 0.25 mg/l trichloroethylene
in combination with 46 other compounds; 103% removal of trichloroethylene
was obtained through stripping(1).
Environmental Bioconcentration:
BCF values of 17 and 39(1) were measured in
bluegill sunfish and rainbow trout, respectively. In carp, BCF values of 4.3 to
17 and 4.0 to 16.0 were reported for trichloroethylene
at 70 and 7 ug/l, respectively(2). A BCF of 302 was measured in a green alga(4).
According to a classification scheme(3), these BCF values suggest the potential
for bioconcentration in aquatic organisms is moderate to low. Marine monitoring
data suggest only moderate bioconcentration (2-25 times) of trichloroethylene(5,6).
Soil Adsorption/Mobility:
Measured Koc values of 100(1), 110(2), 72 to
180 (organic matter of <1.0 to 5%(3), 66(8), 49 (peat soil)(10), 72, 96,
142(5) and 58 (peat soil)(5). The average Kd value for trichloroethylene,
applied with a mixture of organic compounds to low organic, subsurface soils
(average foc=0.00017), was 0.093(4). Kp values of 1.06 (coarse sand), 0.67 (silty-clay
loam), 0.17 (fine sand), 6.0 (podzolic sand, % organic content=0.90), 4.2 (sandy
soil, % organic content=6.07), 32 (peat soil, % organic content=59.3) and 1.24 (Bandelier
tuff, % organic content=0.11) have been reported for trichloroethylene(11).
A study of 32 soils(foc range of 0.0012 to 0.31) reported an average Koc of
101(5). Koc values for trichloroethylene in a loess
sand, weathered shale, and unweathered shale were 123, 363, and 2691,
respectively(6). In nine different soils (foc ranging from 0.13 to 1.2%), Koc
values ranged from 69 to 209(7). Trichloroethylene from
soil samples which had been contaminated for 18 years was found to be resistant
to desorption, requiring extended periods of time for equilibration(9).
According to a classification scheme(12), these Koc values generally suggest
that trichloroethylene is expected to have moderate to
high mobility in soil. Trichloroethylene partitioned
from an aqueous solution of Bandelier tuff under equilibrium conditions to
64-81% in water, 16-23% in vapor phase, and 2-20% in the tuff(13).
In a field groundwater test, no sorption of trichloroethylene
onto organic carbon or mineral surfaces present in the sand aquifer was
observed(1). Two field studies, both of shallow confined aquifers, reported
retardation factors from 5 to 9 (foc=0.11%) and 11.4 (foc=0.11%)(2). In
undisturbed rock cores from the Coventry sandstone aquifer system (foc=0.7 to
0.8%), trichloroethylene had a retardation factor of
less than 3 indicating that it should migrate readily with water(2). Other
column studies using sand aquifer material reported retardation factors from 1.1
to 4.7(2). A retardation factor of 1.1 was reported for trichloroethylene
in the aquifer underlying the Canadian Forces Base in Borden, Ontario(3). The
initial percentage of trichloroethylene in the gas (24,
52, 57%), liquid (5, 3, 4%) and adsorbed (71, 45, 39%) phases was determined in
three soils, respectively (Rindge, 11.2% organic matter, 35.4% moisture; Yolo,
2.2% organic matter, 11.7% moisture; Reiff, 1.4% organic matter, 13.9%
moisture)(9). Sorption in these soils followed reversible, linear sorption
isotherms(9). Sorption of trichloroethylene vapor to
soil is possible; linear sorption coefficients of trichloroethylene
from the vapor phase were about one to four orders of magnitude greater than
those from the aqueous phase based on studies using six different US EPA soils
and sediments under varying moisture contents(10).
Volatilization from Water/Soil:
The Henry's Law constant for trichloroethylene
is 9.85X10-3 atm-cu m/mole(1). This Henry's Law constant indicates that trichloroethylene
is expected to volatilize rapidly from water surfaces(2). Based on this Henry's
Law constant, the volatilization half-life from a model river (1 m deep, flowing
1 m/sec, wind velocity of 3 m/sec)(2) is estimated as 3.5 hours(SRC). The
volatilization half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind
velocity of 0.5 m/sec)(2) is estimated as 5 days(SRC). Half-lives of evaporation
from laboratory water surfaces (distilled water) have been reported to be on the
order of several minutes to hours, depending upon the turbulence(4,5).
Half-lives of trichloroethylene from an experimental
marine ecosystem (MERL) under field conditions and during periods when
volatilization appeared to dominate ranged from 10.7 to 28 days; turbulence is
expected to be greater in open water resulting in even faster half-lives(6). The
potential for volatilization of trichloroethylene from
dry soil surfaces exists(SRC) based upon a vapor pressure of 69 mm Hg(3).
The transport behavior of trichloroethylene
vapor in a section of unsaturated sands and silts at a field site in Borden,
Ontario was studied(1). Movement of trichloroethylene
vapor through unsaturated layers was shown to be lateral based on the
density-induced advective flow of the contaminated soil gas(1). Gas-phase
diffusion coefficients for trichloroethylene in tuff
soils with varying moisture content were measured(2). Under wet conditions
(12-15% moisture), diffusion coefficients of 0.0022-0.0067 and 0.0067-0.0070 sq
cm/sec were determined for trichloroethylene; under dry
conditions (1-3% moisture, diffusion coefficients of 0.0211-0.0230 and
0.0237-0.0292 sq cm/sec were determined(2). Soil diffusion coefficients were
measured for trichloroethylene at 3 different soil
porosities (0.29 to 0.43); values ranged from 0.254X10-3 to 1.986X10-3 sq
cm/sec, with the larger values associated with higher soil porosity levels(4).
The total amount of trichloroethylene that volatilizes
in 100 days may be reduced from 84.6% volatilized without vapor sorption to
73.2% in a soil with increasing water content with depth, based on a flexible
finite element transport model(3). Using the same model, vapor sorption enhanced
the rate of volatilization in 100 days for a soil with low water content at
depth from 72.4% without vapor sorption to 90.3% with vapor sorption(3). Very
dry soil conditions combined with a soil type having strong vapor sorption
characteristics may significantly retard the transport of trichloroethylene
(in the vapor phase)(3).
Environmental Water Concentrations:
GROUNDWATER: Trichloroethylene
was the most frequently detected organic chemical and in highest concentration;
28% of wells from 8 states sampled positive with a max conc reported at 35,000
ppb(2); 38.5% of 13 US cities tested positive with a mean concn 29.72 ppb, range
0.2-125 ppb(1). A study in New Jersey of 670 wells showed that 1.8% and 4.0% of
wells had concn >100 ppb and >10 ppb, respectively(3). Groundwater samples
in the Netherlands collected from 1976-78, at 232 pumping stations, showed that
67% were positive (>0.01 ppb) for trichloroethylene(4).
GROUNDWATER: Trichloroethylene
concns measured at 6 landfill sites in southern Ontario ranged from below the
method detection limit (not given)(3 of 6 sites) to 21 ug/l(1). 10 of 27
groundwater sites in Kanagawa Prefecture, Japan (samples collected 1995-1998),
contained trichloroethylene at concns from <0.1 to
220 ug/l(2). In a study of groundwater beneath 27 Swedish landfills, median and
maximum concns of <0.1 and 5.0 ug/l trichloroethylene
were reported(3). 13% of groundwater alluvial wells monitored in Denver
metropolitan in 1993 contained trichloroethylene (max
concn 2 ug/l)(4). Trichloroethylene was detected in
10.1% (n=208 wells) of groundwater samples collected in urban areas by the
National Water-Quality Assessment Program at a maximum concn of 230 ug/l
(reporting limit=0.2 ug/l; 3 wells exceeded MCL or health advisory level)(5). An
assessment of untreated ambient groundwater in the US from 1985 to 1995 was
conducted as part of the National Water-Quality Assessment Program; trichloroethylene
was detected in 11.6% of urban wells (n=406) and 1.6% of rural wells
(n=2542)(6). 26 of 1,083 shallow wells and 14 of 277 deep wells sampled in 15
cities in Japan in 1983 contained measurable concns of trichloroethylene(7).
Of 210 urban wells and springs sampled during the USGS National water-Quality
Assessment Program, 10% contained trichloroethylene(8).
DRINKING WATER: 28 of 113 US public water
supplies tested positive for trichloroethylene, mean
2.1 ppb(1). Trichloroethylene was found in finished
groundwater in 36% of 25 US cities at a mean concn of 6.76 ppb, range 0.11-53.0
ppb(2). Samples from the Love Canal, Niagara Falls, NY showed that 7 of 9
samples tested positive, with a concn range of 10-250 parts/trillion(3). 466
random samples of finished groundwater showed that 6.4% pos, 1 ppb median concn,
78 ppb max concn(4). State data, 2894 samples, showed that 28.0% tested positive
for trichloroethylene from a trace to 35,000 ppb; in
the US National Screening Program, of 142 samples, 25.4% tested positive with a
trace to 53 ppb and in a Community Water Supply Survey, 3.3% of 452 samples were
positive, with a concn range of 0.5-210 ppb(5).
DRINKING WATER: Trichloroethylene
was detected in drinking water from Zagreb, Croatia at concns ranging from
<0.05 to 22.93 ug/l(1). Trichloroethylene tap water
concns ranged from 0.03 to 2.1 ug/l according to the EPA's National Organics
Monitoring Survey, published in 1977(2). Concns of trichloroethylene
in groundwater before and after treatment from June 1995 to May 1996 at a
water-pumping station in Zagreb, Croatia, ranged from 5.05-12.90 ug/l (mean=8.55
ug/l) and 2.16 to 15.29 ug/l (mean=8.53 ug/l), respectively(3). The Eau Clair
Municipal Well field, WI, supplies drinking water to 57,600 residents; concns of
trichloroethylene in water samples at this site ranged
from 0.02 to 13 ug/l(4). This is currently listed as a Superfund site(4). Trichloroethylene
was measurable in 8, 12, and 66% of collected drinking water samples in Los
Angeles (Jan/Feb 1984), Los Angeles (May 1984), and Contra Costa (June 1984),
respectively(5).
SURFACE WATER: Trichloroethylene
concns of 1-24 ppb were measured in industrial rivers in US, with Lake Erie -
188 ppb, 88 of 204 samples pos(1). It is the third most frequently detected
compound in Ohio River - 2427 of 4972 samples pos, 86% 0.1-1.0 ppb(2). Samples
from Zurich, Switzerland lake surface contained 38 ppb, and at a 30 m depth - 65
ppb(3). Results reported in the USEPA STORET database of 9,295 data points,
showed that 28.0% were positive for trichloroethylene,
0.10 ppb median(4).
SURFACE WATER: Trichloroethylene
was present in water samples from Jackfish Bay, Lake Superior, at concns from
4.1 to 120 ng/l; Jackfish Bay receives 94,000 cu m/d of bleached-kraft mill
effluent(1). Estuarine waters containing trichloroethylene
were collected from sites in the UK (Humber, <10-40.6 ng/l; Tees, <10-269;
Tyne, <10-43.7; Wear, <10-132; Tweed, <10; Mersey, 250-4200), The
Netherlands/Belgium (Scheldt in 1987-1989, <10-1570; Scheldt in 1993, 54.7),
Germany (Elbe, <700), and the US (Back River, <132-30,000 and 260-13800;
Brazos river, 6-280)(2). Seawaters (beach, bay, fjord, coastal and shelf
seawaters) containing trichloroethylene were collected
from the following sites: Liverpool Bay, UK (<3600 ng/l), Swansea Bay, UK
(<10), Byfjorden, Sweden(0.28 ng/l), Skagerrak (<2.6 to <5.8), Firth of
Forth, UK (<10), Moray Forth, UK(<10), North Minch, UK (<10), Bristol
Channel, UK (<10), Belgian continental shelf (4.9- 7.3)(2). Open seawaters
containing trichloroethylene were collected from the
following sites: the NE Atlantic Ocean (5-11 ng/l), Antarctica in 1990 (3.8 ng/l),
Sea of Japan in 1991 (<10 ng/l), and the East Pacific Ocean in 1981 (0.1 to
0.7 ng/l)(2). Trichloroethylene was measured in two
sites in the River Elbe near Hamburg in 1992/1993; at Zollenspieker, upstream of
Hamburg, concns ranged from 20-132 ng/l (median=57 ng/l) and at Seemannshoft,
downstream of Hamburg, concns ranged from 13-117 ng/l (median=39 ng/l)(3). Trichloroethylene
was found in water samples collected from 30 sites within the urban rivers and
estuaries of Osaka, Japan; a median concn of 0.39 ug/l (78 of 136 samples
positive, range=0.31-45 ug/l) was reported(4). The average concn of trichloroethylene
in marine water samples was 0.3 ppb, max 3.6 ppb(6). A mean concn of 14.93 ng/l
was reported for trichloroethylene based on data
collected in the southern North Sea from Sept 1994 to December 1995(5).
RAIN/SNOW/FOG: Concns of trichloroethylene
in rainwater from La Jolla, California cnotained 5 parts/trillion, and from an
industrial area in England 150 parts/trillion(4). Samples from 7 rain events in
Portland, OR, Feb-Apr 1984 showed were 100% pos, concns ranging from 0.78-16
parts/trillion, 5.6 avg(5). 117 rain samples collected over 1991 in Kobe, Japan
contained unmeasurable concns of trichloroethylene
(<0.001 mg/l)(1). Cloud water samples were collected during 1987 and 1988 at
Mt. Mitchell State Park, NC; concns of trichloroethylene
ranged from 0-6.7 ng/ml with an average concn of 1.38 ng/ml(2). Surface snow,
snow collected from 0.5 m depth and surface ice sampled in the Terranova Bay
area in Antarctica, 1991-1992, contained trichloroethylene
at 14, 8.5, and 11 ng/l, respectively(3). Snow collected from a snow pit at 0.5,
1.0, 1.5, 2.0, 2.5, and 3.0 m contained trichloroethylene
at concns of 5.7, 2.9, 8.3, 8.9, 3.9, 8.0, and 9.0 ng /l, respectively (Terranova
Bay area, Antarctica, 1992-1993)(3). Snow samples from Southern California
contained 30 parts/trillion, central California 1.5 parts/trillion, and Alaska
39 parts/trillion(4).
Effluent Concentrations:
Landfill gas at seven U.K. waste disposal
sites contained trichloroethylene at <0.1 (4 sites)
to 152 mg/cu m(1). Gas samples from 3 old and 1 active municipal landfills in
Southern Finland contained trichloroethylene at average
concns of 0.1 to 5.25 mg/cu m and a maximum concn of 13 mg/cu m(2). Average trichloroethylene
concns of 710 and 2079 ppbV were measured in samples of landfill gas(3). 6% of
urban runoff samples (n=86) from 4 of 19 different cities contained trichloroethylene
at concns from 0.3 to 10 ug/l(4). Emissions of trichloroethylene
from hazardous waste incinerators in the US were estimated as 81.8 ng/l or 0.7
tons/yr(5). Primary sludge from seven US publicly owned treatment works
contained trichloroethylene at 35-284 ug/l(6).
Stationary source emissions of 2640 tons/yr trichloroethylene
were reported for The Netherlands in 1980(7). Landfill gas from 6 abandoned
hazardous waste sites and 1 sanitary landfill contained trichloroethylene
at mean concns of 0.08 to 2.43 ppbV and an overall maximum value of 12.3
ppbV(8). Emissions from a municipal waste incineration plant contained trichloroethylene
at 4.0 ug/cu m(9). Bleaching effluent from 3 different kraft pulp mills in
Finland contained trichloroethylene at concns of 0.1 to
0.7 ug/l(10). Trichloroethylene has been identified in
spent chlorination and alkali extraction liquors from pulp bleaching(11).
Effluent from 4 wastewater treatment plants in the Great Lakes basin contained trichloroethylene
at concns of <1 to 1 ppb(12). Trichloroethylene was
reported in the flue gas from the combustion of pulverized coal at minimum and
maximum concns of 4.747X10-7 and 5.685X10-7 lb/10+6 Btu, respectively(13). The
combustion of waste plastics containing vinyl chloride polymer in an incinerator
resulted in concns of trichloroethylene in the exhaust
gas of 47-82 ug/cu m, depending on the combustion and exit chamber
temperatures(14). Concn of trichloroethylene in sewage
sludge generally ranges from 1 to 10 mg/kg dry weight(15). Pyrolysis of military
HC smokepots resulted in the production of trichloroethylene(16).
Leachate samples from 5 hazardous waste landfills and 4 sanitary landfills
contained trichloroethylene at concns of 30 to 9500 ug/l
and 2.3 to 7.9 ug/l, respectively(17). Emissions from coal-fired power stations
contained trichloroethylene at concns of 5.7 ug/N-cu m;
the concn in coal is 0.02 ug/g(18). Diesel engines are reported to emit 4.5 ug/N-cu
m(18).
Trichloroethylene was
detected not quantified in wastewater in vicinity of a specialty chemicals
plant(1). Industries with mean trichloroethylene concns
greater than 75 ppb: paint and ink formulation, electrical/electronic
components, and rubber processing mean range, 7-530 ppb, max range 3-1600
ppb(2). Concn results of trichloroethylene reported in
the USEPA STORET database are as follows: 1,480 data points, 19.6% pos, 5.0 ppb
median(3). Groundwater samples at 178 CERCLA hazardous waste disposal sites were
51.3% pos(4). Trichloroethylene was detected in MN
municipal solid waste landfills: leachates from 6 sites, 83.3% pos, 0.7-125 ppb;
contaminated groundwater (by inorganic indices), 13 sites, 69.2% pos, 0.2-144
ppb; other groundwater (apparently not contaminated as indicated by inorganic
indices), 7 sites, 28.6% pos, 0.2-6.8 ppb(5).
Off-gas from a conventional activated sludge
treatment facility contained trichloroethylene at
average concns of 175, 86, and 242 mg/cu m for three different weeks of
operation in 1995/1996 (1). Trichloroethylene
represented 1.1% of the total mass distribution of different species emitted in
1990 from the United Kingdom(2). Influent and effluent samples collected from
the 14 water pollution control plants (11 with full secondary treatment)in New
York city between 1989 and 1993 contained trichloroethylene
at concn ranges of 1 to 46 ug /l (27% positive, n=84) and 2 to 3 ug /l (7%
positive, n=84), respectively(3). Groundwater samples collected from beneath an
active landfill in Orange County, Florida, in 1989/1990 and 1992/1993 contained trichloroethylene
at concns ranging from below detection to 9.21 ug/l and 0.09 to 0.54 ug/l,
respectively(4). 30 of 49 Superfund sites citing municipal well contamination,
distributed in 21 US states, contained trichloroethylene
in groundwater samples(5). Emissions of trichloroethylene
from wastewater treatment plants in Los Angeles, CA were 366, 12, 3, and 5 kg/yr
for Hyperion, Terminal Island, Tillman, and LA-Glendale plants, respectively(6).
Trichloroethylene was emitted during coal combustion at
concns ranging from 4.747X10-7 to 5.685X10-7 lb/10+6 Btu(7). Concns of trichloroethylene
in municipal landfill leachate ranged from 1 to 15 mg /l; concns in landfill
gases ranged from 1.2 to 175 mg/cu m (median 0.66 mg/cu m)(8). Trichloroethylene
was emitted from 8 municipal solid waste composting facilities at a maximum
concn of 1300 ug/cu m; fresh, mid-aged, old, and curing compost contained trichloroethylene
at average concns of 98, 3, 3, and 2 ug/cu m, respectively(9). Global
atmospheric emission fluxes of trichloroethylene were
reported in 1988 to 1992; values ranged from 197 to 241 kt/year(10).
Sediment/Soil Concentrations:
SEDIMENT: Trichloroethylene
was not detected in sediment in the vicinity of a specialty chemicals plant(1).
The compound was detected in marine sediments from Liverpool Bay, England at a
max of 9.9 ppb(2). It has been reported in the USEPA STORET database, based on
338 data points where 6.0% were reported positive, at <5.0 ppb median
concn(3). Trichloroethylene was detected in sediment
from Lake Pontchartrain at Passes; from 3 sites, 66.7% were positive at a concn
of 0.1-0.2 ppb, wet weight(4).
SOIL: Average concns of trichloroethylene
in a pine and agricultural soil ranged from 0.08 to 0.8 and <0.01 to 0.06 ug/kg
dry weight, respectively(1).
Atmospheric Concentrations:
Global concn of trichloroethylene
has been reported as follows: avg 8 parts/trillion, Northern hemisphere 15-16
parts/trillion, Southern hemisphere <3 parts/trillion(1,2). Concns in major
USA cities have been reported at a mean concn of 96-483 parts/trillion, with a
max of 236-3097 parts/trillion, and a min of 5-36 parts/trillion(3,4). Sampling
studies conducted in Portland, OR, from Feb-Apr 1984, showed a concn in air (ng/cu
m) during 7 rain envents as follows: 100% pos, 240-3900, 1537 avg(11).
Industrial area concns have been reported at a 1.2 ppb mean; urban/suburban-
0.25 ppb mean, and rural- trace-0.10 ppb(5-7). Results from a study based in
England are as follows: industrial 40-60 ppb, suburban 1-20 ppb, rural 5 ppb(8).
Air samples taken from the Love Canal region, Niagara Falls, NY resulted in 2 of
3 samples being pos (1.6 and 3.4 ppb), and home basement levels estimated at
0.83 ppb(9). Waste disposal site in Edison, NJ showed trichloroethylene
concns ranging from a trace-61 ppb(10).
URBAN/SUBURBAN: Air samples collected in
Bilbao, Spain in March 1996 contained trichloroethylene
at a mean concn of 0.7 ppbV(1). 14.6% of air samples collected outside 50 homes
in the Los Angeles area contained trichloroethylene(2).
Mean concns of 1.0 (n=103) and 2.1 (n=83) ug/cu m were reported in air samples
collected from 1986 to 1990 in Southeast Chicago and East St. Louis,
respectively(3). Air samples collected as part of the Urban Baseline VOC
Measurement Program in the District of Columbia from March 1990 to March 1991
contained trichloroethylene in 66.07% of the samples at
a mean concn of 0.33 ppbv (range=0.17-2.83 ppbv)(4). A maximum outdoor air concn
of <2 ug/cu m was reported in a study of 300 Dutch homes(5). Trichloroethylene
was measured in air samples collected from urban and suburban locations in
Chicago at average concns of 0.82-1.16 and 0.52 ug/cu m, respectively(6). The
national VOC database, representing 300 cities from 42 states, reports outdoor
air samples (n=3021) contained trichloroethylene at
average and median concns of 0.495 and 0.158 ppbv, respectively (data reported
up to 1985)(7).
URBAN/SUBURBAN: Trichloroethylene
was detected in air samples set up by the North Rhine-Westphalia State Centre
for Air Quality Control and Noise Abatement (76 stationary stations and 8 mobile
monitoring stations); annual average concns in 1990 ranged from 0.17 to 0.62 ug/cu
m(1). Air samples collected in Porto Alegre, Brazil from March 1996 to April
1997 contained trichloroethylene at an average concn of
0.367 ppb (range=0.1-1.2 ppb, n=23, 6 samples at detection limit of 0.1 ppb)(2).
32% of air samples collected at 10 different locations in Boston, Chicago,
Houston and the Seattle/Tacoma area in 1988/1989 as part of the Toxic Air
Monitoring System network contained trichloroethylene
at concns greater than 0.10 ppbv(3). Yearly mean concns of trichloroethylene
across several Canadian cities in 1990 and in the US were 0.28 (maximum=20 ug/cu
m) and 6.0 ug/cu m, respectively(4). Air samples collected between 1994 and 1996
at a site in Phoenix, AZ and at Tucson, AZ contained trichloroethylene
at average concns of 0.05 (range 0.00 to 0.26 ppbv) and 0.04 ppbv (range 0.00 to
0.25 ppbv), respectively(5).
INDOOR: Indoor air samples, collected from 12
Canadian homes in November/December 1986 contained trichloroethylene
at concns from below detection (detection limit not stated) to 2 ug/cu m
(average concn of 0.5 ug/cu m, average concn in Feb/March of 1.6 ug/cu m);
ambient air collected outside each home contained trichloroethylene
at below detection to 2 ug/cu m with an average of 0.2 ug/cu m in
November/December and 0.8 in Feb/March(1). A WHO summary of indoor air studies
from homes in Italy, The Netherlands, USA, and Germany reported that the average
home in these studies contained 5 ug/cu m trichloroethylene(2).
50% of air samples collected from the kitchens of 50 homes in the Los Angeles
area contained trichloroethylene(3). Indoor air samples
from nonsmoking and smoking homes contained trichloroethylene
at mean concns of 1.84 (range of 0.00 to 9.08 ug/cu m) and 0.66 (range of 0.00
to 3.41 ug/cu m) ug/cu m, respectively(4). Air samples collected from a newly
constructed office facility in 1987/1988 contained trichloroethylene
at concns of 16.4, 7.2, 58.2, and 14.8 ug/cu m at four different sampling
events; air samples collected from the roof contained this compound at 0.9 ug/cu
m(5). 27% of indoor air samples from 26 "sick" houses contained trichloroethylene
at concns ranging from not detected to 4.30 ug/cu m; 50 "normal"
houses contained trichloroethylene at mean and median
concns of 0.97 and 0.25 ug/cu m (max= 20.38 ug/cu m)(6).
INDOOR AIR: An emission rate of 3.6 ug/sq m/hr
was measured for the release of trichloroethylene from
linoleum tile(1). A summary of US studies monitoring VOCs in indoor air reports
that trichloroethylene has been measured at an average
concn of 1.347 ppb in 2134 measurements(1). A maximum indoor air concn of 106 ug/cu
m was reported in a study of 300 Dutch homes(1). Trichloroethylene
was reported in air samples during a study of West German homes with a concn
range of <1.0 to 1200 ug/cu m (mean concn of 13 ug/cu m)(1). Air samples
collected from 757 randomly selected Canadian homes in 1992 contained trichloroethylene
at unreported concns(2).
RURAL/REMOTE: Mean concns of trichloroethylene
in air samples collected from Talladega National Forest were 0.2 ppb(1). Air
samples collected from 4 forests in southwest Germany between 1986 and 1988
contained trichloroethylene at mean concns of 0.45,
0.55, 0.5, and 0.45 ug/cu m(2). A mean concn of 0.6 ug/cu m (n=23) was reported
in air samples collected from 1987 to 1990 from a rural site near Champaign,
IL(3). Concns of trichloroethylene were measured in air
samples collected above the Pacific Ocean (1977, mean=0.07 ug/cu m), Panama
Canal Zone (1977, 0.08 ug/cu m), and in the northern hemisphere (1985, 0.06-0.09
ug/cu m) and southern hemisphere (1981, <0.02 ug/cu m). Air samples from
rural locations contained trichloroethylene: Badger
Pass, CA (1977, mean=0.06 ug/cu m, range=0.005-0.09 ug/cu m), Whiteface
Mountains, NY (1974, mean=0.5 ug/cu, range=<0.3-1.9 ug/cu m), Reese River, NV
(1977, mean=0.06 ug/cu m, range=0.005-0.09 ug/cu m), Jetmar, KS (1978, mean=0.07
ug/cu m, range=0.04-0.11 ug/cu m)(4). Trichloroethylene
was measured in marine air masses surveyed over an area in the western Pacific
between 43 deg N, 150 deg E and 4 deg N, 113 deg E in September 1994 at mean and
median concns of 3.52 and 0.32 parts/trillion volume, respectively
(range=0.03-141.2 parts/trillion volume)(5). Ambient concns of trichloroethylene
in air samples from the western Pacific, 1991 to 1994, ranged from 0.36 to 70
parts/trillion volume with mean concns from 3 different cruises of 1.90 to 9.5
parts/trillion volume(6). The national VOC database reports remote and rural
median concns of 0.013 (n=14) and 0.010 (n=84) ppbv for trichloroethylene(7).
RURAL/REMOTE: Air samples from the Antarctic
from April 1985 to February 1986 contained trichloroethylene
at 3.1X10-11 mol/cu m(1). Trichloroethylene concns in
Arctic air samples peaked in December and January and declined to almost zero in
June/July(2). A mean concn of 141.1 parts/trillion volume was measured for trichloroethylene
in the air above the southern North Sea during cruises from Sept 1994 to Dec
1995(3). Air samples collected between 1994 and 1996 at a site in Payson, AZ and
at Casa Grande, AZ contained trichloroethylene at avg
concns of 0.10 (range 0.00 to 1.13 ppbv) and 0.09 ppbv (range 0.00 to 1.46 ppbv),
respectively(4).
Food Survey Values:
Trichloroethylene was
detected in the following food samples: intermediates grain-based food (1984): 9
varieties, 44.4% pos, 0.77-2.7 ppb, 1.9 ppb (max concn in yellow corn meal;
wheat, corn, oats (1984)), 10, 2, and 1 samples, respectively: not detected(1).
Sampling table-ready foods showed trichloroethylene
concns as follows: 19 varieties, 47% pos, 1.7-8.0 ppb, 1.5 ppb avg, max concn in
plain granola; butter, 7 samples, 100% pos; 1.6-20 ppb, 9.7 ppb avg; margarine,
7 samples, 100% pos, 3.7-980 ppb, 4.3 ppb avg of pos, max concn in Mozzarella
cheese(2). Trace amounts of trichloroethylene were
detected in extracted edible oils(1). It was also detected in meat, beverages,
dairy products, fruits and vegetables, oil and fats, range 0.02-60 ug/kg(1).
Concns of trichloroethylene in food samples were as
follows: Cheshire cheese: 3 mg/kg; English butter: 10 mg/kg; eggs: 0.6 mg/kg;
shin of beef: 16 mg/kg; beef fat: 12 mg/kg; pig liver: 22 mg/kg; margarine: 6
mg/kg; olive oil (Spanish): 9 mg/kg; cod liver oil: 19 mg/kg; vegetable oil for
frying: 7 mg/kg; fruit juices: 5 mg/kg; light beer: 0.7 mg/kg; freeze-dried
coffee: 4 mg/kg; tea in bags: 60 mg/kg; Yugoslavian wine: 0.02; potatoes: 3
mg/kg; apples: 5 mg/kg; pears: 5 mg/kg; fresh bread: 7 mg/kg(3).
5 of 372 samples of food, obtained from the
Food and Drug Administration's "market basket" collections, contained trichloroethylene
at concns ranging from 2 to 94 ng/g (mean=49 ng/g)(1). Trichloroethylene
was present in samples of butter from not detected to 0.3 ug/kg, in margarine at
concns from not detected to 0.4 ug/kg, in peanut butter at concns from not
detected to 0.7 ug/kg, and in pastry mix at a concn of 0.2 ug/kg(2). Floured
chickpeas contained trichloroethylene at unreported
concns(3). Trichloroethylene has been reported as a
component of chicken meat volatiles(4).
Plant Concentrations:
Tree cores obtained from bald cypress, tupelo,
sweet gum, oak, sycamore, and loblolly pine growing over shallow groundwater
contaminated with trichloroethylene contained this
compound at concns from <50 to 35,040 nmol /l (n=138, sampled
January-February 1998, Savannah River Site, SC)(1).
Fish/Seafood Concentrations:
Conger conger (eel): gill, gut: 29 ng/g;
brain, muscle: 62-70 ng/g; Gaddus morhua (cod): stomach, muscle: 7-8 ng/g;
brain, liver: 56-66 ng/g; Pollachius birens (coal fish): muscle: 8 ng/g;
alimentary canal: 306 ng/g; Scylliorhinus canicula (dog fish): muscle, gut,
brain: 40-41 ng/g; liver: 479 ng/g; Trisopterus luscus (bib): gill: 40 ng/g;
muscle, skeletal tissue: 185-187 ng/g.
Trichloroethylene has
been reported in marine fish at the following concns: flesh - 0.04-1.1 ppm,
liver - 0.66-20.0 ppb, mussels - 50 day exposure 1.37 ppm(1). Shelfish from Lake
Pontachartrain at Passes contained the following concns: oysters, 5 samples, 2.2
ppb avg; clams, composite samples from 2 sites, 5.7 and 0.8 ppb(2).
Animal Concentrations:
Clams collected in 1995/1996 from the Ariho,
Koe and Okita Rivers, Japan, did not contain measurable quantities of trichloroethylene
(detection limit <0.5 ug/kg)(1). Earthworms collected from a forest site
adjacent to a former landfill site and chemical plant in West Germany during
1989 contained trichloroethylene at concns below
detection (detection limit not reported) to 170 ng/g wet weight(2). In a
sampling study conducted near Liverpool Bay, UK, trichloroethylene
concns in Alca torda (Razorbill Auk), Uria aalge (Guillemot), and Rissa
tridactyla (Kittiwake) sea bird eggs were 23-33 mg/kg. Levels of 2.4 mg/kg for
Phalacrocrax aristotelis (Shag) were also noted(3).
Milk Concentrations:
Trichloroethylene has
been detected in dairy products(1). In mother's milk samples from 4 U.S. urban
areas, 8 of 8 samples tested positive for the compound(2). The concn of trichloroethylene
in fresh milk was 0.3 mg/kg(3).
Other Environmental Concentrations:
Trichloroethylene was
found in 2.2% of 1159 household products; automotive products (0.1%
weight/weight, 1.2% positive hits in category), household cleaner/polishes
(0.0%, 0.9%), paint-related products (3.0%, 1.1%), fabric and leather treatments
(0.0%, 2.2%), cleaners for electronic equipment (0.3%, 1.4%), oils, greases and
lubricants (0.3%, 1.8%), adhesive-related products (34.7%, 2.6%) and
miscellaneous products (33.9%, 14.1%)(1). Household cleaning agents and
pesticides contained trichloroethylene at an average
concn of 7 ug/cu m (2). Trichloroethylene was
identified in 3 of 26 samples of hobby glue at 0.007 to 0.15 weight percent(3).
In the European Community, trichloroethylene is used by
some producers during the decaffeinating of coffee(4).
Environmental Standards & Regulations:
CERCLA Reportable Quantities:
Persons in charge of vessels or facilities are
required to notify the National Response Center (NRC) immediately, when there is
a release of this designated hazardous substance, in an amount equal to or
greater than its reportable quantity of 100 lb or 45.4 kg. The toll free number
of the NRC is (800) 424-8802; In the Washington D.C. metropolitan area (202)
426-2675. The rule for determining when notification is required is stated in 40
CFR 302.4 (section IV. D.3.b).
RCRA Requirements:
U228; As stipulated in 40 CFR 261.33, when trichloroethylene,
as a commercial chemical product or manufacturing chemical intermediate or an
off-specification commercial chemical product or a manufacturing chemical
intermediate, becomes a waste, it must be managed according to Federal and/or
State hazardous waste regulations. Also defined as a hazardous waste is any
residue, contaminated soil, water, or other debris resulting from the cleanup of
a spill, into water or on dry land, of this waste. Generators of small
quantities of this waste may qualify for partial exclusion from hazardous waste
regulations (40 CFR 261.5).
D040; A solid waste containing trichloroethylene
may or may not become characterized as a hazardous waste when subjected to the
Toxicity Characteristic Leaching Procedure listed in 40 CFR 261.24, and if so
characterized, must be managed as a hazardous waste.
F002; When trichloroethylene
is a spent solvent, it is classified as a hazardous waste from a nonspecific
source (F002), as stated in 40 CFR 261.31, and must be managed according to
state and/or federal hazardous waste regulations.
Atmospheric Standards:
This action promulgates standards of
performance for equipment leaks of Volatile Organic Compounds (VOC) in the
Synthetic Organic Chemical Manufacturing Industry (SOCMI). The intended effect
of these standards is to require all newly constructed, modified, and
reconstructed SOCMI process units to use the best demonstrated system of
continuous emission reduction for equipment leaks of VOC, considering costs, non
air quality health and environmental impact and energy requirements. Trichloroethylene
is produced, as an intermediate or a final product, by process units covered
under this subpart.
Listed as a hazardous air pollutant (HAP)
generally known or suspected to cause serious health problems. The Clean Air
Act, as amended in 1990, directs EPA to set standards requiring major sources to
sharply reduce routine emissions of toxic pollutants. EPA is required to
establish and phase in specific performance based standards for all air emission
sources that emit one or more of the listed pollutants. Trichloroethylene
is included on this list.
Clean Water Act Requirements:
Toxic pollutant designated pursuant to section
307(a)(1) of the Federal Water Pollution Control Act and is subject to effluent
limitations.
Trichloroethylene is
designated as a hazardous substance under section 311(b)(2)(A) of the Federal
Water Pollution Control Act and further regulated by the Clean Water Act
Amendments of 1977 and 1978. These regulations apply to discharges of this
substance. This designation includes any isomers and hydrates, as well as any
solutions and mixtures containing this substance.
Federal Drinking Water Standards:
EPA 5 ug/l
State Drinking Water Standards:
(FL) FLORIDA 3 ug/l
(NJ) NEW JERSEY 1 ug/l
State Drinking Water Guidelines:
(AZ) ARIZONA 3.2 ug/l
(CT) CONNECTICUT 5 ug/l
(ME) MAINE 5 ug/l
(MN) MINNESOTA 30 ug/l
FDA Requirements:
Trichloroethylene is
an indirect food additive for use as a component of adhesives.
Tolerances are established for residues of trichloroethylene
resulting from its use as a solvent in the manufacture of foods as follows:
decaffeinated ground coffee 25 ppm; decaffeinated soluble (instant) coffee
extract 10 ppm; and spice oleoresins 30 ppm (provided that if residues of other
chlorinated solvents are also present, the total of all residues of such
solvents in spice oleoresins shall not exceed 30 ppm).
Allowable Tolerances:
Tolerances are established for residues of trichloroethylene
resulting from its use as a solvent in the manufacture of foods as follows:
decaffeinated ground coffee 25 ppm; decaffeinated soluble (instant) coffee
extract 10 ppm; and spice oleoresins 30 ppm (provided that if residues of other
chlorinated solvents are also present, the total of all residues of such
solvents in spice oleoresins shall not exceed 30 ppm).
Chemical/Physical Properties:
Molecular Formula:
C2-H-Cl3
Molecular Weight:
131.39
Color/Form:
CLEAR, COLORLESS, OR BLUE MOBILE LIQUID
Colorless liquid (unless dyed blue).
Odor:
Ethereal odor
Sweet smelling
Characteristic odor resembling that of
chloroform
Boiling Point:
87.2 deg C
Melting Point:
-84.7 deg C
Corrosivity:
Non-corrosive
Critical Temperature & Pressure:
Critical temperature: 300.2 deg C; Critical
pressure: 4.986 MPa
Density/Specific Gravity:
1.4642 @ 20 deg C/4 deg C
Heat of Combustion:
-6.56 kJ/g
Heat of Vaporization:
8,314.7 gcal/gmole
Octanol/Water Partition Coefficient:
log Kow= 2.61
Solubilities:
Soluble in ethanol, diethyl ether, acetone,
and chloroform
Miscible in oil.
In water, 1,280 mg/l @ 25 deg C
Spectral Properties:
SADTLER REF NUMBER: 185 (IR, PRISM); MAX
ABSORPTION: LESS THAN 200 NM (VAPOR)
Index of refraction: 1.4773 @ 20 deg C/D
IR: 62 (Sadtler Research Laboratories IR
Grating Collection)
NMR: 9266 (Sadtler Research Laboratories
Spectral Collection)
MASS: 583 (Atlas of Mass Spectral Data, John
Wiley & Sons, New York)
Intense mass spectral peaks: 60 m/z, 95 m/z,
130 m/z
Surface Tension:
29.3 dynes/cm = 0.0293 N/m at 20 deg C
Vapor Density:
4.53 /Air=1/
Vapor Pressure:
69 mm Hg @ 25 deg C
Viscosity:
0.00550 poise at 25 deg C
Other Chemical/Physical Properties:
Percent in saturated air: 10.2 (25 DEG C);
Equivalencies: 1 mg/l= 185.8 ppm and 1 ppm= 5.38 mg/cu m @ 25 deg C, 760 mm Hg)
Ratio of Specific Heats of Vapor (gas) : 1.116
Olive oil/water partition coefficient 522:1 at
37 deg C.
Liquid heat capacity: 0.231 Btu/lb-F;
saturated vapor pressure: 1.166 lb/sq in; saturated vapor density: 0.02695 lb/cu
ft (all at 70 deg F)
Saturated liquid density: 90.770 lb/cu ft;
ideal gas heat capacity: 0.146 Btu/lb-F (All at 75 deg F)
Weight per gallon @ 20 deg C: 12.20 lb.
Partition coefficients at 37 deg C for trichloroethylene
into blood = 9.5; into oil = 718.
Dielectric constant: @ 16 deg C 3.42;
coefficient of cubic expansion: 0.00119 (at 0-40 deg C); heat of formation:
-42.3 kJ/mol (liquid), -7.78 kJ/mol (vapor); latent heat of vaporization: 238
kJ/kg (at boiling point)
Henry's Law Constant=9.85X10-3 atm-cu m/mol @
25 deg C
Hydroxyl radical rate constant = 2.36X10-12 cu
cm/molecule-sec at 25 deg C
Slowly dec (with formation of HCl) by light in
the presence of moisture
Will not attack the common metals even in the
presence of moisture
Photo-oxidized in air by sunlight (half-time,
five days) giving phosgene and dichloroacetyl chloride
Chemical Safety & Handling:
Hazards Summary:
Trichloroethylene (TCE)
is a hazardous substance due primarily to its toxicity. Effects result from both
high-level, acute and lower-level, chronic exposures. Protection must be
afforded against both dermal contact and inhalation. Dermal protection is
accomplished by routinely wearing neoprene constructed gloves, worksuit, apron,
and shoes. Safety goggles or a face shield is necessary to protect against
splash potential. The TLV for TCE is 50 ppm with a short term exposure limit (STEL)
of 200 ppm. These levels should be attained through local exhaust
(pressure/vacuum) ventilation. If the STEL is exceeded, an organic vapor-acid
canister respirator or air-supplied, self-contained breathing apparatus (in
emergencies) is recommended. The ethereal, chloroform-like odor of TCE is
detectable at 50 ppm, with levels above 200 ppm becoming disagreeable. Its
clear, colorless appearance and liquid form do not serve similarly as warnings
against dermal contact. The potential fire hazard from TCE alone is low.
However, TCE, when exposed to flames or an electric arc in the presence of iron,
copper, zinc, or aluminum, can form phosgene, a highly toxic gas. Also, TCE in
the presence of heat and strong oxidizers (eg, tetraoxide) reacts violently.
Even without a heat source, TCE can react with strong alkali (eg, sodium
hydroxide) to form the dangerously toxic, flammable and explosive
dichloroacetylene. Perchloric acid also reacts violently with TCE. Further TCE
forms impact-explosive mixtures with finely divided aluminum, beryllium,
lithium, magnesium or titanium. TCE should be packaged in steel drums. These
drums should be stored in a cool, dry, well-ventilated area because TCE will
slowly decompose to corrosive HCL when exposed to light & moisture. Should a
TCE fire occur, it may be combated with water, fog, dry chemical, carbon dioxide
or foam extinguisher. Spills of TCE should be isolated by flushing with water to
an impoundment. Density stratification will cause the formation of a bottom TCE
layer which can be pumped and containerized.
DOT Emergency Guidelines:
Health: Vapors may cause dizziness or
suffocation. Exposure in an enclosed area may be very harmful. Contact may
irritate or burn skin and eyes. Fire may produce irritating and/or toxic gases.
Runoff from fire control or dilution water may cause pollution.
Fire or explosion: Some of these materials may
burn, but none ignite readily. Most vapors are heavier than air. Air/vapor
mixtures may explode when ignited. Container may explode in heat of fire.
Public safety: CALL Emergency Response
Telephone Number ... . Isolate spill or leak area immediately for at least 25 to
50 meters (80 to 160 feet) in all directions. Keep unauthorized personnel away.
Stay upwind. Many gases are heavier than air and will spread along ground and
collect in low or confined areas (sewers, basements, tanks). Keep out of low
areas. Ventilate closed spaces before entering.
Protective clothing: Wear positive pressure
self-contained breathing apparatus (SCBA). Structural firefighters' protective
clothing will only provide limited protection.
Evacuation: ... Fire: If tank, rail car or
tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all
directions; also, consider initial evacuation for 800 meters (1/2 mile) in all
directions.
Fire: Small fires: Dry chemical, CO2 or water
spray. Large fires: Dry chemical, CO2, alcohol-resistant foam or water spray.
Move containers from fire area if you can do it without risk. Dike fire control
water for later disposal; do not scatter the material. Fire involving tanks or
car/trailer loads: Fight fire from maximum distance or use unmanned hose holders
or monitor nozzles. Cool containers with flooding quantities of water until well
after fire is out. Withdraw immediately in case of rising sound from venting
safety devices or discoloration of tank. ALWAYS stay away from tanks engulfed in
fire.
Spill or leak: Eliminate all ignition sources
(no smoking, flares, sparks or flames in immediate area). Stop leak if you can
do it without risk. Small liquid spills: Take up with sand, earth or other
noncombustible absorbent material. Large spills: Dike far ahead of liquid spill
for later disposal. Prevent entry into waterways, sewers, basements or confined
areas.
First aid: Move victim to fresh air. Call 911
or emergency medical service. Apply artificial respiration if victim is not
breathing. Administer oxygen if breathing is difficult. Remove and isolate
contaminated clothing and shoes. In case of contact with substance, immediately
flush skin or eyes with running water for at least 20 minutes. For minor skin
contact, avoid spreading material on unaffected skin. Wash skin with soap and
water. Keep victim warm and quiet. Ensure that medical personnel are aware of
the material(s) involved, and take precautions to protect themselves.
Odor Threshold:
10 mg/l (in water) /Purity not specified/
5.00X10-1 mg/l (liquid) (detection in water)
2.14X10+1 ppm (recognition in air) (chemically
pure)
Skin, Eye and Respiratory Irritations:
Exposure to trichloroethylene
vapor may cause irritation of the eyes, nose, and throat.
Liquid: irritating to skin and eyes.
Fire Potential:
FIRE HAZARD: LOW, WHEN EXPOSED TO HEAT. HIGH
CONCN OF TRICHLOROETHYLENE VAPOR IN HIGH TEMP AIR CAN
BE MADE TO BURN MILDLY IF APPLIED WITH STRONG FLAME. THOUGH SUCH CONDITION IS
DIFFICULT TO PRODUCE, FLAMES OR ARCS SHOULD NOT BE USED IN CLOSED EQUIPMENT
WHICH CONTAINS ANY SOLVENT RESIDUE OR VAPOR.
At normal handling temperatures, trichloroethylene
behaves as a non-flammable, non-burnable substance.
NFPA Hazard Classification:
Health: 2. 2= Materials that, on intense or
continued (but not chronic) exposure, could cause temporary incapacitation or
possible residual injury, including those requiring the use of respiratory
protective equipment that has an independent air supply. These materials are
hazardous to health, but areas may be entered freely if personnel are provided
with full-face mask self-contained breathing apparatus that provides complete
eye protection.
Flammability: 1. 1= This degree includes
materials that must be preheated before ignition will occur, such as Class IIIB
combustible liquids and solids and semi-solids whose flash point exceeds 200 deg
F (93.4 deg C), as well as most ordinary combustible materials. Water may cause
frothing if it sinks below the surface of the burning liquid and turns to steam.
However, a water fog that is gently applied to the surface of the liquid will
cause frothing that will extinguish the fire.
Reactivity: 0. 0= This degree includes
materials that are normally stable, even under fire exposure conditions, and
that do not react with water. Normal fire fighting procedures may be used.
Flammable Limits:
Lower flammable limit: 8% by volume at 25 deg
C; Upper flammable limit: 10.5% by volume at 25 deg C
Lower flammable limit: 7.8% by volume at 100
deg C; Upper flammable limit: 52% by volume at 100 deg C
Autoignition Temperature:
420 DEG C (788 DEG F)
Fire Fighting Procedures:
Approach fire from upwind to avoid hazardous
vapors and toxic decomposition products. Use water spray to keep fire-exposed
containers cool. Use water spray, dry chemical, foam, or carbon dioxide.
Extinguish fire using agent suitable for surrounding fire.
If material involved in fire: Extinguish fire
using agent suitable for type of surrounding fire. (Material itself does not
burn or burns with difficulty.)
Toxic Combustion Products:
Combustion may produce irritants and toxic gas
including hydrogen chloride.
Explosive Limits & Potential:
UPPER (77 DEG F) 10.5% VOL; LOWER (77 DEG F)
8% VOL
UPPER 90% VOL; LOWER 12.5% VOL
... Under ordinary conditions of use, trichloroethylene
is non-flammable and non-explosive... .
Hazardous Reactivities & Incompatibilities:
Strong caustics and alkalis; chemically-active
metals (such as barium, lithium, sodium, magnesium, titanium, and berylium).
1-Chloro-2,3-epoxypropane, the mono- and
di-2,3-epoxypropyl ethers of 1,4-butanediol, and 2,2-bis-4(2',3'-epoxypropoxy)-phenyl-propane
can, in presence of catalytic quantities of halide ions, cause
dehydrochlorination of trichloroethylene to
dichloroacetylene, which causes minor explosions when the mixture is boiled
under reflux.
Granular barium in contact with trichloroethylene
is susceptible to detonation.
Mixtures of powdered beryllium with trichloroethylene
will flash on heavy impact.
Mixtures of lithium shavings and trichloroethylene
are impact-sensitive and willexplode, sometimes violently.
Mixtures of powdered magnesium with trichloroethylene
will flash on heavy impact.
Mixtures of powdered titanium and trichloroethylene
flash or spark under heavy impact.
Trichloroethylene
reacts violently with the anhydrous perchloric acid.
Mixtures of dinitrogen tetraoxide with trichloroethylene
react violently on heating to 150 deg C.
Mixture of liquid oxygen with dichloromethane,
1,1,1-trichloroethane, trichloroethylene, and
chlorinated dye penetrants 1 and 2 exploded violently when initiated with a
blasting cap.
In the presence of strong alkali (eg, sodium
hydroxide), trichloroethylene can decompose into
dichloroacetylene, an explosive, flammable, and highly toxic compound.
Formation of phosgene, a highly toxic gas, was
observed when trichloroethylene came into contact with
iron, copper, zinc, or aluminum over the temperature range 250 deg C to 600 deg
C.
Mixtures of trichloroethylene
and oxygen will ignite at temperatures above 25.5 deg C when the trichloroethylene
concentration is between 10.3 and 64.5%.
PHOTOREACTIVE LIQUID; WILL NOT ATTACK COMMON
METALS EVEN IN PRESENCE OF MOISTURE
An emulsion, formed during extraction of a
strongly alkaline liquor with trichloroethylene,
decomposed with the evolution of the spontaneously flammable gas,
dichloroacetylene. This reaction could also occur if alkaline metal-stripping
preparations were used in conjunction with trichloroethylene
degreasing preparations, some of which also contain amine inhibitors which could
cause the same reaction.
Mixtures of dinitrogen tetraoxide with trichloroethylene
are explosive when subjected to shock of 25 g TNT equivalent or less.
Aluminum powder reaction when /exposed/ to trichloroethylene.
Incompatibilities: Strong caustics; when
acidic reacts with aluminum; chemical active metals-barium, lithium, sodium,
magnesium, titanium.
Hazardous Decomposition:
SLOWLY DECOMPOSED WITH FORMATION OF
HYDROCHLORIC ACID BY LIGHT IN PRESENCE OF MOISTURE
Autoxidation products, such as phosgene and
dichloroacetylene, added stabilizers, such as epichlorohydrin, and decomp
products, such as chlorine and hydrochloric acid, may be responsible for some of
the toxic and carcinogenic effects reported for trichloroethylene.
Immediately Dangerous to Life or Health:
NIOSH considers trichloroethylene
to be a potential occupational carcinogen.
Protective Equipment & Clothing:
Wear appropriate personal protective clothing
to prevent skin contact.
Facilities for quickly drenching the body
should be provided within the immediate work area for emergency use where there
is a possibility of exposure. [Note: It is intended that these facilities
provide a sufficient quantity or flow of water to quickly remove the substance
from any body areas likely to be exposed. The actual determination of what
constitutes an adequate quick drench facility depends on the specific
circumstances. In certain instances, a deluge shower should be readily
available, whereas in others, the availability of water from a sink or hose
could be considered adequate.]
Eyewash fountains should be provided in areas
where there is any possbility that workers could be exposed to the substance;
this is irrespective of the recommendation involving the wearing of eye
protection.
Wear appropriate eye protection to prevent eye
contact.
Recommendations for respirator selection.
Condition: At concentrations above the NIOSH REL, or where there is no REL, at
any detectable concentration: Respirator Class(es): Any self-contained breathing
apparatus that has a full facepiece and is operated in a pressure-demand or
other positive-pressure mode. Any supplied-air respirator that has a full
facepiece and is operated in a pressure-demand or other positive-pressure mode
in combination with an auxiliary self-contained breathing apparatus operated in
pressure-demand or other positive-pressure mode.
Recommendations for respirator selection.
Condition: Escape from suddenly occurring respiratory hazards: Respirator
Class(es): Any air-purifying, full-facepiece respirator (gas mask) with a
chin-style, front- or back-mounted organic vapor canister. Any appropriate
escape-type, self-contained breathing apparatus.
ORGANIC VAPOR-ACID CANISTER; SELF-CONTAINED
BREATHING APPARATUS FOR EMERGENCIES; NEOPRENE OR VINYL GLOVES; CHEMICAL SAFETY
GOGGLES; FACE-SHIELD; NEOPRENE SAFETY SHOES; NEOPRENE SUIT OR APRON FOR SPLASH
PROTECTION.
/Wear/ positive-pressure hose masks, airline
masks or an industrial canister-type gas mask fitted with an appropriate
canister for absorbing trichloroethylene vapor are
acceptable.
PRECAUTIONS FOR "CARCINOGENS": ...
Dispensers of liq detergent /should be available./ ... Safety pipettes should be
used for all pipetting. ... In animal laboratory, personnel should ... wear
protective suits (preferably disposable, one-piece & close-fitting at ankles
& wrists), gloves, hair covering & overshoes. ... In chemical
laboratory, gloves & gowns should always be worn ... however, gloves should
not be assumed to provide full protection. Carefully fitted masks or respirators
may be necessary when working with particulates or gases, & disposable
plastic aprons might provide addnl protection. ... Gowns ... /should be/ of
distinctive color, this is a reminder that they are not to be worn outside the
laboratory. /Chemical Carcinogens/
Cleaning of confined spaces presents serious
hazards: the gas should be dispelled by mobile ventilators before workers are
permitted to enter, safety belts & lifelines & respiratory protective
equipment of the self-contained or supplied-air type should be avail, &
another worker should be posted outside for supervision & rescue, if
necessary.
Preventive Measures:
Recommended ventilation design concentrations:
100 ppm; dilution rate: 30,000 cu ft air/lb solvent flow.
PVC and natural rubber should not be used when
cleaning up a TCE spill. Equipment should not be iron or metal, or be
susceptible to hydrogen chloride.
Processes employing trichloroethylene
should be designed so that the operator is not exposed to direct contact with
the solvent or its vapor. Open electric heaters, high-temp processes, arc
welding or open flames should not be used in environments with trichloroethylene
vapor. ... Workers should be given instruction in the safe handling ... and be
well acquainted with the hazards that may result from improper use. ... Adequate
sanitary facilities should be provided and workers encouraged to wash before
eating and at the end of the shift.
Trichloroethylene
should not be stored near foodstuffs, strong acids, alkalis, or oxidizing
agents.
Stop discharge if possible. Keep people away.
Avoid contact with liquid and vapor. Call fire department. Isolate and remove
discharged material. Notify local health and pollution control agencies.
Avoid long contact with skin.
Contact lenses should not be worn when working
with this chemical.
SRP: The scientific literature for the use of
contact lenses in industry is conflicting. The benefit or detrimental effects of
wearing contact lenses depend not only upon the substance, but also on factors
including the form of the substance, characteristics and duration of the
exposure, the uses of other eye protection equipment, and the hygiene of the
lenses. However, there may be individual substances whose irritating or
corrosive properties are such that the wearing of contact lenses would be
harmful to the eye. In those specific cases, contact lenses should not be worn.
In any event, the usual eye protection equipment should be worn even when
contact lenses are in place.
The worker should immediately wash the skin
when it becomes contaminated.
Work clothing that becomes wet or
significantly contaminated should be removed and replaced.
If material not involved in fire: Keep
material out of water sources and sewers. Build dikes to contain flow as
necessary.
Personnel protection: Keep upwind. ... Avoid
breathing vapors or dusts. Wash away any material which may have contacted the
body with copious amounts of water or soap and water.
PRECAUTIONS FOR "CARCINOGENS":
Smoking, drinking, eating, storage of food or of food & beverage containers
or utensils, & the application of cosmetics should be prohibited in any
laboratory. All personnel should remove gloves, if worn, after completion of
procedures in which carcinogens have been used. They should ... wash ... hands,
preferably using dispensers of liq detergent, & rinse ... thoroughly.
Consideration should be given to appropriate methods for cleaning the skin,
depending on nature of the contaminant. No standard procedure can be
recommended, but the use of organic solvents should be avoided. Safety pipettes
should be used for all pipetting. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": In
animal laboratory, personnel should remove their outdoor clothes & wear
protective suits (preferably disposable, one-piece & close-fitting at ankles
& wrists), gloves, hair covering & overshoes. ... Clothing should be
changed daily but ... discarded immediately if obvious contamination occurs ...
/also,/ workers should shower immediately. In chemical laboratory, gloves &
gowns should always be worn ... however, gloves should not be assumed to provide
full protection. Carefully fitted masks or respirators may be necessary when
working with particulates or gases, & disposable plastic aprons might
provide addnl protection. If gowns are of distinctive color, this is a reminder
that they should not be worn outside of lab. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": ...
Operations connected with synth & purification ... should be carried out
under well-ventilated hood. Analytical procedures ... should be carried out with
care & vapors evolved during ... procedures should be removed. ... Expert
advice should be obtained before existing fume cupboards are used ... & when
new fume cupboards are installed. It is desirable that there be means for
decreasing the rate of air extraction, so that carcinogenic powders can be
handled without ... powder being blown around the hood. Glove boxes should be
kept under negative air pressure. Air changes should be adequate, so that concn
of vapors of volatile carcinogens will not occur. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS":
Vertical laminar-flow biological safety cabinets may be used for containment of
in vitro procedures ... provided that the exhaust air flow is sufficient to
provide an inward air flow at the face opening of the cabinet, &
contaminated air plenums that are under positive pressure are leak-tight.
Horizontal laminar-flow hoods or safety cabinets, where filtered air is blown
across the working area towards the operator, should never be used ... Each
cabinet or fume cupboard to be used ... should be tested before work is begun (eg,
with fume bomb) & label fixed to it, giving date of test & avg air-flow
measured. This test should be repeated periodically & after any structural
changes. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS":
Principles that apply to chem or biochem lab also apply to microbiological &
cell-culture labs ... Special consideration should be given to route of admin.
... Safest method of administering volatile carcinogen is by injection of a soln.
Admin by topical application, gavage, or intratracheal instillation should be
performed under hood. If chem will be exhaled, animals should be kept under hood
during this period. Inhalation exposure requires special equipment. ... Unless
specifically required, routes of admin other than in the diet should be used.
Mixing of carcinogen in diet should be carried out in sealed mixers under fume
hood, from which the exhaust is fitted with an efficient particulate filter.
Techniques for cleaning mixer & hood should be devised before expt begun.
When mixing diets, special protective clothing &, possibly, respirators may
be required. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": When
... admin in diet or applied to skin, animals should be kept in cages with solid
bottoms & sides & fitted with a filter top. When volatile carcinogens
are given, filter tops should not be used. Cages which have been used to house
animals that received carcinogens should be decontaminated. Cage-cleaning
facilities should be installed in area in which carcinogens are being used, to
avoid moving of ... contaminated /cages/. It is difficult to ensure that cages
are decontaminated, & monitoring methods are necessary. Situations may exist
in which the use of disposable cages should be recommended, depending on type
& amt of carcinogen & efficiency with which it can be removed. /Chemical
Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": To
eliminate risk that ... contamination in lab could build up during conduct of
expt, periodic checks should be carried out on lab atmospheres, surfaces, such
as walls, floors & benches, & ... interior of fume hoods & airducts.
As well as regular monitoring, check must be carried out after cleaning-up of
spillage. Sensitive methods are required when testing lab atmospheres. ...
Methods ... should ... where possible, be simple & sensitive. /Chemical
Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": Rooms
in which obvious contamination has occurred, such as spillage, should be
decontaminated by lab personnel engaged in expt. Design of expt should ... avoid
contamination of permanent equipment. ... Procedures should ensure that
maintenance workers are not exposed to carcinogens. ... Particular care should
be taken to avoid contamination of drains or ventilation ducts. In cleaning
labs, procedures should be used which do not produce aerosols or dispersal of
dust, ie, wet mop or vacuum cleaner equipped with high-efficiency particulate
filter on exhaust, which are avail commercially, should be used. Sweeping,
brushing & use of dry dusters or mops should be prohibited. Grossly
contaminated cleaning materials should not be re-used ... If gowns or towels are
contaminated, they should not be sent to laundry, but ... decontaminated or
burnt, to avoid any hazard to laundry personnel. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": Doors
leading into areas where carcinogens are used ... should be marked distinctively
with appropriate labels. Access ... limited to persons involved in expt. ... A
prominently displayed notice should give the name of the Scientific Investigator
or other person who can advise in an emergency & who can inform others (such
as firemen) on the handling of carcinogenic substances. /Chemical Carcinogens/
Stability/Shelf Life:
RELATIVELY STABLE IN AIR
UNSTABLE IN LIGHT AND MOISTURE
Shipment Methods and Regulations:
PRECAUTIONS FOR "CARCINOGENS":
Procurement ... of unduly large amt ... should be avoided. To avoid spilling,
carcinogens should be transported in securely sealed glass bottles or ampoules,
which should themselves be placed inside strong screw-cap or snap-top container
that will not open when dropped & will resist attack from the carcinogen.
Both bottle & the outside container should be appropriately labelled. ...
National post offices, railway companies, road haulage companies & airlines
have regulations governing transport of hazardous materials. These authorities
should be consulted before ... material is shipped. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": When
no regulations exist, the following procedure must be adopted. The carcinogen
should be enclosed in a securely sealed, watertight container (primary
container), which should be enclosed in a second, unbreakable, leakproof
container that will withstand chem attack from the carcinogen (secondary
container). The space between primary & secondary container should be filled
with absorbent material, which would withstand chem attack from the carcinogen
& is sufficient to absorb the entire contents of the primary container in
the event of breakage or leakage. Each secondary container should then be
enclosed in a strong outer box. The space between the secondary container &
the outer box should be filled with an appropriate quantity of shock-absorbent
material. Sender should use fastest & most secure form of transport &
notify recipient of its departure. If parcel is not received when expected,
carrier should be informed so that immediate effort can be made to find it.
Traffic schedules should be consulted to avoid ... arrival on weekend or holiday
... /Chemical Carcinogens/
No person may /transport,/ offer or accept a
hazardous material for transportation in commerce unless that person is
registered in conformance ... and the hazardous material is properly classed,
described, packaged, marked, labeled, and in condition for shipment as required
or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./
The International Air Transport Association (IATA)
Dangerous Goods Regulations are published by the IATA Dangerous Goods Board
pursuant to IATA Resolutions 618 and 619 and constitute a manual of industry
carrier regulations to be followed by all IATA Member airlines when transporting
hazardous materials.
The International Maritime Dangerous Goods
Code lays down basic principles for transporting hazardous chemicals. Detailed
recommendations for individual substances and a number of recommendations for
good practice are included in the classes dealing with such substances. A
general index of technical names has also been compiled. This index should
always be consulted when attempting to locate the appropriate procedures to be
used when shipping any substance or article.
Storage Conditions:
STORE IN COOL, DRY, WELL-VENTILATED LOCATION.
SEPARATE FROM ACTIVE METALS. ISOLATE FROM OPEN FLAMES AND COMBUSTIBLES.
Store trichloroethylene
in cans or in dark glass bottles to minimize decomposition.
All containers for trichloroethylene
should bear a label giving the following or similar information: TRICHLOROETHYLENE-WARNING
Vapor harmful. Use only with adequate ventilation. /safe handling & storage
of chemicals/
... May be stored satisfactorily in galvanized
iron, black iron, or steel containers.
Preserve trichloroethylene
in sealed, light-resistant ampules or in frangible, light-resistant glass tubes.
Storage temp: ambient
Storage areas should be cool, well-ventilated,
flame-proof, and shielded from direct sunlight, high-temperature surfaces, or
sparks.
PRECAUTIONS FOR "CARCINOGENS":
Storage site should be as close as practical to lab in which carcinogens are to
be used, so that only small quantities required for ... expt need to be carried.
Carcinogens should be kept in only one section of cupboard, an explosion-proof
refrigerator or freezer (depending on chemicophysical properties ...) that bears
appropriate label. An inventory ... should be kept, showing quantity of
carcinogen & date it was acquired ... Facilities for dispensing ... should
be contiguous to storage area. /Chemical Carcinogens/
Cleanup Methods:
Contain and isolate spill by using clay/bentonite
dams, interceptor trenches, or impoundments. /SRP: If time permits, pits, ponds,
lagoons, soak holes, or holding areas should be sealed with an impermeable
flexible membrane liner./ Construct swale to divert uncontaminated portion of
watershed around contaminated portion. ... Density stratification and
impoundment -- remove product from bottom layer by pumping through manifold or
polyethylene rope mop collection or remove clarified upper portion by skimmers
or siphon. Treatment is required for both clarified and concentrated fractions.
Treatment alternatives include powdered activated carbon, granular activated
carbon, and biodegradation. /Other/ treatment alternatives for contaminated
soils include well point collection and treatment of leachates as for
contaminated waters, bentonite/cement injection to immobilize spill.
Waste water treatment: evaporation from water
at 25 deg C of 1 ppm solution: 50% after 19-24 min, 90% after 63-80 min
Environmental considerations: Land spill: Dig
a pit, pond, lagoon, holding area to contain liquid or solid material. /SRP: If
time permits, pits, ponds, lagoons, soak holes, or holding areas should be
sealed with an impermeable flexible membrane liner./ Dike surface flow using
soil, sand bags, foamed polyurethane, or foamed concrete. Absorb bulk liquid
with fly ash or cement powder.
Environmental consideration: Water spill: If
dissolved, in region of 10 ppm or greater concentations, apply activated carbon
at ten times the spilled amount. Remove trapped material with suction hoses. Use
mechanical dredges or lifts to remove immobilized masses of pollutants and
precipitates.
Environmental considerations: Air spill: Apply
water spray or mist to knock down vapors. Combustion products include corrosive
or toxic vapors.
PRECAUTIONS FOR "CARCINOGENS": A
high-efficiency particulate arrestor (HEPA) or charcoal filters can be used to
minimize amt of carcinogen in exhausted air ventilated safety cabinets, lab
hoods, glove boxes or animal rooms ... Filter housing that is designed so that
used filters can be transferred into plastic bag without contaminating
maintenance staff is avail commercially. Filters should be placed in plastic
bags immediately after removal ... The plastic bag should be sealed immediately
... The sealed bag should be labelled properly ... Waste liquids ... should be
placed or collected in proper containers for disposal. The lid should be secured
& the bottles properly labelled. Once filled, bottles should be placed in
plastic bag, so that outer surface ... is not contaminated ... The plastic bag
should also be sealed & labelled. ... Broken glassware ... should be
decontaminated by solvent extraction, by chemical destruction, or in specially
designed incinerators. /Chemical Carcinogens/
Disposal Methods:
Generators of waste (equal to or greater than
100 kg/mo) containing this contaminant, EPA hazardous waste numbers U228, D040,
and F002 must conform with USEPA regulations in storage, transportation,
treatment and disposal of waste.
Incineration, preferably after mixing with
another combustible fuel. Care must be exercised to assure complete combustion
to prevent the formation of phosgene. An acid scrubber is necessary to remove
the halo acids produced. An alternative to disposal for trichloroethylene
is recovery and recycling.
Group I Containers: Combustible containers
from organic or metallo-organic pesticides (except organic mercury, lead,
cadmium, or arsenic compounds) should be disposed of in pesticide incinerators
or in specified landfill sites. /Organic or metallo-organic pesticides/
This compound should be susceptible to removal
from wastewater by air stripping.
Chemical Treatability of Trichloroethylene;
Concentration Process: Activated Carbon; Chemical Classification: Halogens;
Scale of Study: Pilot Scale/Continuous Flow; Type of Wastewater Used: Hazardous
Material Spill; Influent Concentration: 21 ppb; Results of Study: 98.6% removal
with 0.3 ppb detected in effluent after 8.5 min contact time (250,000 gal
spilled materials treated with EPA mobile treatment trailer).
The following wastewater treatment technology
has been investigated for trichloroethylene:
Concentration process: Biological treatment.
The following wastewater treatment technology
has been investigated for trichloroethylene:
Concentration process: Chemical precipitation.
The following wastewater treatment technology
has been investigated for trichloroethylene:
Concentration process: Stripping.
The following wastewater treatment technology
has been investigated for trichloroethylene:
Concentration process: Solvent extraction.
The following wastewater treatment technology
has been investigated for trichloroethylene:
Concentration process: Activated carbon.
Trichloroethylene is
a waste chemical stream constituent which may be subjected to ultimate disposal
by controlled incineration. Incineration, preferably after mixing with another
combustible fuel; care must be exercised to assure complete combustion to
prevent the formation of phosgene. An acid scrubber is necessary to remove the
halo acids produced.
A potential candidate for rotary kiln
incineration at a temperature range of 820 to 1,600 deg C and residence times of
seconds for liquids and gases, and hours for solids. A potential candidate for
fluidized bed incineration at a temperature range of 450 to 980 deg C and
residence times of seconds for liquids and gases, and longer for solids. A
potential candidate for liquid injection incineration at a temperature range of
650 to 1,600 deg C and a residence time of 0.1 to 2 seconds.
Recovering: Incineration, preferably after
mixing with another combustible fuel. Care must be exercised to assure complete
combustion to prevent the formation of phosgene. An acid scrubber is necessary
to remove the halo acids produced. An alternative to disposal for TCE /trichloroethylene/
is recovery and recycling. Recommendable method: Incineration. Not recommendable
method: Discharge to sewer.
Incineration & evaporation: Small
quantities may be poured onto a 10% soda ash and sand mixture, then placed in a
paper container and incinerated. Wastes from cleaning operations should be
stored in a well ventilated area until they can be incinerated or chemically
treated to reduce the toxicity. Residues may be poured on sand, soil or ashes,
at a safe distance from occupied areas and allowed to evaporate in the
atmosphere.
PRECAUTIONS FOR "CARCINOGENS": There
is no universal method of disposal that has been proved satisfactory for all
carcinogenic compounds & specific methods of chem destruction ... published
have not been tested on all kinds of carcinogen-containing waste. ... summary of
avail methods & recommendations ... /given/ must be treated as guide only.
/Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": ...
Incineration may be only feasible method for disposal of contaminated laboratory
waste from biological expt. However, not all incinerators are suitable for this
purpose. The most efficient type ... is probably the gas-fired type, in which a
first-stage combustion with a less than stoichiometric air:fuel ratio is
followed by a second stage with excess air. Some ... are designed to accept ...
aqueous & organic-solvent solutions, otherwise it is necessary ... to absorb
soln onto suitable combustible material, such as sawdust. Alternatively, chem
destruction may be used, esp when small quantities ... are to be destroyed in
laboratory. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": HEPA
(high-efficiency particulate arrestor) filters ... can be disposed of by
incineration. For spent charcoal filters, the adsorbed material can be stripped
off at high temp & carcinogenic wastes generated by this treatment conducted
to & burned in an incinerator. ... LIQUID WASTE: ... Disposal should be
carried out by incineration at temp that ... ensure complete combustion. SOLID
WASTE: Carcasses of lab animals, cage litter & misc solid wastes ... should
be disposed of by incineration at temp high enough to ensure destruction of chem
carcinogens or their metabolites. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": ...
Small quantities of ... some carcinogens can be destroyed using chem reactions
... but no general rules can be given. ... As a general technique ... treatment
with sodium dichromate in strong sulfuric acid can be used. The time necessary
for destruction ... is seldom known ... but 1-2 days is generally considered
sufficient when freshly prepd reagent is used. ... Carcinogens that are easily
oxidizable can be destroyed with milder oxidative agents, such as saturated soln
of potassium permanganate in acetone, which appears to be a suitable agent for
destruction of hydrazines or of compounds containing isolated carbon-carbon
double bonds. Concn or 50% aqueous sodium hypochlorite can also be used as an
oxidizing agent. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS":
Carcinogens that are alkylating, arylating or acylating agents per se can be
destroyed by reaction with appropriate nucleophiles, such as water, hydroxyl
ions, ammonia, thiols & thiosulfate. The reactivity of various alkylating
agents varies greatly ... & is also influenced by sol of agent in the
reaction medium. To facilitate the complete reaction, it is suggested that the
agents be dissolved in ethanol or similar solvents. ... No method should be
applied ... until it has been thoroughly tested for its effectiveness &
safety on material to be inactivated. For example, in case of destruction of
alkylating agents, it is possible to detect residual compounds by reaction with
4(4-nitrobenzyl)-pyridine. /Chemical Carcinogens/
Occupational Exposure Standards:
OSHA Standards:
Permissible Exposure Limit: Table Z-2 8-hr
Time Weighted Avg: 100 ppm.
Permissible Exposure Limit: Table Z-2
Acceptable Ceiling Concentration: 200 ppm.
Permissible Exposure Limit: Table Z-2
Acceptable maximum peak above the acceptable ceiling concentration for an 8-hour
shift. Concentration: 300 ppm. Maximum Duration: 5 minutes in any 2 hours.
Vacated 1989 OSHA PEL TWA 50 ppm (270 mg/cu
m); STEL 200 ppm (1080 mg/cu m) is still enforced in some states.
Threshold Limit Values:
8 hr Time Weighted Avg (TWA) 50 ppm; Short
Term Exposure Limit (STEL) 100 ppm
BEI (Biological Exposure Index) for Trichloroethylene:
Trichloroacetic acid in urine at end of workweek is 100 mg/g creatinine. The
determinant is nonspecific, since it is observed after exposure to other
chemicals. (1986 Adoption)
BEI (Biological Exposure Index) for Trichloroethylene:
Trichloroacetic acid and trichloroethanol in urine at end of shift at end of
workweek is 300 mg/g creatinine. The determinant is nonspecific, since it is
observed after exposure to other chemicals. (1986 adoption)
BEI (Biological Exposure Index) for Trichloroethylene:
Trichloroethylene in end-exhaled air. The biological
determinant is an indicator of exposure to the chemical, but the quantitative
interpretation of the measurement is ambiguous. These determinants should be
used as a screening test if a quantitative test is not practical or as a
confirmatory test if the quantitative test is not specific and the origin of the
determinant is in question.
A5: Not suspected as a human carcinogen.
BEI (Biological Exposure Index) for Trichloroethylene:
Free trichloroethanol in blood at end of shift at end of workweek is 4 mg/l. The
determinant is nonspecific, since it is observed after exposure to other
chemicals. (1986 adoption)
BEI (Biological Exposure Index) for Trichloroethylene:
Trichloroethylene in blood. The biological determinant
is an indicator of exposure to the chemical, but the quantitative interpretation
of the measurement is ambiguous. These determinants should be used as a
screening test if a quantitative test is not practical or as a confirmatory test
if the quantitative test is not specific and the origin of the determinant is in
question. (1993 adoption) /No value specified in text/
NIOSH Recommendations:
NIOSH considers trichloroethylene
to be a potential occupational carcinogen.
NIOSH usually recommends that occupational
exposures to carcinogens be limited to the lowest feasible concentration.
Recommended Exposure Limit: 60 Min Ceiling
Value: 2 ppm. /During the usage of trichloroethylene as
an anesthetic agent/
Recommended Exposure Limit: 10 Hr
Time-Weighted Avg: 25 ppm. /During exposures to trichloroethylene
other than as an anesthetic agent/
Immediately Dangerous to Life or Health:
NIOSH considers trichloroethylene
to be a potential occupational carcinogen.
Other Occupational Permissible Levels:
Occupational exposure limits used in various
countries are as follows: (time-weighted values) Australia: 535 mg/cu m;
Austria: 260 mg/cu m; Belgium: 535 mg/cu m; Bulgaria: 10 mg/cu m;
Czechoslovakia: 250 mg/cu m, ceiling value 1250 mg/cu m; Egypt: 267; Finland:
260 mg/cu m; France: 405 mg/cu m, ceiling value 1080 mg/cu m; German Democratic
Republic: 250 mg/cu m, ceiling limit: 750 mg/cu m; Germany, Federal Republic:
260 mg/cu m; Hungary: 50 mg/cu m; Italy: 400 mg/cu m, skin irritation 1000 mg/cu
m; Japan: 268 mg/cu m; Netherlands: 190 mg/cu m; Poland: 50 mg/cu m (ceiling
value); Romania: 200 mg/cu m, 300 mg/cu m (ceiling value); Spain: 535 mg/cu m;
Sweden: 110 mg/cu m, short-term exposure limit 250 mg/cu m; Switzerland: 260
mg/cu m; United Kingdom: 535 mg/cu m; USSR: 10 mg/cu m (ceiling value);
Yugoslavia: 200 mg/cu m.
Emergency Response Planning Guidelines (ERPG):
ERPG(1) 100 ppm (no more than mild, transient effects) for up to 1 hr exposure;
ERPG(2) 500 ppm (without serious, adverse effects) for up to 1 hr exposure;
ERPG(3) 5000 ppm (not life threatening) up to 1 hr exposure.
Manufacturing/Use Information:
Major Uses:
For Trichloroethylene
(USEPA/OPP Pesticide Code: 081202) there are 0 labels match. /SRP: Not
registered for current use in the U.S., but approved pesticide uses may change
periodically and so federal, state and local authorities must be consulted for
currently approved uses./
Therap cat: anesthetic (inhalation)/former
use/; Therap cat (vet): anesthetic (inhalation)
IN GAS PURIFICATION, AS A SOLVENT OF SULFUR
& PHOSPHORUS
Aerospace operations (flushing liquid oxygen)
AGENT IN REMOVAL OF BASTING THREADS IN TEXTILE
PROCESSING
CHEM INT FOR 1,1,2,2-TETRACHLOROETHYL SULFENYL
CHLORIDE
SOLVENT BASE FOR METAL PHOSPHATIZING SYSTEMS
SOLVENT IN CHARACTERIZATION TEST FOR ASPHALT
ENTRAINER FOR RECOVERY OF FORMIC ACID
Used as household cleaner; with
trichloroethane it is used in most typewriter correction fluid. /SRP: Former
use/
Used in wool-fabric scouring
Intermediate in the production of
pentachloroethane.
Carrier solvent for the active ingredients of
insecticides, and fungicides.
MEDICATION
MEDICATION (VET)
Used in the preparation of insecticidal
fumigants.
Trichloroethylene was
used earlier as an extraction solvent for natural fats and oils, such as palm,
coconut and soya bean oils. It was also an extraction solvent for spices, hops
and the decaffeination of coffee. The United States Food and Drug Administration
banned these uses of trichloroethylene...its use in
cosmetic and drug products was also discontinued...It was used as both an
anesthetic and an analgesic in obstetrics. /Former uses/
Trichloroethylene has
been used, in limited quantities, to control relative molecular mass in the
manufacture of polyvinyl chloride. It has also been used as a solvent in the
rubber industry, some adhesive formulations and in research laboratories. In the
textile industry, it is used as a carrier solvent for spotting fluids and as a
solvent in dyeing and finishing. It is also used as a solvent in printing inks,
paint, lacquers, varnishes, adhesives and paint strippers.
The major use of trichloroethylene
is in metal cleaning or degreasing. Trichloroethylene
is used in degreasing operations in five main industrial groups: furniture and
fixtures, fabricated metal products, electric and electronic equipment,
transport equipment and miscellaneous manufacturing industries. It is also used
in plastics, appliances, jewellery, automobile, plumbing fixtures, textiles,
paper, glass and printing industries.
Used as a chemical intermediate in the
synthesis of captafol; chloroacetic acid; 1-chloro-2,2,2-trifluoroethane
Stabilized grades are produced for vapor
cleaning applications
Use of trichloroethylene
in fluorocarbon production and as a metal cleaning and degreasing solvent are
both increasing. In vapor degreasing, trichloroethylene
has regained some market share as a result of the phaseout of
1,1,1-trichloroethane for emissive uses. Growth prospects for trichloroethylene
as a fluorocarbon feedstock hold more potential, however, particularly its use
as a precursor for the workhorse hydrofluorocarbon product, HFC-134a.
Manufacturers:
Dow Chemical USA, Hq, 2030 Dow Center,
Midland, MI 48674, (517) 636-1000; Production site: Freeport, TX 77541
PPG Industries, Inc., Hq, One PPG Place, 36
East, Pittsburgh, PA 15272, (412) 434-3131; Chemicals Group; Production site:
Lake Charles, LA 70602
Methods of Manufacturing:
Until 1968, about 85% of United States
production capacity of trichloroethylene was based on
acetylene. The acetylene-based process consists of two steps: acetylene is first
chlorinated to 1,1,2,2-tetrachloroethane, with a ferric chloride, phosphorus
chloride or antimony chloride catalyst, and the product is then
dehydrohalogenated to trichloroethylene. The current
method of manufacture is from ethylene or 1,2-dichloroethane. In a process used
by one plant in the United States, trichloroethylene is
produced by noncatalytic chlorination of ethylene dichloride and other C2
hydrocarbons with a mixture of oxygen and chlorine or hydrogen chloride.
Ethylene dichloride + chlorine (chlorination;
coproduced with perchloroethylene)
Ethylene dichloride + chlorine + oxygen (oxychlorination/dehydrochlorination;
coproduced with perchloroethylene)
General Manufacturing Information:
Since there are now only two producers (Dow
& PPG), the USITC stopped publicly reporting production and other statistics
at the end of 1982
Depending on the condition, dissociation of
HCl at elevated temperatures in the presence of carbon in a chemical plasma will
produce 1,1,2-trichloroethane, 1,2-dichloroethane, trichloroethylene,
and perchloroethylene.
Cancelled for use in fumigant mixture or as a
solvent with other ingredient on grains.
Formulations/Preparations:
Trichloroethylene for
medicinal purposes may contain thymol as a preservative. Industrial grades ...
may contain stabilizers, such as triethanolamine.
Grades: USP; technical; high purity;
electronic; metal degreasing; extraction.
Trichloroethylene is
available in the USA in high-purity, electronic USP, technical, metal degreasing
and extraction grades
Commercial grades of trichloroethylene,
formulated to meet use requirements, differ in the amount and type of added
inhibitor. Typical grades contain >99% trichloroethylene;
they include a neutrally inhibited vapor-degreasing grade and a technical grade
for use in formulations.
Stabilizers that have been used in
formulations of trichloroethylene include neutral
inhibitors and free-radical scavengers, amyl alcohol, n-propanol, isobutanol,
2-pentanol, diethylamine, triethylamine, dipropylamine, diisopropylamine,
diethanolamine, triethanolamine, morpholine, N-methylmorpholine, aniline,
acetone, ethyl acetate, borate esters, ethylene oxide, propylene oxide,
1,2-epoxybutane, cyclohexene oxide, butadiene dioxide, styrene oxide, pentene
oxide, 2,3-epoxy-1-propenol, 3-methoxy-1,2-epoxypropane, stearates,
2,2,4-trimethyl-1-pentene, 2-methyl-1,2-epoxypropanol, epoxycyclopentanol,
epichlorohydrin, tetrahydrofuran, tetrahydropyran, 1,4-dioxane, dioxalane,
trioxane, alkoxyaldehyde hydrazones, methyl ethyl ketone, nitromethanes,
nitropropanes, phenol, ortho-cresol, thymol, para-tert-butylphenol,
para-tert-amylphenol, isoeugenol, pyrrole, N-methylpyrrole, N-ethylpyrrole,
(2-pyrryl)trimethylsilane, glycidyl acetate, isocyanates and thiazoles.
Impurities:
Acidity (as hydrochloric acid), 0.0005% max;
alkalinity (as sodium hydroxide), 0.001% max; residue on evaporation, 0.005%
max; antioxidants, such as amine (0.001-0.01% or more) or combinations of
epoxides such as epichlorohydrin & esters (0.2-2% total)
Apart from added stabilizers, commercial
grades of trichloroethylene should not contain more
than the following amounts of impurities: water, 100 ppm; acidity (as HCl), 5
ppm; insoluble residue, 10 ppm. Free chlorine should not be detectable.
Impurities that have been found in commercial trichloroethylene
products include: carbon tetrachloride, chloroform, 1,2-dichloroethane,
trans-1,2-dichloroethylene, cis-1,2-dichloroethylene, pentachloroethane,
1,1,1,2-tetrachloroethane, 1,1,2,2-tetrachloroethane, 1,1,1-trichloroethane,
1,1,2-trichloroethane, 1,1-dichloroethylene, tetrachloroethylene,
bromodichloromethane, bromodichloroethylene, and benzene.
Consumption Patterns:
Demand: (1982): 240 million pounds; (1983):
Est 235 million pounds; 1987: Est 215 million pounds.
Vapor degreasing of fabricated metal parts,
80%; chemical intermediate, 5%; miscellaneous used, 5%; exports, 10% (1985)
Vapor degreasing of fabricated metal parts,
66%; chemical intermediates, miscellaneous domestic uses, 5%; exports, 22%.
Vapor degreasing of fabricated metal parts,
65%; chemical intermediates and miscellaneous uses, 35%.
Demand: 1996: 180 million pounds; 1997: 190
million pounds; 2001: 230 million pounds (includes exports)
U. S. Production:
USA production: (1981): 258,182 pounds.
Production quantities (1976): 610X10+6 pounds.
(1985) 7.72X10+10 g /Estimated/
(1991) 320 million lb
U. S. Imports:
(1985) 1.98X10+10 g
Imports last year totaled approximately 10
million pounds, averaging 12 million pounds during the period.
U. S. Exports:
(1985) 1.06X10+10 g
Exports were 65 million pounds during 1996,
but averaged 83 million pounds per year in the 1992-1996 period.
Laboratory Methods:
Clinical Laboratory Methods:
GAS CHROMATOGRAPHY USED TO DETERMINE HUMAN
SERUM AND ADIPOSE TISSUE LEVELS OF VOLATILE PURGEABLE HALOGENATED HYDROCARBONS.
Practical recommendation for the biologic
monitoring of exposure to trichloroethylene is as
following: Biological parameter: trichloroethanol. Biological material: Urine. /SRP:
Permissable/ value: 150 mg/g creatinine /From table/
Practical recommendation for the biologic
monitoring of exposure to trichloroethylene is as
following: Biological parameter: trichloroacetic acid. Biological material:
plasma. Permissable value: 5 mg/100 ml /After 5-day exposure, from table/
Practical recommendation for the biologic
monitoring of exposure to trichloroethylene is as
following: Biological parameter: trichloroethanol. Biological material: plasma.
Permissable value: 0.25 mg/100 ml /After 5-day exposure, from table/
Matrix: breath; conventional reference range:
< 1 ppm; international recommended reference range: <8 umolar
A method is presented which is suitable for
the analysis of certain halocarbons in blood and tissue samples. Among these
halocarbons is ... trichloroethylene. ... Blood samples
are warmed and an inert gas is passed through the sample to extract the volatile
halocarbons. Treated samples are macerated in water, then treated the same as
for blood samples. A Tenax gas chromatography cartridge is used to trap the
vapors which are then recovered by thermal desorption and analyzed on gas
chromatography/mass spectrometry. The limits of detection of this method are
approximately 3 ng/ml for a 10 ml blood sample and 6 ng/g for 5 g tissue
samples.
Analytic Laboratory Methods:
RECOVERIES WERE FROM FORTIFIED WHEAT SAMPLES,
USING GAS LIQUID CHROMATOGRAPHIC COLUMN & ELECTRON CAPTURE DETECTOR.
Trichloroethylene in
grain is analyzed by gas chromatography with source-heated electron capture
detector and glass-lined injection block. Construct calibration curve daily of
peak heights against ng fumigant/125 ml acetone for suitable range.
Trichloroethylene in
spice oleoresins is analyzed by gas chromatographic method.
Fujiwara Test: Trichloroethylene
is treated with pyridine in an alkaline environment. Solution absorbance is then
determined at 535 or 470 nm (absorptivity: 18-32 l/g/cm with a sensitivity of
about 1 mg/kg.
Infra-red spectroscopy: In the gaseous phase,
quantities are determined by measuring the optical density at the selected
wavelength of 11.8 um. ... This corresponds to a detection sensitivity of not
less than 0.5 ug/l.
High-resolution gas chromatography with
electron capture detector/mass spectrophotometry...for determination of trichloroethylene
in soil /has been utilized/ as a confirmatory technique with a detection
threshold of approximately 10 mg/kg (10 ppm).
EPA Method 8010. Direct Injection or Purge and
Trap Gas Chromatography with halogen-specific detector for the analysis of
halogenated volatile organics including trichloroethylene
in solid waste. Under the prescribed conditions for trichloroethylene,
the method has a detection limit of 0.12 ug/l. Precision and method accuracy
were found to be directly related to the concentration of the parameter and
essentially independent of the sample matrix.
EPA Method 502.1. Volatile Halogenated Organic
Compounds in Water by Purge and Trap Gas Chromatography. Revision 2.0. Analysis
by GC with electrolytic conductivity detection. Detection limit= 0.001 ug/l in
drinking water.
EPA Method 502.2. Volatile Organic Compounds
in Water by Purge and Trap Capillary Column Gas Chromatography with
Photoionization and Electrolytic Conductivity Detectors in Series. Revision 2.0.
Detection limit= 0.01 ug/l in drinking water.
EPA Method 503.1. Volatile Aromatic and
Unsaturated Organic Compounds in Water by Purge and Trap Gas
Chromatography" Revision 2.0 Analysis by gas chromatography with
photoionization detection. Detection limit= 0.01 ug/l in drinking water.
EPA Method 524.1. Measurement of Purgeable
Organic Compounds in Water by Packed Column Gas Chromatography and Mass
Spectrometry. Revision 3.0. Detection limit= 0.4 ug/l in drinking water.
EPA Method 524.2. Measurement of Purgeable
Organic Compounds in Water by Capillary Column Gas Chromatography/Mass
Spectrometry. Revision 4.0. Detection limit= 0.19 ug/l in drinking water.
EPA Method 551. Determination of Chlorination
Disinfection Byproducts and Chlorinated Solvents in Drinking Water by
Liquid-Liquid Extraction and Gas Chromatography with Electron-Capture Detection.
Detection limit= 0.002 ug/l in drinking water.
EPA Method 601. Purgeable Halocarbons in
Wastewater by Gas Chromatography with Electrolytic Conductivity Detection.
Detection limit= 0.120 ug/l in drinking water.
EPA Method 624. Protocol for the Analysis of
Purgeable Organic Priority Pollutants in Industrial and Municipal Wastewater.
Detection limit= 1.9 ug/l in wastewater.
EPA Method 8240. Determination of Volatile
Organics Compounds by Gas Chromatography/Mass Spectrometry (GC/MS). Estimated
quantitation limit= 5 ug/l.
EPA Method 8021. Analysis of Halogenated and
Aromatic Volatiles By Gas Chromatography using Electrolytic Conductivity and
Photoionization Detectors in Series: Capillary Column Technique. Detection
limit= 0.01-0.02 ug/l.
EPA Method 8260B. Volatile Organic Compounds
by Gas Chromatography/Mass Spectrometry (GC/MS): Capillary Column Technique.
EPA Method 1624. Volatile Organic Compounds by
Isotope Dilution GCMS. Detection limit= 2 ug/kg in soil.
NIOSH Method: 3701. Analtye: Trichloroethylene.
Matrix: Air. Procedure: Gas chromatography (portable), photoionization detector.
For trichloroethylene this method has an estimated
detection limit of 0.25 ng/injection/sample. The precision/RSD is 0.078 and the
recovery is not given. Applicability: The working range is 10 to 1000 ppm (54 to
5100 mg/cu m) in relatively non-complex atmospheres where trichloroethylene
is known to be present. Interferences: None found.
NIOSH Method: 1022. Analyte: Trichloroethylene.
Matrix: Air. Procedure: Gas chromatography, flame ionization detector. For trichloroethylene
this method has an estimated detection limit of 0.01 mg/sample. The precision/RSD
is 0.038 @ 1.6 to 6.4 mg/sample and the recovery is not given. Applicability:
The working range is 27 to 875 ppm (150 to 4700 mg/cu m for a 3.4 liter air
sample. Interferences: None studied.
Gas chromatograph/mass spectrometric analysis
of volatiles including trichloroethylene. The Contract
Required Quantitation Limits are 5.0 ug/kg in solids at low level, 500 ug/kg in
solids at medium level, and 5 ug/l in water as used in EPA Contract Laboratory
Program.
EPA Method 0-3115. Purge and trap gas
chromatography/mass spectrometric method for the determination of organic
substances including trichloroethylene in water and
fluvial sediments. The estimated detection limit is 3 ug/l as used in US
Geological Survey Techniques of Water Resources.
Sampling Procedures:
Water samples were collected in 125 ml serum
vial that had been cleaned by detergent wash, distilled water rinse, dichromic
acid wash, and oven-drying at 150 deg C. Vials were completely filled and stored
at 4 deg C. Minimum loss occurred during storage at 4 deg C up to 28 days.
Sampling ... /is conducted by utilizing/
activated carbon felt badges.
Sampling ... /is conducted by utilizing/
activated carbon tubes.
EPA Method 8010. For the analysis of solid
waste, a representative sample (solid or liquid) is collected in a standard
40-ml glass screw-cap VOA vial equipped with a Teflon-faced silicone septum.
Sample agitation, as well as contamination of the sample with air, must be
avoided. Two vials are filled per sample location, then placed in separate
plastic bags for shipment and storage.
NIOSH Method: 3701. Analyte: Trichloroethylene.
Matrix: Air. Sampler: Air bag (Tedlar). Flow Rate: 0.02 to 0.05 l/min or higher;
fill bag to equal to or greater than 80% of capacity; spot samples possible.
Sample Stability: Bags should be analyzed as soon after collection as possible
(equal to or greater than 4 hrs).
NIOSH Method: 1022. Analyte: Trichloroethylene.
Matrix: Air. Sampler: Solid sorbent tube (coconut shell charcoal 100 mg/50 mg).
Flow Rate: 0.01 to 0.2 l/min. Sample Size: 3.4 liters. Shipment: Routine. Sample
Stability: Not determined.
Special References:
Special Reports:
Health and Safety Executive Monograph: Trichloroethylene
#6 (1982).
USEPA; Ambient Water Quality Criteria
Document: Trichloroethylene (1980) EPA-440/5/80-007.
NTP; Division of Toxicology Research and
Testing; Management Status Report; 07/22/92; p.27. NTP TR No 002; Route: oral,
gavage; Species: rats and mice. NTIS No PB264122/AS.
WHO; Environ Health Criteria 50: Trichloroethylene
(1985).
Municipal Environmental Research Laboratory;
USEPA, Survey of Two Municipal Wastewater Treatment Plants for Toxic Substances,
March (1977)
DHHS/ATSDR; Toxicological Profile for Trichloroethylene
(Update) TP-92/19 (1993)
NTP TR No 243; Route: gavage; Species: rats
and mice. NTIS No PB91111815/AS.
Bruening T; Bolt HM; Critical Reviews in
Toxicology 30 (3): 253-285 (2000). Renal toxicity and carcinogenicity of trichloroethylene:
Key results, mechanisms, and controversies.
Lash LH; Parker JC; Scott CS; Environ Health
Perspect 108 (2): 225-240 (2000). Modes of action of trichloroethylene
for kidney tumorigenesis.
Moore MM; Harrington-Brock K; Environmental
Health Perspectives 108 (2): 215-223 (2000). Mutagenicity of trichloroethylene
and its metabolites: implications for the risk assessment of trichloroethylene.
Wartenberg D; Reyner D; Scott C; Environmental
Health Perspectives 108 (2): 161-176 (2000). Trichloroethylene
is an organic chemical that has been used in dry cleaning, for metal degreasing,
and as a solvent for oils and resins. It has been shown to cause liver and
kidney cancer in experimental animals. This article reviews over 80 published
papers and letters on the cancer epidemiology of people exposed to trichloroethylene.
U.S. Department of Health & Human
Services/National Toxicology Program; Tenth Report on Carcinogens. National
Institutes of Environmental Health Sciences. The Report on Carcinogens is an
informational scientific and public health document that identifies and
discusses substances (including agents, mixtures, or exposure circumstances)
that may pose a carcinogenic hazard to human health. Trichloroethylene
(79-01-6) was first listed in the Ninth Report on Carcinogens (2000) as
reasonably anticipated to be a human carcinogen.
Synonyms and Identifiers:
Synonyms:
ACETYLENE TRICHLORIDE
**PEER REVIEWED**
AI3-00052
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ALGYLEN
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ANAMENTH
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BENZINOL
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Caswell No 876
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CECOLENE
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CHLORILEN
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1-CHLORO-2,2-DICHLOROETHYLENE
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Chlorylea, Chorylen, CirCosolv, Crawhaspol,
Dow-Tri, Dukeron, Per-A-Clor, Triad, Trial, TRI-Plus M, Vitran
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DENSINFLUAT
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1,1-Dichloro-2-chloroethylene
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Pesticide Code: 081202
**QC REVIEWED**
EPA Pesticide Chemical Code 081202
**PEER REVIEWED**
ETHENE, TRICHLORO-
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ETHINYL TRICHLORIDE
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ETHYLENE TRICHLORIDE
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ETHYLENE, TRICHLORO-
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FLECK-FLIP
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FLOCK FLIP
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FLUATE
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GERMALGENE
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LANADIN
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LETHURIN
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NARCOGEN
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NARKOSOID
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NCI-C04546
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NIALK
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NSC 389
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PERM-A-CHLOR
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PETZINOL
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PHILEX
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THRETHYLEN
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THRETHYLENE
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TRETHYLENE
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TRI
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TRIASOL
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Trichloraethen
(German)
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Trichloraethylen, tri (German)
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TRICHLORAN
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TRICHLOREN
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Trichlorethene (French)
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TRICHLORETHYLENE
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Trichlorethylene, tri (French)
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TRICHLOROETHENE
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1,1,2-TRICHLOROETHYLENE
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TRICLENE
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Tricloretene
(Italian)
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Tricloroetilene
(Italian)
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Trielin
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Trielina (Italian)
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TRIKLONE
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TRILENE
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TRIMAR
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TRI-PLUS
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VESTROL
**PEER REVIEWED**
Formulations/Preparations:
Trichloroethylene for
medicinal purposes may contain thymol as a preservative. Industrial grades ...
may contain stabilizers, such as triethanolamine.
Grades: USP; technical; high purity;
electronic; metal degreasing; extraction.
Trichloroethylene is
available in the USA in high-purity, electronic USP, technical, metal degreasing
and extraction grades
Commercial grades of trichloroethylene,
formulated to meet use requirements, differ in the amount and type of added
inhibitor. Typical grades contain >99% trichloroethylene;
they include a neutrally inhibited vapor-degreasing grade and a technical grade
for use in formulations.
Stabilizers that have been used in
formulations of trichloroethylene include neutral
inhibitors and free-radical scavengers, amyl alcohol, n-propanol, isobutanol,
2-pentanol, diethylamine, triethylamine, dipropylamine, diisopropylamine,
diethanolamine, triethanolamine, morpholine, N-methylmorpholine, aniline,
acetone, ethyl acetate, borate esters, ethylene oxide, propylene oxide,
1,2-epoxybutane, cyclohexene oxide, butadiene dioxide, styrene oxide, pentene
oxide, 2,3-epoxy-1-propenol, 3-methoxy-1,2-epoxypropane, stearates,
2,2,4-trimethyl-1-pentene, 2-methyl-1,2-epoxypropanol, epoxycyclopentanol,
epichlorohydrin, tetrahydrofuran, tetrahydropyran, 1,4-dioxane, dioxalane,
trioxane, alkoxyaldehyde hydrazones, methyl ethyl ketone, nitromethanes,
nitropropanes, phenol, ortho-cresol, thymol, para-tert-butylphenol,
para-tert-amylphenol, isoeugenol, pyrrole, N-methylpyrrole, N-ethylpyrrole,
(2-pyrryl)trimethylsilane, glycidyl acetate, isocyanates and thiazoles.
Shipping Name/ Number DOT/UN/NA/IMO:
UN 1710; Trichloroethylene
IMO 6.1; Trichloroethylene
Standard Transportation Number:
49 411 71; Trichloroethylene
EPA Hazardous Waste Number:
U228; A toxic waste when a discarded
commercial chemical product or manufacturing chemical intermediate or an
off-specification commercial chemical product or manufacturing chemical
intermediate.
F002; A hazardous waste from nonspecific
sources when a spent solvent.
D040; A waste containing trichloroethylene
may or may not be characterized as a hazardous waste following testing by the
Toxicity Characteristic Leaching Procedure as prescribed by the Resource
Conservation and Recovery Act (RCRA) regulations.
Administrative Information:
Hazardous Substances Databank Number: 133
Last Revision Date: 20030829
Last Review Date: Reviewed by SRP on 1/20/2001
Update History:
Complete Update on 2003-08-29, 1 fields
added/edited/deleted
Complete Update on 03/05/2003, 3 fields added/edited/deleted.
Field Update on 02/14/2003, 1 field added/edited/deleted.
Field Update on 11/08/2002, 1 field added/edited/deleted.
Complete Update on 10/16/2002, 2 fields added/edited/deleted.
Complete Update on 08/06/2002, 1 field added/edited/deleted.
Complete Update on 05/13/2002, 1 field added/edited/deleted.
Complete Update on 01/14/2002, 1 field added/edited/deleted.
Complete Update on 08/09/2001, 1 field added/edited/deleted.
Complete Update on 05/23/2001, 92 fields added/edited/deleted.
Field Update on 05/15/2001, 1 field added/edited/deleted.
Field Update on 09/12/2000, 1 field added/edited/deleted.
Complete Update on 02/08/2000, 1 field added/edited/deleted.
Complete Update on 02/02/2000, 1 field added/edited/deleted.
Complete Update on 01/11/2000, 8 fields added/edited/deleted.
Field Update on 11/18/1999, 1 field added/edited/deleted.
Field Update on 09/21/1999, 1 field added/edited/deleted.
Complete Update on 06/03/1999, 3 fields added/edited/deleted.
Field Update on 05/17/1999, 1 field added/edited/deleted.
Field Update on 05/04/1999, 1 field added/edited/deleted.
Complete Update on 03/29/1999, 1 field added/edited/deleted.
Complete Update on 02/01/1999, 1 field added/edited/deleted.
Complete Update on 01/20/1999, 2 fields added/edited/deleted.
Complete Update on 11/16/1998, 1 field added/edited/deleted.
Complete Update on 11/12/1998, 1 field added/edited/deleted.
Complete Update on 06/02/1998, 1 field added/edited/deleted.
Complete Update on 10/17/1997, 1 field added/edited/deleted.
Complete Update on 05/08/1997, 1 field added/edited/deleted.
Complete Update on 03/27/1997, 2 fields added/edited/deleted.
Complete Update on 03/11/1997, 3 fields added/edited/deleted.
Complete Update on 02/26/1997, 1 field added/edited/deleted.
Complete Update on 01/09/1997, 2 fields added/edited/deleted.
Complete Update on 10/12/1996, 1 field added/edited/deleted.
Complete Update on 06/27/1996, 1 field added/edited/deleted.
Complete Update on 06/11/1996, 2 fields added/edited/deleted.
Complete Update on 05/17/1996, 2 fields added/edited/deleted.
Complete Update on 04/16/1996, 29 fields added/edited/deleted.
Field Update on 01/18/1996, 1 field added/edited/deleted.
Field Update on 09/26/1995, 1 field added/edited/deleted.
Field Update on 09/26/1995, 1 field added/edited/deleted.
Field Update on 08/31/1995, 1 field added/edited/deleted.
Field Update on 08/21/1995, 1 field added/edited/deleted.
Field Update on 04/20/1995, 1 field added/edited/deleted.
Field Update on 04/20/1995, 1 field added/edited/deleted.
Field Update on 01/24/1995, 1 field added/edited/deleted.
Field Update on 12/19/1994, 1 field added/edited/deleted.
Field Update on 08/04/1994, 1 field added/edited/deleted.
Complete Update on 05/05/1994, 1 field added/edited/deleted.
Complete Update on 03/25/1994, 1 field added/edited/deleted.
Complete Update on 02/02/1994, 1 field added/edited/deleted.
Complete Update on 01/12/1994, 92 fields added/edited/deleted.
Field Update on 11/05/1993, 1 field added/edited/deleted.
Field Update on 09/16/1993, 1 field added/edited/deleted.
Field Update on 08/03/1993, 1 field added/edited/deleted.
Field update on 12/11/1992, 1 field added/edited/deleted.
Complete Update on 08/17/1992, 87 fields added/edited/deleted.
Complete Update on 04/27/1992, 1 field added/edited/deleted.
Complete Update on 01/23/1992, 1 field added/edited/deleted.
Complete Update on 09/26/1991, 2 fields added/edited/deleted.
Complete Update on 10/22/1990, 1 field added/edited/deleted.
Complete Update on 06/28/1990, 12 fields added/edited/deleted.
Field Update on 05/14/1990, 1 field added/edited/deleted.
Field Update on 01/15/1990, 1 field added/edited/deleted.
Complete Update on 01/11/1990, 9 fields added/edited/deleted.
Field Update on 05/05/1989, 1 field added/edited/deleted.
Field Update on 03/01/1989, 1 field added/edited/deleted.
Complete Update on 09/23/1988, 2 fields added/edited/deleted.
Complete Update on 08/18/1988, 114 fields added/edited/deleted.
Complete Update on 07/24/1985
Created 19830401 by GCF
GLCC RELATED TOXIC SUBSTANCES
FOUND IN THE CAMP POND AND CAMP WATER WELL 2003 AND 2004