Tca 2
Tca 2
Tca 2
TRICHLOROACETIC ACID
FOREWORD
INTRODUCTION
TRICHLOROACETIC ACID
CAS N: 76-03-9
UNEP PUBLICATIONS
OECD SIDS
TRICHLOROACETIC ACID
SIDS INITIAL ASSESSMENT PROFILE
CAS Nr.
Chemical Name
Structural formula
76-03-9
Trichloroacetic acid
CCl3-COOH
CONCLUSIONS AND RECOMMENDATIONS
Environment: A potential risk to the aquatic compartment is identified due to high toxicity to algae
and local exposure from use as auxiliary in textile dyes, waste water from electroplating facilities,
textile washing and pulp mills. A potential risk to the terrestrial environment is identified due to
high toxicity to plants and global exposure from the decomposition of C2-chlorocarbons.
Human health: The chemical is reprotoxic, corrosive and an eye irritant but adequate protection
measures are currently being applied. Trichloroacetic acid is currently considered of low potential
risk and low priority for further work.
SHORT SUMMARY WHICH SUPPORTS THE REASONS FOR THE CONCLUSIONS
AND RECOMMENDATIONS
The production volume of trichloroacetic acid (TCA) is ca. 1000 t/a in Germany. TCA is mostly
used in the production of TCA Na-salt used as a herbicide. TCA is also used as an auxiliary in
textile dying processes.
TCA is stable in neutral solution and is classified as "non biodegradable" with a "low
bioaccumulation potential" for fish and a "high bioaccumulation potential" for terrestrial plants.
The most sensitive environmental species to TCA is the alga Chlorella pyrenoidosa (14d-NOEC =
0.01 mg/l) and pine (60d-EC10 = 0.12 mg/kg).
The acute oral, dermal and inhalation toxicity is low. This chemical is corrosive and strongly
irritant to the eyes. The NOEL in a 90-day study in dogs - the most sensitive species tested - was
determined as 500 ppm (approx. 30 mg/kg bw/day). The NOEL for repeated dose toxicity in a 4month feeding study with rats was 4000 ppm (365 mg/kg bw/day), the NOEL in a 2-year feeding
study in rats was 1600 ppm (80 mg/kg bw/day).
An inconsistent picture was found in tests on genotoxic action. Point-mutation tests were
predominantly negative. In-vivo tests of chromosome mutations were mostly positive, but effects
only appeared after high loading of the animals. The SCE test in mice was negative. The results of
a micronucleus test in mice are apparently not reproducible. The end point of the sperm anomaly
test is not necessarily due to genetic damage. The validity of the positive test results described for
the clastogenic effects in mice suffers from the partly insufficient experimental procedure.
Drinking water studies in male and female mice to 52 or 61 weeks gave an increased incidence of
tumours in the livers of the male mice only. A 2-year feeding study with rats and a drinking water
study over 100 - 104 weeks in rats showed no evidence of carcinogenicity.
Reproduction toxicology investigations in rats showed maternal and embryonic toxicity from 330
mg/kg bodyweight and from 800 mg/kg also embryo-lethality. In all dose-groups there was a doseUNEP Publications
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dependent increase in visceral anomalies, particularly in the cardiovascular system. The mean
frequency of soft tissue malformations ranged from 9% at the low dose (330 mg/kg) to 97% at the
high dose (1800 mg/kg/day). A NOAEL could not be established. Based on these findings TCA
was considered to be developmentally toxic in the pregnant rat at doses of 330 mg/kg and above.
The aquatic local PEC probably due to its use in textile finishing industry was estimated to be 7 27 g/l. The PEC in natural soil due to atmospheric oxidation of C2-chlorocarbons is 8 - 150
g/kg.
In conclusion, TCA represents a risk to both the hydrosphere as well as the soil compartment.
Considering the low exposure potential to humans, available toxicity data support a low risk to
human health. The tumorigenic action in male mouse liver corresponds to the type, which leads to
liver tumours preferentially in male mice via peroxisome proliferation, hepatotoxicity and liver cell
proliferation.
IF FURTHER WORK IS RECOMMENDED, SUMMARISE ITS NATURE
There is a need for consideration of risk management measures, concerning the environment and
these should be addressed by the Risk Management Advisory Group.
Measurements in forest soils should be performed to actualise the soil pollution.
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FULL SIDS SUMMARY
CAS-NO.: 76-03-9
PROTOCOL
RESULTS
PHYSICAL CHEMICAL
2.1
Melting-Point
NA
56
2.2
Boiling-Point
DIN 53171
197
C (at101.3 kPa)
2.3
Density
NA
2.4
Vapour Pressure
NA
0.12
2.5
exp.
-0.27
calc.
1.33
NA
miscible at
20C
C
2.6 A
B
2.12
Water solubility
pH
at
pKa
NA
0.7
mV
kPa at 50C
ENVIRONMENTAL FATE /
BIODEGRADATION
3.1.1
Photodegradation
3.1.2
Stability in water
3.2
Monitoring data
3.5
calc. (Atkinson)
NA
In air T1/2
= 446days
ca 1% hydrolysation in 4 - 6
weeks
In air
= / mg/m3
In surface water =0.09 - 370
g/l
In soil / sediment = 0.02 - 0.4
g/g
In biota = ND - 0.1 g/g
calculated
(fugacity
level 1 type)
In air
/%
In water / %
In sediment / %
In soil / %
In biota / %
Biodegradation
OECD 302 B
10% after 27 d
OECD 302 A
0 - 46% after 28 d
OECD
max. 10%
confirmatory test
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ECOTOXICOLOGY
(lowest effect data only)
Pimephales
promelas
Daphnia magna
4.1
4.2
acute/prolonged toxicity to
aquatic invertebrates ( daphnia ) Somatochlora
cingulata
NA
2000mg/l
NA
2000mg/l
NA
LOEC (8h) =
0.01
mg/l
4.3
Chlorella
pyrenoidosa
NA
4.4
toxicity to microorganisms
NA
EC50 (14 d) =5
mg/l
4.5.1
NA
LOEC (63d) = 7
mg/l
4.6.1
Spirulina
platensis
Cyprinus
carpio
Eisenia foetida
4.6.2
87/302/EEC
NA
Allolobophora
rosea
Avena sativa
BBA (1984)
NA
LC100 (90d) =
20mg/kg dw
TOXICOLOGY
5.1.1
dog
rat
mouse
Hoechst
internal
LD50
LD50
LD50
=1590 - 2000mg/kg
=3310 - 6900mg/kg
=4970 mg/kg
5.1.2
Hoechst
internal
5.1.3
rat
Hoechst
internal
LD50
5.4
rat
dog
Hoechst
internal
5.5
several
5.6
mouse
mouse
mouse
5.8
toxicity to reproduction
5.9
developmental toxicity /
teratogenicity
rat
5.11
168
NA
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Trichloroacetic acid
CAS Nr.:
76-03-9
Empirical Formula:
C2HCl3O2
Structural Formula:
CCl3-COOH
98%
Major impurities
2. Exposure
2.1 General discussion
In 1993, ca. 1000 t were produced in Germany (6). There is no information available on production
volumes in other countries.
In Germany and in the USA, trichloracetic acid is industrially produced by chlorination of acetic
acid (5) (6).
The use pattern in Germany is the following (6):
670 t
250 t
50 t
30 t
export
processing to sodium trichloroacetate (NaTCA)
processing to trichloroacetic acid-ethylester
sale in Germany (mainly to producers of pharmaceuticals)
Of the produced NaTCA, ca. 110 t/a are sold in Germany and the rest is exported.
For production and processing, discharges occur at the German site into waste water in amounts of
ca. 1 kg/a and about 17 kg/a via exhaust air (6).
At a second German site, where ca. 100 t of NaTCA are used in the formulation of textile finishing
products, 2 t/a are released to a waste water treatment plant (6).
The main application for NaTCA is its use as a selective herbicide and in formulations with 2,4-D
and 2,4,5-T preparations as a total herbicide. In Germany and in Switzerland, the sale and import of
NaTCA as a herbicide is prohibited since 1989. In the USA, NaTCA is still used as a herbicide.
Several other uses are reported in literature (1). TCA is employed as an etching or pickling agent in
the surface treatment of metals, as an albumin precipitating agent in medicine, as an auxiliary in
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textile finishing, and as an additive to improve high-pressure properties in mineral lubricating oils.
Because it is strongly corrosive, TCA is used to remove warts and hard skin and to treat various
skin afflictions. Particularly the esters of TCA are important starting materials in organic syntheses.
For Germany, the only environmentally exposure-relevant use of TCA, which could be identified, is
its use as an auxiliary in textile finishing (ca. 110 t/a (6)). According to the German producer, TCA
is included in dyes as an alcali-liberating auxiliary for fixing reactive dyes on fibres for printing
processes. In the usual formulations, the relative ratio to the actual dye is 1:1. Its average
concentration in the formulations is 40 g/kg. Ca. 2.9 g TCA are necessary to completely dye 100 g
textile.
According to a US-importer, TCA is also used as a glue precipitant, and as an etching agent in the
manufacture of photographic films (5).
Furthermore, TCA is formed as a by-product:
- from chlorination of drinking water and swimming pools;
- in chemical cleaning units using tetrachloroethylene;
- in electroplating facilities treating cyanide containing waste water with NaOCl;
- in textile washing facilities using NaOCl as bleaching or disinfection agent;
- during bleaching of paper in paper mills;
- during the atmospheric oxidation of C2-chlorocarbons. This subject is elaborated more
detailed in Appendix I.
Some authors set up the hypothesis that TCA could be formed in soils by enzymatic chlorination of
naturally occuring compounds. In an in vitro laboratory test, TCA formation was simulated
incubating different natural occuring short chained aliphatic acids with the chlorinating enzyme
chloroperoxidase in the presence of sodium chloride and hydrogenperoxide. Trichloromethane and
chlorinated acetones were identified as main products, while TCA was formed in low yields (8%
with acetic acid, less than 1% with malic acid, lactic acid, fumaric acid, malonic acid, citric acid and
acetonedicarboxylic acid ). As a high peroxide concentration (3 g/l) was used, it seems to be
questionable that under natural conditions TCA is formed in any significant amount (19).
2.2 Environmental exposure
2.2.1 General/Environmental fate
TCA is miscible with water. The pure solid compound has a vapour pressure of 120 Pa at 50 C. In
aqueous solution, TCA dissociates (pKa = 0.7) and volatilization from water is not to be expected to
a high degree. The measured log Pow amounts to - 0.27 (probably dissociated form). The log Pow
of the undissociated TCA was calculated to be 1.33. Bioaccumulation factors of 0.4 - 1.0 and <1.7
have been determined experimentally (OECD GL 305C). Bioaccumulation in fish is therefore
considered to be low.
In plants, a rapid uptake and distribution of TCA occurs. 22 days old seedlings of oat and wheat
were exposed to a solution containing 0.03 mg/l 14 C-TCA for 42.5 h. After exposure the seedlings
were transferred into pots containing clay laom soil and were grown to appropriate stages of
maturity. Uptake and distribution of 14 C was examined with time for 16 weeks. A rapid translocation of 14 C-TCA from roots to shoots was observed especially for wheat. In the roots of both
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plants a substantial reduction of 14 C was found 3 weeks after absorption. However, elimination from
shoots was very slow and uncomplete (50% after 16 weeks).
With barley and oat as test species bioaccumulation of 14 C-TCA in plants was examined. The plants
were grown in a closed aerated system in sandy agricultural soil treated with TCA (1 mg/kg dw)
and were thus able to take up the chemical both by the roots from the soil and by the leaves from
the air where the TCA has been volatilized. Also non-contaminated soil was placed in the closed
system and protected against contamination by the air by a special close cover. In this soil plants
were grown, the roots being in non-contaminated soil and the leaves in contaminated air. High
bioconcentration factors (330 - 970) were determined 7 days after application. Uptake was both by
roots and by leaves and transport within the plants was in both directions. The 14 C residues in the
plants grown in treated soil contained only small portions of the parent compound. For barley, only
8.5 % of total 14 C present in shoots was TCA, and only 10.6 % in roots. For oats the corresponding
figures were 8.7 % in shoots and 9.9 % in roots. The plants grown in untreated soil contained only
unknown polar metabolites.
The uptake of TCA in the needles of two year old potted Scots pine (Pinus sylvestris) seedlings was
studied (18). Two exposure set-ups, the root route and the atmospheric route simulating wet
deposition of fog were used. Seedlings were exposed via roots by applying 5 ml of a TCA solution
containing 0.02 mg/l respectively 1 mg/l into each pot, giving doses of 0.1 g and 5 g TCA
respectively. The wet deposition treatments to the foliage were done inside teflon chambers which
were placed over the seedlings during the treatment. 10 ml of a TCA solution (1 mg/l and 50 mg/l)
were fumigated with bottled synthetic air by nebulizers. The aqueous TCA fog was distributed on
all surfaces in the chamber, thus the exact TCA dose obtained by the needles is not known. The pots
of the seedlings exposed to TCA by wet deposition were covered with a piece of plastic to prevent
contamination of the soil. In both experiments seedlings were exposed 3 times a week for 9 weeks.
TCA was effectively incorporated into the needles via roots. TCA concentrations were 700 800 g/kg and 40 - 60 g/kg at the end of the experiment in the second year needles (C+1) treated
with 5 g and 0.1 g TCA respecitvely. The levels in the current year needles (C) were 2-3 times
lower. About 80 % of the TCA applied as wet deposition remained on the surface of the needles and
could be removed by rinsing with water. The TCA levels inside the C+1 needles at the end of the
exposure were about 270 - 320 g/kg and 60 - 80 g/kg in the needle treated with high and low
doses of TCA respecitvely. The C-needles exhibited about 1.5-4 times lower concentrations than
the older C+1 needles.
Bioaccumulation of TCA in plants is therefore considered to be high.
Due to the ionic nature of TCA, the leaching behaviour in soil can not be described with log Pow
and water solubility only. Binding to the mineral parts of soil is possible, although not quantifiable.
As found in a laboratory test, there is strong indication that TCA is physically or chemically bound
on humic acids. TCA was added to aqueous solutions of humic acids in different concentrations,
and the recovery rate for TCA analysis was detemined. With the lowest tested humic acid concentration of 3 mg/l, only about 10% of the TCA could be extracted, and the recovery rate deteriorated
with increasing humic acid concentrations (19).
Tests on ready biodegradability of TCA in the aquatic medium are not available. Nevertheless
several test results on inherent biodegradability are available. In two Zahn-Wellens-Tests with
industrial activated sludge, TCA proved to be non biodegradable (ca. 5 - 10 % DOC removal after
27 days). In a modified MITI-II-Test (with 100 mg/l instead of 30 mg/l test substance; 100 mg/l
inoculum) biodegradation rates of 0 - 46% in 28 days were recorded.
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On the other hand, in a modified OECD confirmatory test, no significant biodegradation was
observed; even after increasing the retention time up to 48 hours, only a maximum of 10 %
biodegradation with regard to Cl- -liberation could be achieved.
In aerated lagoons receiving the effluents from mills producing pulp from wood the removal was
22% in one treatment plant (age 3 years; hydraulic retention time 2.5 days) and 99 % in a second
(age 10 years; hydraulic retention time 5 days).
Despite the many negative biodegradation results in laboratory tests, a significant elimination of
TCA in waste water treatment plants can be expected, based on monitoring data.
Indeed, the elimination of TCA was monitored in 5 domestic waste water treatment plants (wwtps)
in Switzerland ranging from 24 to 90 %. An average removal rate of 66% was recorded (average
influent concentration: 1.4 g/l; effluent conc.: 0.43 g/l). The elimination variation in the different
wwtp cannot be conclusively explained as data on operating conditions of the wwtps are available
only for 2 plants. A possible explanation would be a difference in hydraulic retention times, being
19 hours in one (87% elimination) and 12.5 hours in the second (47% elimination). The average
hydraulic retention time in domestic wwtps is estimated to be about 7 - 14 hours though. Therefore,
for a realistic worst case estimation, it would be appropriate to assume a wwtp elimination of 24%.
On the other hand, for a complete exposure assessment, the sequential use of worst case situations,
which would lead to unrealistic worst case situations have to be avoided. As other worst case
assumption are already included in most of the exposure scenarios (e.g. a dilution factor in surface
waters of 10), the average elimination rate of 66% can nevertheless be used in the following
exposure estimation.
Biodegradation of TCA in soil was also investigated, but no standardized investigations or
measurements comparable with standard procedures are available.
In suspensions of different soils the dt50-values of TCA biodegradation (with respect to Cl- liberation) amounted to 10 to 30 days with probes of the upper 5 cm of soil profiles and 16 to 68
days for deeper soil levels, depending on the origin of soil samples. The high numbers of
microorganisms in soil probes that were able to grow with TCA as sole source of energy indicate
that there might be a preadaptation of the soil microorganisms to TCA.
In a laboratory study, after 5 month, biodegradation reached 29% in a fine sand and 81.7% in a
humus soil estimated from remaining radioactivity in soil. The high numbers of microorganisms in
soil probes that were able to grow with TCA as sole source of energy indicate also here that there
might be a preadaptation of the soil microorganisms to TCA.
In two field studies, it could be demonstrated that TCA is biologically degraded from soil
microorganisms. In one study dt50 values varied between 18.1 and 25.5 days depending on soil
types and experimental conditions. The initial chemical burden of soils could not be estimated from
literature in both studies. It is demonstrated that replicated treatment of soil with TCA reduces the
lag-period and dt50-values significantly.
As a conclusion, TCA is biologically degraded from adapted soil organisms. Biodegradability of
TCA from non-adapted soil organisms can not be finally assessed from available data.
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For the assessment, only a very slow biodegradation rate can be assumed. Based on the above
results, at best a biodegradation half-life of 150 days can be assumed. This half-life is derived from
the 5 month study measuring remaining radioactivity in soil.
Zakordonec et al. (1987) found dichloroacetic acid and monochloroacetic acid as metabolites of
NaTCA degradation in forest soil.
2.2.2 Monitoring data
atmosphere
Only one investigation on the occurence of TCA in the atmosphere is available. In 1992, it was
detected in concentrations of 0.4 to 3 ng/m3 in unfiltered air sampled in a German rural area (15).
hydrosphere
The average concentration in the lake "Greifensee" in Switzerland was measured to be 0.09 g/l.
The 90-percentile value was 0.12 g/l (50 samples over a depth of 0 - 30 m from 6.12.92 - 4.10.93).
The concentration in other Swiss lakes was below 0.1 g/l.
The concentration in several Swiss rivers varied from 0 - 0.34 g/l (average 0.14 g/l). The 90percentile was 0.33g/l (30 samples from 7 rivers).
The TCA-concentration in the Austrian river "Pls" downstream of a pulp mill varied between 148
and 558 g/l (10 samples; average: 370 g/l). In the river "Mur", downstream of another pulp mill
the concentrations were < 3 - 104 g/l (6 samples; average 56 g/l).
rain water
The measured TCA-concentrations in rain water in 1989 in Germany (Hessen) are 0.2 - 6.5 g/l (94
samples from 8 locations). The average concentration was 1.7 g/l. Further rain samples were taken
over a year in 1990/91 in Berlin with concentrations of 0.1 - 20 g/l. The yearly average was
2.1 g/l in wooded areas and 0.9 g/l elsewhere.
In 1991/92, TCA was measured in the rain water in a distance of about 30 km from Siegen
(Germany), where metal industry is settled. The concentrations were < 0.1 g/l in December and
2 g/l in June with an annual average of 0.57 g/l. At a site in the vicinity, 0.1 - 0.21 g/l were
detected, without seasonal dependence (19).
The average concentration in rain water was determined as 0.3 g/l in Switzerland in 1993 (44
samples at 2 locations). The 90-percentile value was 0.62 g/l (11).
In the summer of 1993, TCA concentrations between 0.044 and 0.710 g/l were measured in the
city of Zrich. The mean TCA concentrations decreased from 0.3 to 0.13 g/l in the period 19931995. Simultaneously the concentrations of some chlorohydrocarbons decreased at a sampling point
in the vicinity indicating that they could be the precursors. In Alpthal (a rural area in Switzerland)
similar TCA concentrations than in Zrich were measured. The deposition by canopy runoff from
the trees was larger than by rain in the open field. This is explained by the authors by dry deposition
onto trees with subsequent rinsing (14).
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During a monitoring program in Germany in 1993/94, TCA was measured in the rain water both in
open fields and forested areas at 9 rural sites. The maximum concentrations (2-months-mixed
samples) were in the range from 0.37 - 2.2 g/l with mean values (averaged over 15 months) of 0.2
-0.85 g/l in forested areas. In open fields (the sampling sites were in the near vicinity of the forest
sites), the maximum values were 0.33 - 0.47 g/l and the mean values 0.17 - 0.28 g/l (20).
The rain water monitoring data reveal that the TCA concentrations in urban and industrialized
regions are substantially higher than in rural regions. Several investigations show a seasonal
dependence, the concentrations in summer are higher than in winter. These results indicate that the
main source of the atmospheric TCA is the photochemical degradation of tetrachloroethylene (cf
Appendix I). TCA is not only deposited by rain water, but by dry deposition e.g. on leaves and
needles from which it is rinsed during rainfalls; this leads to an advanced pollution of forest soils.
waste water
The average effluent concentration from 5 domestic wwtps in Switzerland was 0.43 g/l. The
effluent concentration in the wwtp of a paper mill in Switzerland was measured at 104 g/l (one
24h-sample). The untreated waste water of 4 electroplating facilities, treating their waste water with
NaOCl contained 0.1 - 87 g/l TCA (6 samples; average: 32 g/l). The untreated waste water of 4
textile washing facilities, using NaOCl for bleaching, contained 2,3 - 205 g/l TCA (7 samples;
average: 97 g/l).
swimming pools
The water in 34 swimming pools in Switzerland were analyzed. The average TCA concentration
was 64 g/l.
soil compartment and biota
In 1986, trichloroacetic acid was measured in fir and spruce needles of forest trees (Black Forest,
Northern Alps, Germany) in concentrations up to 0.1 mg/kg fresh needle weight. The TCA
concentration greatly depended on the needle age, time and place of the sampling as well as on the
meteorological conditions. The TCA concentrations were relatively high (up to 300 g/kg needles)
after dry- and sunny periods, while it dropped to 1/10 or less after rainy periods. The youngest
needles on one spruce branch contained 30 g/kg, and older needles contained 80 g/kg. In soil
samples from the same forests (20 cm depth) TCA was also detected at concentrations of 0.02 - 0.4
mg/kg soil in 1988 (not clear wether wet weight or dry weight). The high concentrations can be
explained by the characteristics of the sampling sites: on the mountains a high photolytical activity
is combined with high rainfall levels.
Further pine needles in the area of Berlin were sampled over 2 years in 1990/91. The concentrations
were in the range of 0.7 to 175 g/kg with monthly average concentrations of 10 - 55 g/kg fresh
weight.
In another monitoring programme in Germany, soil leachate (passing through a 10 cm layer of
natural soil) was sampled at 4 locations. The concentrations (mean values for each location) were in
the range of 0.14 to 2.80 g/l (overall average 0.7 g/l). Compared to the above reported concentrations in rain water (average 1.7 g/l), which were measured during the same time at the same
locations, the concentration is diminished during the passage of the rain water through the soil
layer. The cause can be that TCA is degraded in soils by microorganisms or adsorbs onto soil solids
(cf. 2.2.1).
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In 1991/92, TCA was measured in the soil of 4 rural sites in the Netherlands. The concentrations
were 1.0 - 2.7 g/kg at a peat-moor, 2.6 - 4.6 g/kg at a peat-bog, 0.2 - 0.9 g/kg in a forest with
beech trees and 0.2 - 1.3 g/kg in a douglas forest. In douglas needles at the last site, 23 g/kg were
detected (21).
2.2.3 Exposure estimation / PEC - calculations
In the following, the releases leading to high local concentrations are modelized.
2.2.3.1 hydrosphere
- local concentration due to formulation of textile dyes
At one German site, 2 t NaTCA/a are released to a wwtp during formulation of textile dyes
(processing of 100 t NaTCA/a). With an assumed elimination rate in the wwtp of 66%, 0.7 t/a are
released into surface waters. The site being located on the upper Rhine, a concentration at low flow
(ca. 550 m3/s) is estimated at PEC local = 0.04 g/l. No data are available regarding other chemical
producers performing the same operations. For a more generic approach, a site independant
exposure scenario for intermediates is proposed in the the EU-Technical Guidance Documents (2),
using a flow of 60 m3/s of the receiving river. Assuming the same processing volumes and release
rates for other chemical producers, a PEC local of 0.37 g/l can be estimated.
- local concentration due to the use as auxiliary in textile dyes
According to the TGD, the colouring capacities of dye-houses vary within a wide range. An average
weight of processed goods of 3000 kg/day is assumed implying a daily use of 86 kg TCA for dying
the whole cloth. During the steaming process for fixation, TCA is decomposed under formation of
sodium bicarbonate, soda and chloroform (3). In a laboratory simulation test, performed by the
producer, TCA decomposed to 96.5%. With this decomposition rate, a daily release rate of 3 kg is
estimated.
The default volumes of water used during wet process of textile material (including pretreatment
like scouring, desizing, mercerizing, bleaching etc.) is ca. 250 m3/1000 kg textile (2). For those
textile processing units, which do not perform all the pretreatment processes, lower waste water
volumes would occur and subsequent higher concentrations of TCA.
With the above indicated waste water volumes, and the decomposition rate of 96.5 % a
concentration in the raw waste water of 4 mg/l is calculated.
Most textile processing sites are rejecting their waste water into domestic waste water treatment
plants (ca. 93 % in Germany ). Assuming a dilution factor of 5 upon entering the wwtp, an influent
concentration of ca 0.8 mg/l is calculated.
Elimination during biological treatment is assumed to be 66 % (see above). With an elimination rate
of 66% in wwtps and assuming a further dilution factor of 10 upon entering the surface water, a
PEC local of ca. 27 g/l is calculated. Distribution processes immediately upon entering the surface
water are not to be expected (see above).
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For estimating the successive dilution steps, other data are available: in a recent survey of textile
processing units by ETAD, the 20-percentile of the water flow of 25 waste water treatment plants
receiving waste water from textile processing units is 5000 m3/d. The 20-percentile of the water
flow of 18 rivers receiving waste water from these wwtps is 45000 m3/d.
With an release of 3 kg/d TCA, an elimination in wwtps of 66% and dilution in a total of 5000 +
45000 m3/d, the resulting PEClocal is 20 g/l.
The above scenario assumes that the whole cloth is dyed. On the other hand, print colour is usually
applied only to specific areas by screen printing systems to achieve the planned design. For
comparison, the PEC will be calculated for an average use of 30 kg dye per day (2), i.e. 30 kg TCA.
With a decomposition rate of 96.5%, 1.05 kg TCA are rejected per day into the waste water.
Eliminated in wwtps at a rate of 66% and diluted in 50000 m3/d, the resulting PEClocal is 7 g/l.
In conclusion, the expected PEC local in surface waters will be in the range of 7 to 27 g/l.
- local concentration due to the treatment of cyanide containing waste water from electroplating
facilites
The above described measurements in untreated waste water, reporting concentrations averaging 32
g/l can be used for a PEC estimation. Assuming an elimination of 66% in wwtps and a dilution
factor of 10 in receiving surface waters, a PEC local of 1 g/l is estimated.
- local concentration due to textile washing with NaOCl bleach
The above described measurements in untreated waste water, reporting concentrations averaging 97
g/l can be used for a PEC estimation. Assuming an elimination of 66% in wwtps and a dilution
factor of 10 in receiving surface waters, a PEC local of 3.3 g/l is estimated.
- local concentration due to pulp mill effluents
Monitoring data in surface water are available for this pathway. Due to the low number of samples
(6 - 10), only the average concentrations can be used. A PEC local of 56 - 370 g/l can be expected.
- regional concentration
The measured concentrations in the Swiss lake "Greifensee" can be considered as representative for
a background concentration, i.e. PEC regional = 0.12 g/l. For a correct exposure assessment, this
background concentration needs to be added to the concentration due to point emissions, unless the
latter are based on measurements in the receiving surface water.
In the following table, an overview of the different PECs are presented:
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Concentration [g/l]
0.37
0.04
7 - 27
1
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pulp mills
56 - 370
Concentration [g/l]
2.2.3.2 atmosphere
There are no direct emissions of TCA into the atmosphere during its production or use. However,
the substance is formed due to the photooxidation of tetrachloroethene and 1,1,1-trichloroethane.
The relative importance of both precursors to the environmental TCA is elaborated in Appendix I.
The result is that tetrachloroethylene is the main source of TCA formed in the atmosphere.
Due to its low volatility, TCA is removed from the atmosphere by dry and wet deposition, which
leads to an ubiquitary pollution of soils. Air-born TCA was detected in fir and spruce needles (cf.
2.2.2).
2.2.3.3 soil
As adsorption onto sludge is not to be expected to a significant extent (log Pow max. 1.33; no
adsorption was observed in the Zahn-Wellens-Tests), agricultural soils are not polluted by this
route.
The main release to soil, apart from its use as a herbicide, is expected through atmospheric deposition. The question whether TCA is formed in soil by a natural process (cf. 2.1) is not decided
finally.
A realistic TCA concentration in soil can presently not be modelled as fundamental parameters like
distribution constant and degradation rate are not known exactly. Thus, the assessment is performed
on the basis of monitoring data.
The measured data in soil were 20 - 400 g/kg (assumed these are based on wet soil => ca. 23 - 450
g/kg dw). As the tetrachloroethylene concentrations in German rural areas decreased by a factor of
about 3 since 1986 (cf. Appendix III, Schauinsland), it can be assumed, as an approximation, that
the TCA concentration also decreased by this factor. Thus, 8 - 150 g/kg dw can be assumed as the
present concentration range being chosen for the PECsoil in this assessment.
Di- and monochloroacetic acid were found to be metabolites of TCA in soils (16). Several authors
state that these compounds are more toxic than TCA, so the real risk which is only based on TCA is
underestimated.
2.3 Consumer exposure
In the USA, TCA is found as a disinfection by-product in drinking water. The quarterly median
concentrations ranged from 4.0 to 6.0 g/l (35 water utilities). These concentrations being median
values, the actual concentrations will be higher in 50% of all cases.
The extent to which TCA is used in consumer products is unknown.
2.4 Occupational exposure
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development. No further findings of toxicological relevance were discovered. The NOEL was
determined as 4000 ppm (365 mg/kg bodyweight/day).
In a subchronic feeding study, Na-TCA was administered daily over a 90-days period in the
(moist feed) to five groups each consisting of 3 male and 3 female beagle dogs in
concentrations of 0, 500, 2000, 4000 and 8000 ppm. Toxicological examinations were carried
on behaviour, general health, body weights, food consumption, haematology, urinalyses
histopathological examination of the organs.
diet
test
out
and
In the two highest dose groups, 5 males had to be killed in moribund state and one female died
intercurrently of pleuritis. From 2000 ppm upwards body weight decreases occurred accompanied
by impairment of general health, necroses of the gums and oral mucosa, anaemia (diminution of red
cells, haemoglobin and haematocrit) and changes in the leucocyte count (leucocytosis and
lymphocytopenia). From 2000 ppm upwards, the histopathological examinations showed hepatic
and myocardial changes. Oligospermia and azoospermia were seen in 2 animals dosed with 2000
ppm and in all animals in the 4000 and 8000 ppm groups. From 4000 ppm upwards atrophy of
skeletal muscles occurred. Urinalysis of the males from the 4000 ppm and 8000 ppm groups killed
during the study revealed positive protein and bilirubin reactions.
Based on these findings the "no effct level" in this study was 500 ppm, equivalent to approx. 30 mg
Na-TCA/kg body weight/day.
In a 2-year study in rats, 250, 630, 1600 or 10,000 ppm sodium trichloroacetate was administered
with the daily feed. A significantly reduced bodyweight development was caused by 10,000 ppm.
All other parameters investigated, such as the feed consumption, substance uptake, blood picture,
serum enzymes, urine findings, and organ weights were in the normal range. Histopathological
examinations showed that feeding with sodium trichloroacetate over 2 years in rats did not lead to
any morphologically discernible organ damage. In particular, no evidence was found of a
carcinogenic action. The NOEL was determined as 1600 ppm (approx. 80 mg/kg bodyweight/day).
Human experience: no data available
c. Carcinogenicity
Animal data:
Drinking water studies of the carcinogenicity of trichloroacetic acid in male and female mice for 52
weeks (1000 or 2000 mg TCA/l) or 61 weeks (5000 mg TCA/l only in male mice) gave a
significantly increased incidence of tumours in the livers of the male mice. Females showed no
significant differences from the controls.
In a 2-year feeding study, TCA was administered to male and female rats in concentrations of 250,
630, 1600 or 10,000 mg/kg feed. There was no evidence of substance-specific neoplastic alterations
in any of the groups.
A drinking water study over 100 - 104 weeks in rats with concentrations of 0, 50, 500 or 5000 mg
TCA/l showed liver toxicity but no evidence of carcinogenicity.
Mechanistic investigations showed that TCA induces peroxisome proliferation in rat and mouse
hepatocyte cultures, but not in human liver-cell cultures.
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It is known that the male B6C3F1 mouse in particular is unusually sensitive to the development of
liver tumours.
Because TCA causes liver tumours only in the male B6C3F1 mouse after the administration of very
high concentrations, and the peroxisome proliferation detected represents an extensively rodentspecific process, which has a subordinate meaning in humans, a tumour-initiating action is unlikely
for TCA.
Human experience: no data available.
Conclusion: While in male B6C3F1 mouse TCA is hepatocarcinogenic, there is no evidence that
humans are at significant risk for hepatocellular toxicity.
Recommendation: No need for follow-up test. NTP has not conducted short-term toxicology or
long-term toxicology and carcinogenesis bioassays on TCA.
Priority setting: low priority or concern
d. Reproductive Toxicity
Animal data:
Reproduction toxicology investigations after treatment of pregnant rats from 6th to the 15th day of
gestation showed maternal and embryonic toxicity from 330 mg/kg bodyweight, and from 800
mg/kg also embryo-lethality. In all dose groups there was a dose-dependent increase in visceral
anomalies, particularly in the cardiovascular system. Maternal spleen and kidney weights increased
in a dose related manner. The mean frequency of soft tissue malformations especially in the
cardiovascular system, ranged from 9% at the low dose (330 mg/kg/day) to 97% at the high dose
(1800 mg/kg/day).
Human experience: no data available.
Conclusion: The authors of the developmental toxicity study considered TCA to be a developmental
toxin in the rat at doses 330 mg/kg bodyweight.
Recommendation: no need for follow-up test
Priority setting: Low priority or concern considering the low exposure potential
e. Genetic Toxicity
Experimental data:
Trichloroacetic acid has been tested for genotoxicity in a series of Ames tests, in the Rec assay
using Bacillus subtilis, and on the basis of point mutations in Aspergillus nidulans in vitro. In all
these studies trichloroacetic acid gave negative results, except in one, in which dimethyl sulfoxide
(DMSO) was used as a solubilizer. In the authors' opinion TCA reacts with DMSO to give a
mutagenic intermediate which subsequently decomposes, because after an hour the mixture is no
longer mutagenic.
Free as well as neutralized TCA were incubated with human lymphocytes (500, 2000 and 3500
g/ml) and examined for induction of chromosome aberrations. The free acid acted clastogenic with
and without S9-mix, however only in concentrations at which the pH value was significantly
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reduced. The neutralized TCA did not cause a significant increase in chormosome damage (Styles
et al., 1992).
TCA did not induce any DNA-strand breaks in hepatocyte cultures of B6C3F1-mice and Fisher-344
rats after a 4-hour incubation with up to 10 mM. No DNA-strand breaks were determined also after
a 2-hour incubation with human CCRF-CEF cells (same concentration, Chang et al., 1992).
TCA was examined on the mouse for induction of chromosome aberrations, micronuclei and spermhead anomalies. Three adults Swiss mice each were used per end-point; per animal, 100 metaphases
were examined for chromosome aberrations, 1000 poly- and normochromatic erythrocytes for
micronuclei and 500 sperms for anomalies. The study on chromosome aberration took place under
various exposure conditions: the preparation of the bone marrow occured 24 hours after the last
application following intraperitoneal injection of 125, 250 or 500 mg TCA/kg bw or 100 mg
TCA/kg bw and day for 5 days or after oral administration of 500 mg/kg bw. After intraperitoneal
injection of 500 mg/kg bw, the bone marrow preparation took place after 6, 24 and 48 hours. An
increase in chromosome aberrations in the range of 3- 6 % compared to the controls (0.16-0.2 %),
could be observed under all test conditions. Hereby, the single administration of the substance was
more effective than the fractionated application. Moreover, the results depended on the time of the
bone marrow preparation (strongest effects after 24 hours) and on the application route (effects after
intraperitoneal application were stronger than after oral application; Bhunya and Behera, 1987).
In the micronucleus test, mice were intraperitoneally treated twice within 24-hour intervals with
125, 250 or 500 mg TCA/kg bw. The preparation of the bone marrow was performed 6 hours after
the last application. There was an increase in the micronuclei in poly- and normochromatic
erythrocytes. Nevertheless, the findings were not dosage-dependent, because the weakest effects
were shown at a dosage of 250 mg/kg bw (Bhunya and Behera, 1987)
In vivo, a negative result was obtained in a well conducted and well reported bone marrow
micronucleus study in mice (Mackay et al. 1995). In contrast, statistically significant (but non-doserelated) increases in the frequency of cells containing micronuclei were observed in the Bhunya and
Behera-study, 1987. The study by Mackay et al. was conducted to GLP and QA standards in an
attempt to confirm the study by Bhunya and Behera. It employed the same study design, but with
the addition of an extra sampling time at 24 hours. Mackay et al. proposed the positive results
previously observed with TCA may have been due to a non-genotoxic mechanism, possible caused
by physicochemically induced stress, resulting from intraperitoneal pH changes. In addition,
Bhunya and Behera reported a positive test for chromosome aberration in mouse bone marrow. It is
possible that these results may have also arisen via a non-genotoxic mechanism attributable to pH
changes as proposed by Mackay et al.
For studying sperm-head anomalies, the animals were treated for 5 days intraperitoneally with 125,
250 or 500 mg TCA/kg bw and day. The preparations were produced 35 days after the last
application. A dosage-dependent increase in sperm-head anomalies of 4.4-7.6 % was found
compared to the controls (2.06 %; Bhunya and Behera, 1987).
None of the cited studies carried along positive controls in order to define the sensibility of the test
systems.
Two other micronuclei tests produced negative results (DeAngelo et al., 1989; Styles et al., 1992).
In one test, the mice were intraperitoneally administered neutralized TCA twice within 24 hours
(25 %, 50 % and 80 % of the mean lethal dosage, corresponding up to 1300 mg/kg bw). On the
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The initiating and promoting properties of TCA were studied in a short-term carcinogenicity test on
the male Spargue-Dawley rat. This test is based on the detection of preneoplastic lesions in form of
enzyme-altered foci in the rat liver. 24 hours after a 2/3 hepatectomy, the rats obtained either a
single oral application of 1500 mg/kg bw or 5000 ppm TCA in drinking water (ca. 350 mg/kg bw)
for 10, 20 or 30 days. Two weeks after ending the treatment, the animals were treated for 3 or 6
month with 500 ppm phenobarbital in drinking water as a promoter. TCA had no effects as an
initiator, becaues it did not induce any gamma-glutamyl-transpeptidase (GGT)-positive foci in the
rat liver (Parnell et al., 1986).
Furthermore, male Sprague-Dawley rats (6 animals per group) were orally treated after a 2/3
hepatectomy with a single dose of 10 mg/kg bw of the initiator diethylnitrosamine. They then
received 50, 500 or 5000 ppm TCA in drinking water (ca. 4, 40 or 350 mg/kg bw) for 3 or 6 month.
In all dosage groups, there was a significant increase in GGT-positive foci in the rat liver after 6
month. A slight stimulation (10-20 % above the control) of cyanide-insensitive palmitoyl-CoAoxidation could be observed simultaneously only in the highest dosage group. Hepatomegaly was
not observed. According to the authors, TCA seems to have weakly promoting properties and thus
seems to possibly be a weak epigenetically effective carcinogen (Parnell et al., 1986).
Human experience:
The herbicide sodium trichloroacetate increases chromosome aberration frequency in the culture of
human peripheral lymphocytes.
Conclusion:
Overall, on balance, the available evidence does not suggest that TCA is a mutagen. This
conclusion is consistent with the view that the liver tumours observed in mice treated with TCA
(see carcinogenicity comments) arose by a non-genotoxic mechanism (peroxisome proliferation).
Recommendation:
48h-LC50
48h-LC50
48h-LC50
>10000 mg/l
9160 mg/l
277 mg/l
96h-LC50
96h-LC50
9300 mg/l
2000 mg/l
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The highest toxicity to fish was recorded with Oncorhynchus tschawytscha (48h-LC50 = 10 mg/l)
but no information is available on the test conditions, especially if the test medium was neutralized
or not. The LC50-values for neutralized solutions are consistently high. The lowest acute toxicity in
a valid test was recorded at 2000 mg/l. Furthermore the results from a long-term test are available:
Cyprinus carpio
63d-LOEC
7 mg/l *
The weight loss was ca. 10% compared to the controls. No other behavioural or clinical changes
were observed. Histopathological changes were muscular atrophy and hyaline degeneration as well
as cell necrosis in the gills.
b) toxicity to invertebrates
Daphnia magna
24h-EC50
24h-EC50
48h-EC50
8370 mg/l
>10000 mg/l*
2000 mg/l
Daphnia magna
(the test medium was not neutralized)
24h-EC50
110 mg/l
Nitocra spinipes
48h-EC50
4800 mg/l
Thamnocephalus platyurus
24h-EC50
Streptocephalus proboscideus
24h-EC50
(no information about neutralization; Centeno et al. 1995)
16.9 mg/l
1.5 mg/l
The EC50-values for neutralized solutions are consistently high. The lowest acute toxicity in a valid
test was recorded at 2000 mg/l. No long-term test results are available. Sublethal effects were
determined with Dragonfly nymphs (several different species: Somatochlora cingulata, Aeschna
umbrosa and species of genera Aeschna and Basiaeschna); significant effects were recorded on the
oxygen consumption rate at 0.01 mg/l and 0.1 mg/l and the ammonia excretion rate at 0.01 mg/l.
This is the lowest recorded effect concentration with TCA.
c) toxicity to algae
Scenedesmus quadricauda
7d-TT
Effect: growth inhibition (biomass); TT = toxicity threshold
200 mg/l*
Ankistrodesmus minutissimus
Chlorella pyrenoidosa
98 mg/l*
0.3 mg/l*
0.01 mg/l*
0.46 mg/l*
0.01 mg/l*
1.2 mg/l*
7 mg/l*
8.8 mg/l*
Chlorella mucosa
Chlorococcum sp.
Dictospaerium pulchellum
Scenedesmus acutus
Effect: growth inhibition (biomass)
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14d-EC50
14d-EC50
14d-NOEC
14d-EC50
14d-NOEC
14d-EC50
14d-EC50
14d-EC50
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mixed culture of Chlorococcales
Effect: inhibition of oxygen production
TRICHLOROACETIC ACID
24h-EC10
As expected (cf. SIDS for Monochloroacetic acid CAS Nr. 79-11-8), algae are very sensitive to
TCA. Only results from non standardized tests are available. The strongest effects were recorded in
a 14-day test with the species Chlorella pyrenoidosa and Chlorella mucosa (9). Although the
recorded effects are based on biomass after the exponential growth phase, an analysis of the growth
curves reported in the publication shows that the effect concentrations derived from biomass during
the exponential growth phase are of the same order as those reported after 14 days.
d) Toxicity to microorganisms
Protozoae:
Entosiphon sulcatum
16h-TT
Effect: growth inhibition (biomass); TT = toxicity threshold
800 mg/l*
Cyanobacteria:
Microcystis aeruginosa
8d-TT
Anabaena variabilis
14d-EC50
Spirulina platensis
14d-EC50
Effect: growth inhibition (biomass); TT = toxicity threshold
250 mg/l*
8 mg/l*
5 mg/l*
Bacteria:
Photobacterium phosphoreum
Effect: inhibition of bioluminescence
15min-EC50
Pseudomonas putida
16h-TT
Effect: growth inhibition (biomass); TT = toxicity threshold
Pseudomonas cepacia
24h-MIC
Aeromonas hydrophilia
24h-MIC
Bacillus Subtilis
24h-MIC
Effect: growth inhibition (cell count): MIC = Minimum Inhibition concentration
35 mg/l
>1000 mg/l*
1000 mg/l*
1000 mg/l*
1000 mg/l*
24h-EC10
24h-EC20
Determination of PNECaqua
The lowest aquatic effect concentrations were determined with algae (14d-NOEC = 0.01 mg
NaTCA/l = 0.0086 mg TCA/l) and with invertebrates (significant effects at 0.01 mg/l). The acute
sublethal effects recorded with the dragonfly nymphs underline the high sensibility of certain
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organisms with TCA. On the other hand, as this type of recorded effects do not fit the usual
assessment schemes, the effect data from algae are used for the assessment here.
According to the EU-Technical Guidance Documents (2), a safety factor of F = 50 applied to the
lowest NOEC would be appropriate, as long-term tests are available only for species from two
trophic levels. It could be argued that a NOEC is available for the most sensitive species, and that a
safety factor of 10 is sufficient. On the other hand, the very high acute to long-term toxicity ratio
found in fish (nearly 300) lessens this probability.
PNEC aqua = 8.6 g/l / 50 = 0.17 g/l
3.2.2 Terrestrial organisms
a) toxicity to plants
Many results on acute toxicity to plants are available:
Avena sativa
(2 test results)
Brassica rapa
Triticum aestivum
(17)
organic soil
14d-EC50
14d-EC50
15d-EC50
( of 10 test results)
15d-EC50
( of 3 test results)
(effect: growth only, effect on germination not determined)
sandy loam
< 1 - 23 mg/kg dw
308 mg/kg dw
1.46 mg/kg dw
2.79 mg/kg dw
14d-EC50
14d-EC50
14d-EC50
560 mg/kg dw
37 mg/kg dw
48 mg/l
14d-EC50
14d-EC50
14d-EC50
124 mg/kg dw
154 mg/kg dw
59 mg/l
Long-term tests with NaTCA were performed with pine and spruce seeds (species not indicated). At
4 mg/kg dw, the germination was inhibited in 2 - 15 % of the shoots and 27 - 61 % at 64 mg/kg dw.
The most sensitive parameter was the weight of the roots: an inhibition of 34% for pine and 60% for
spruce, compared to the controls was observed at 1 mg/kg dw after 60 days. No NOECs were
determined by the author. For pine, a dose-response curve for weight reduction in the roots can be
established by probit analysis, and a 60d-EC10 of 0.14 mg/kg dw can be derived. For spruce, which
was even more sensitive to TCA than pine, no dose-response curve can be established. The 60dEC10 of 0.14 mg/kg corresponds to an EC10 of 0.12 mg/kg related to TCA.
b) toxicity to invertebrates
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In a ring test involving 21 laboratories, the acute toxicity of TCA to the earthworm Eisenia fetida
according to EEC-Guideline was tested.
The mean result was:
14d-LC50
>1140 mg/kg dw
In the same manner a contact filter paper test was performed by 33 laboratories. The mean result
was:
48h-LC50
0.0964 mg/cm2
Results from a long term test with earthworms are also available. The growth and sexual
development was observed over 3 months for the earthworm species Allolobophora caliginosa, A.
chlorotica, A. rosea and Lumbricus terrestris. Two substrates were used for the test: an equal
volume mixture of clay and farmyard manure and an equal volume mixture of sand and farmyard
manure. Two TCA concentrations were tested: 20 ppm and 40 ppm. In the substrate clay and
farmyard manure TCA caused no or only slight effects at both concentrations. However, in sand
and farmyard manure 20 ppm were lethal to A. rosea and caused retarded growth and in some cases
also mortality for the other species. No NOEC can be derived from this test.
Determination of PNECsoil
As with aquatic organisms, the highest effects were determined with plants. The lowest acute effect
concentrations were determined with Avena sativa (14d-EC50 = <1 - 23 mg/kg dw) and with
Triticum aestivum (15d-EC50 = 1.46 mg/kg dw respectively 2.79 mg/kg dw). The bioavailability in
the different soils is very variable. For TCA, ionic interaction with the mineral part of soils is to be
expected. This is shown especially in the comparative results with Avena sativa and Lactuca sativa.
The long term tests show also high effects in earthworms, although NOECs could not be
determined. With pine a 60d-EC10 of 0.14 mg/kg dw can be derived for the endpoint weight
reduction of the roots, which can be used as a NOEC in the first approach.
For the derivation of the PNEC soil from the available data two approaches are possible. One way is
to use the EC10 from the long-term study with pine and spruce as basic value for the PNECsoil. As
long-term tests with species from two trophic levels are available an assessment factor of 50 is
appropriate. However, it could be stated that a NOEC is available for the most sensitive trophic
level (plants) and that therefore an assessment factor of 10 might be adequate.On the other hand,
there are several reasons that would also justify the use of an assessment factor of 100. One reason
is that no NOEC could be determined with the most sensitive plant species (spruce). Furthermore,
the long-term test with earthworms indicate a high acute to long-term toxicity ratio. In addition,
bioaccumulation of TCA in plants is considered to be high. This could be shown in several tests and
also by measuring the TCA concentration in needles. The chronic effects of bioaccumulating
substances cannot be described adequately as real chronic tests are missing and therefore a more
conservative assessment factor should be chosen for such substances. A 60d-study with pine or
spruce seedlings cannot be regarded as chronic test as for a tree a period of 60 days that consideres
not even seasonal changes is extremely short compared with the lifetime of more than 100 years. As
conclusion an assessment factor not lower than 50 can be applied on the EC10 from the pine study:
PNEC soil = 120 g/kg dw / 50 = 2.4 g/kg dw
A second possible approach is the derivation of the PNEC soil using the available short-term tests.
The lowest EC50 of 1.46 mg/kg dw was found in a 15d-growth inhibition test with wheat (Triticum
aestivum) using a sandy loam as substrate. An assessment factor of 1000 has to be applied to this
value:
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4. Initial Assessment
4.1 Human toxicity
TCA is a relatively strong organic acid. Acute exposure shows mild to moderate skin and eye burns,
but it is not readily absorbed through the skin.
In high concentrations TCA causes peroxisome induction in mice. For many such substances it is
known that they typically lead to liver tumours in male B6C3F1 mice (but not in rats) and with a
lower incidence in female mice. Through a regenerative process at hepatotoxic doses TCA clearly
stimulates the mitosis rate and thus DNA synthesis in the liver.
Point-mutation tests were predominantly negative. In-vivo tests of chromosome mutations were
mostly positive, but effects only appeared after high loading of the animals. The SCE test in mice
was negative. The results of a micronucleus test in mice are apparently not reproducible. The end
point of the sperm anomaly test is not necessarily due to genetic damage.
The validity of the positive test results described for a clastogenic effect in mice suffers from the
partly insufficient experimental procedure.
As an overall conclusion the available data do not suggest any genotoxic mechanism. This is
supported by carcinogenicity studies in which no indications of a carcinogenic effect were observed
aside from an increased incidence of hepatic tumours in the male mouse. The tumorigenic action in
male mouse liver corresponds to the type which leads to liver tumours preferentially in male mice
via peroxisome proliferation, hepatotoxicity and liver-cell proliferation.
The corrosive property of TCA prompts workers to dramatically limit the potential exposure to this
chemical. An OSHA PEL of 7 mg/m3 has been established for TCA. The extent to which TCA is
used in consumer products is unknown. The potential for consumer exposure to TCA has not been
estimated.
4.2 Assessment of environmental hazards
a. aquatic compartment
In the following table, the PEC/PNEC ratios for the different exposure scenarios are presented:
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Scenario
PEClocal + PECregional
[g/l]
PEC/PNEC
0.37 + 0.12
0.04 + 0.12
2.88
0.94
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use as auxiliary in textile dyes
waste water from electroplating facilities
textile washing
pulp mills
TRICHLOROACETIC ACID
7 + 0.12
resp. 27 + 0.12
1 + 0.12
3.3 + 0.12
56 - 370
41
resp. 159
6.6
20
329 - 2176
For most configurations, the ratio PEC/PNEC is greater 1. A risk for the aquatic compartment has to
be expected.
b. terrestrial compartment
As the PECsoil can not be modelled satisfactorily, the risk assessment is performed with the
monitoring data. The PECsoil was estimated to 8 - 150 g/kg dw (cf. 2.2.3.3). With a PNECsoil of
2.4 g/kg dw, the following ratios are calculated:
PEC
[g/kg dw]
8
150
PEC/PNEC
3.3
63
With the measured concentrations in soil, a risk to the terrestrial ecosystem can clearly be deduced.
In addition it has to be kept in mind that plants are not only exposed to TCA via the soil (uptake by
the roots) but also via the atmosphere (uptake via the needle or leaf surface). Therefore it means to
underestimate the risk for plants if only the uptake of TCA via the soil is considered. However, with
the available data it is not possible to quantify the amount of TCA taken up by plants via the
needles or leaves from the atmosphere and to compare it with the uptake by the roots.
Mono- and dichloroacetic acid were found as metabolites of TCA in soil. These compounds are
more toxic than TCA. In addition, all three compounds have a similar mode of action and therefore
additive effects can be assumed. This means that the real risk seems to be underestimated.
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toxicity towards algae: the highest effects were recorded in a non standard test. In a thorough
evaluation of the publication, the validity of the results could be ascertained though. A result
from a standard test with Chlorella pyrenoidosa would probably not improve the assessment.
long-term toxicity towards daphnids: a reproduction tests with daphnids could lower the safety
factor. A lower NOEC than for the algae is not expected though. However, the use of a safety
factor of 10 would not change the overall result of the assessment.
use as auxiliary in textile dyes: the PEC from this use is estimated. Can the releases be
analytically monitored ?
For the terrestrial compartment, the risk assessment results that there is a risk for the terrestrial ecosystem. This risk is caused by TCA which is formed in the atmosphere mainly from tetrachloroethylene. As the PER emissions have decreased in the last years, measurements could be performed
to actualize the soil pollution. The substance should be preferredly measured in forest soils, as it is
known that these soils are highly polluted.
A revision of the PNECsoil by the conduction of further biotests is not possible with justifyable
expense. No guideline exists for the conduction of a real chronic study with conifers that considers
both the long lifetime of a tree and the high bioaccumulation potential of TCA in plants.
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1. Appendix
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Cl
+ O H
Cl
Cl
H
Cl
Cl
-H
Cl
+O
Cl
2
Cl
O
Cl
1,1,1-Trichloroethane
+NO, O
-NO
, O
Cl
Cl
Ox.
H
Cl
C
Cl
Cl
H
aqueous
Trichloroacetaldehyde
C
Cl
O H
Trichloroacetic acid
Cl
5
-3
-3
months (COH = 5.10 molecules.cm ) and 13 months (C Cl = 500 molecules.cm ). With these
figures, 25% of the tetrachloroethylene are degraded by the pathway starting with chlorine atom
addition, which leads with 15% yield to TCA (13).
In the following, only the degradation pathway which leads to TCA is presented (13). The reactions
leading to other products are omitted:
CCl2CCl2 + Cl. CCl3CCl2.
CCl3CCl2. + O2 CCl3CCl2O2.
CCl3CCl2O2. + NO CCl3CCl2O.+NO2
CCl3CCl2O. (85%) CCl3COCl + Cl.
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(1)
With:
f111-T :
C111-T :
k111-T :
Y111-T :
K:
proportionality constant
(2)
As the proportionality constant K includes only parameters describing the environment and the
environmental fate of TCA, and no properties of 1,1,1-trichloroethane and tetrachloroethylene, in
both equations K must be equal. It can be eliminated by division of equations 1 and 2:
f111-T
-------fPER
(3)
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With the elimination of K, most of the uncertainties of the analysis are eliminated.
As 1,1,1-trichloroethane and tetrachloroethylene are the only sources of TCA in the atmosphere and
rural soils, the sum of f1,1,1-T and fPER is equal to the environmental TCA concentrations, which are
known from the measurements (cf. 2.2.2).
An apparent contradiction is that the model describes the formation of TCA as an end product of a
reaction chain, while reaction constants only for the primary transformation reactions of the
precursors are used. In the paragraphs above the reaction pathways and the intermediates are given.
The reaction pathways were investigated in smog chamber experiments, and 1,1,1-trichloroethane,
tetrachloroethylene as well as TCA were detected, but not the intermediates. It can be concluded
that the intermediates have a very short lifetime, so the TCA formation rate is nearly equal with the
rates for the primary degradation steps. The only intermediate found is trichloroacetylchloride
(TCAC), which occurs because dry air was used in the laboratory experiments. Under natural
conditions, the aerosol is a sink of TCAC where it hydrolyses to TCA.
A further problem is that the atmospheric concentrations especially of tetrachloroethylene are
fluctuating dependent on the sampling site and time. These fluctuations become less important
when values from sites are used at which both precursors were measured simultaneously. In
Appendix III, the results of three sampling sites in Germany are given. The quotients of the yearly
averaged values are calculated and the tendency during the last 10 years is shown. Instead of
accidental measured values, the quotients C111-T / CPER are used in the calculations to get more
reliable results.
The sampling site Offenbach is representative for an urban air pollution. In the last years, the C111-T
/ CPER ratio is about 2.5 (cf. Appendix III).
Deuselbach is located near a densely populated region. The ratio is about 1, except the last year. We
assume a fault in the PER value, therefore this value is ignored.
Schauinsland is a summit in the Black Forest, far away from industrialized regions. The ratio is
decreasing slightly in the last years indicating that the emissions of 1,1,1-trichloroethane are nearly
stopped, while the PER pollution was constant in the last 4 years. The ratio C111-T / CPER amounts
about 4.5.
The parameters for the solution of equation 3 are summarized:
C111-T / CPER:
4.5 [-]
k111-T :
5.10-9 s-1
Y111-T :
kPER:
2.0.10-8.s-1
YPER:
15%
As large differences for the formation yield of TCA from 1,1,1-trichloroethane are found in the
literature, the calculation is done with all values. The calculation of the relative contribution of both
sources is done with a concentration ratio C111-T / CPER of 4.5 which is characteristic for rural
regions. The results are:
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Y111-T
fPER
[%]
0.06%
4.5 . 10-3
0.45%
99.55%
10%
0.75
43%
57%
50%
3.8
79%
21%
The result of the analysis above reveals that in most cases tetrachloroethylene is the major source of
TCA formed in the atmosphere. In rural regions, where the PER concentration is relatively low,
1,1,1-trichloroethane could be the main source if it is transformed to TCA with a high yield. In
urban areas PER is the main source of the TCA even when a high transformation yield for 1,1,1trichloroethane is assumed.
UNEP Publications
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rn : 20687
:AJ7875000
: REG
original : ILO , , , , ,
amendment: ZWACH*, ZULAESSIGE WERTE AM ARBEITSPLATZ(PERMITTED VALUES IN
THE WORKPLACE), , , , 1987
*******
rn : 21563
:AJ7875000
: REC
original : ILO , , , , ,
amendment: NMACN*, NATIONALE MAC-LIST(NATIONAL MAC-LIST), , , , 1986
*******
rn : 26238
:AJ7875000
: REG
-------------------------------|subject|specification|descriptor|
|-------+-------------+----------|
| GOODS |
|
PRO
|
-------------------------------SUBSTANCE WHICH MUST NOT FORM PART OF THE COMPOSITION OF COSMETIC
PRODUCTS. THE MARKETING OF COSMETIC PRODUCTS CONTAINING THE SUBSTANCEIS
PROHIBITED. EEC DIRECTIVE 76/768/EEC - OJEC L262,169,1976- AS LAST
AMENDED BY THE REFERENCE GIVEN.
entry date: SEP 1987
effective date: 1JAN1988
amendment: OJEC**, Official Journal of the European (Communities)/Union,
L56 , , 20 , 1987
UNEP Publications
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*******
rn : 40958
:AJ7875000
: REC
*******
200
rn : 100081
:AJ7875000
: REG
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*******
rn : 300361
:AJ7875000
: REG
-------------------------------|subject|specification|descriptor|
|-------+-------------+----------|
| AIR
|
OCC
|
TLV
|
-------------------------------TWA: 1 PPM, 7 MG/M3. PRESCRIBED BY THE CANADA OCCUPATIONAL SAFETY AND
HEALTH REGULATIONS, UNDER THE CANADA LABOUR CODE (ADMINISTERED BY THE
DEPARTMENT OF LABOUR). THE REGULATIONS STATE THAT NO EMPLOYEE SHALL BE
EXPOSED TO A CONCENTRATION OF AN AIRBORNE CHEMICAL AGENT IN EXCESS OF
THE VALUE FOR THAT CHEMICAL AGENT ADOPTED BY ACGIH (AMERICAN CONFERENCE
OF GOVERNMENTAL INDUSTRIAL HYGIENISTS) IN ITS PUBLICATION ENTITLED:
"THRESHOLD LIMIT VALUE AND BIOLOGICAL EXPOSURE INDICES FOR 1985-86".
entry date: MCH 1991
effective date: 13MCH1986
amendment: CAGAAK, Canada Gazette Part II, 120 , 6 , 1105 ,
UNEP Publications
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*******
*******
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CANADA. THESE ARE BASED ONUNITED NATIONS RECOMMENDATIONS. THE ACT AND
REGULATIONS SHOULD BE CONSULTED FOR DETAILS. RECORDS ARE ENTERED UNDER
THE PROPER SHIPPINGNAME FOUND IN THE REGULATIONS; THIS MAY INCLUDE VERY
GENERAL GROUPS OF CHEMICAL SUBSTANCES.
entry date: OCT 1991
effective date: 06DEC1990
amendment: CAGAAK, Canada Gazette Part II, 124 , 26 , 5523 ,
*******
rn : 302406
:AJ7875000
: REC
-------------------------------|subject|specification|descriptor|
|-------+-------------+----------|
| AQ
|
DRINK
|
GL
|
|
|
|
MAC
|
-------------------------------TABLE 2 - UNDER REVIEW FOR POSSIBLE ADDITION TO THE GUIDELINES. THESE
LEVELS ARE SET ACCORDING TO GUIDELINES FOR CANADIAN DRINKINGWATER
QUALITY - 1989. THE GUIDELINES ARE PREPARED BY THE FEDERAL-PROVINCIAL
SUBCOMMITTEE ON DRINKING WATER OF THE FEDERAL-PROVINCIAL ADVISORY
COMMITTEE ON ENVIRONMENTAL AND OCCUPATIONAL HEALTH AND PUBLISHED BY
AUTHORITY OF THE MINISTER OF NATIONAL HEALTH AND WELFARE; THEY SPECIFY
RECOMMENDATIONS AND LIMITS FOR SUBSTANCES ANDCONDITIONS WHICH AFFECT THE
QUALITY OF DRINKING WATER.
entry date: NOV 1991
effective date:
1989
amendment: GWQUEQ, GUIDELINES FOR CANADIAN DRINKING WATER QUALITY, , , ,
*******
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rn : 510579
205
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common name
:TCA
reported name :TRICHLOROACETIC ACID
cas no
:76-03-9
rtecs no
:AJ7875000
area
: DEU
type
: REG
-------------------------------|subject|specification|descriptor|
|-------+-------------+----------|
| CLASS |
|
CLASS |
| LABEL |
|
RQR
|
| PACK |
|
RQR
|
-------------------------------CLASSIFICATION AND LABELLING IN GERMANY IS GENERALLY THE SAME AS FOR THE
EEC (SEE OJEC** L180, 1991). HOWEVER, SLIGHT MODIFICATIONS MAY BE
INTRODUCED FOR SOME SUBSTANCES IN THE GERMAN LEGISLATION.
entry date: APR 1992
effective date: 15JUN1991
title: ORDINANCE ON HAZARDOUS SUBSTANCES. (GEFAHRSTOFFVERORDNUNG)
original : BGZBAD, Bundesgesetzblatt (Federal Law Gazette), , I , 1931 ,
1991
*******
rn : 1120995
:AJ7875000
: REG
-------------------------------|subject|specification|descriptor|
|-------+-------------+----------|
| AIR
|
OCC
|
MAC
|
|
|
|
CLASS |
-------------------------------CLV: 5.0MG/M3 (VAPOUR, AEROSOL) HAZARD CLASS: III
entry date: MAY 1990
effective date: 01JAN1989
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USSR), 12.1.005 , , , 1988
*******
rn : 1315006
:AJ7875000
: REG
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*******
File: 17.01 LEGAL
systematic name:Acetic acid, trichlorocommon name
:TCA
reported name :TRICHLOROACETIC ACID
cas no
:76-03-9
rtecs no
area
: USA
type
-------------------------------|subject|specification|descriptor|
|-------+-------------+----------|
| AIR
|
OCC
|
TLV
|
-------------------------------208
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: REC
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Time Weighted Avg (TWA) 1 ppm, 6.7 MG/M3; Summary - THIS THRESHOLD LIMIT
VALUE IS INTENDED FOR USE IN THE PRACTICE OF INDUSTRIAL HYGIENE AS A
GUIDELINE OR RECOMMENDATION IN THE CONTROL OF POTENTIAL HEALTH HAZARDS.
entry date: DEC 1991
effective date:
1989
title: THRESHOLD LIMIT VALUES
original : ACGIH*, Threshold Limit Values and Biological Exposure
Indices, , , 11 , 1989
amendment: ACGIH*, Threshold Limit Values and Biological Exposure
Indices, , , 11 , 1991
*******
rn : 1421922
:AJ7875000
: REG
-------------------------------|subject|specification|descriptor|
|-------+-------------+----------|
| CLASS |
|
CLASS |
| LABEL |
|
RQR
|
| PACK |
|
RQR
|
-------------------------------CLASS: C - CORROSIVE; CAUSES SEVERE BURNS (R 35). LABEL: C - CORROSIVE;
CAUSES SEVERE BURNS (R 35); AVOID CONTACT WITH SKIN AND EYES (S 24/25);
IN CASE OF CONTACT WITH EYES, RINSE IMMEDIATELY WITH PLENTY OF WATER AND
SEEK MEDICAL ADVICE (S 26). CLASSIFICATION OF PREPARATIONS CONTAINING
THE SUBSTANCE IN CONCENTRATION RANGE: ABOVE 10%: C - CORROSIVE; CAUSES
SEVERE BURNS (R 35). FROM 5% TO 10%: C - CORROSIVE; CAUSES BURNS (R 34).
FROM 1% TO 5%: XI - IRRITANT; IRRITATING TO EYES AND SKIN (R 36/38).
entry date: APR 1992
effective date: 1JUL1992
title: COUNCIL DIRECTIVE 67/548/EEC OF 27 JUNE 1967 ON THE APROXIMATION
OF THE LAWS, REGULATIONS AND ADMINISTRATIVE PROVISIONS RELATING TO THE
CLASSIFICATION, PACKAGING AND LABELLING OF DANGEROUS SUBSTANCES
original : OJEC**, Official Journal of the European (Communities)/Union,
196 , , 1 , 1967
amendment: OJEC**, Official Journal of the European (Communities)/Union,
L 180 , , 79 , 1991
*******
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rn : 1744964
:AJ7875000
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area
TRICHLOROACETIC ACID
: UN
type
: REC
-------------------------------|subject|specification|descriptor|
|-------+-------------+----------|
| TRNSP |
|
CLASS |
| LABEL |
|
|
| PACK |
|
|
-------------------------------HAZARD CLASS: 8 = CORROSIVE. PACKING GROUP: II = MEDIUM DANGER (I=GREAT
DANGER - III=MINOR DANGER). (APPLIES TO TRICHLORACETIC ACID, SOLUTION).
UN NO. 2564
entry date: AUG 1990
amendment: !UNTDG*, UN Transport of Dangerous Goods, Recommendation
prepared by theCommittee of Experts on the Transport of
Dangerous Goods, , , 15 , 1989
*******
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211