National Industrial Chemicals Notification and Assessment Scheme

16.4Environmental hazards

Formulae from the EC Technical Guidance Document (European Commission, ) have been used to predict an environmental concentration for trichloroethylene in Australian receiving waters.

The percentage of trichloroethylene in the STP being lost to the atmosphere is 91%, based on the SIMPLETREAT model, calculated by the UK in the SIAR (United Kingdom, 1996). Therefore, the value of P in the following equations is 0.91.
PEC _local(water) = C_eff/(1+K_p(susp).c_susp).D
Where:
PEC _{local(water) =} predicted environmental concentration (g/L)

C_eff = concentration of the chemical in the sewage treatment plant (g/L)

K_p(susp) = Suspended matter-water adsorption coefficient (L/kg)

c_susp = Concentration of suspended matter in receiving waters (L/kg)

D = Dilution factor.
C_eff = W.(100-P)/100.Q
Where:

W = emission rate (kg/day)

Q = volume of waste water.

P = percentage removal in the sewage treatment plant

1. 
   All trichloroethylene imported into Australia is released to the environment.
   

3) 300 days per year of trichloroethylene handling, meaning a daily release of 10 tonnes.

4) In the absence of data, 40% use of trichloroethylene will be assumed to occur in the Sydney metropolitan area, equating to a release of 4 tonnes per day. Of this, 400 kg will be sent to the sewer, which has a flow of 250 ml per day.
Values:

c_susp = 15 mg/L (default value)

D = 10

W = 400 kg/day

P = 91%

Kow = 195

a = 0.411 (European Commission, 1994)
Using the above formulae, data and assumptions, the predicted environmental concentration in receiving waters is 14.4 µg/L (ppb).

These calculations represent a worst case scenario, and assume no degradation of trichloroethylene by microorganisms in the STP or in receiving waters. The estimates give a predicted environmental concentration two orders of magnitude below the lowest toxic level for aquatic organisms being a 48h EC₅₀ = 7.8 ppm for Daphnia magna. Thus a low aquatic hazard may be concluded.

Because of the relatively short half-life in the atmosphere, trichloroethylene is thought to make only a minor contribution to global warming. It is unlikely to reach the stratosphere, and so is not likely to have an effect on stratospheric ozone. It will not make a significant contribution to photochemical ozone formation. However, the breakdown product, dichloracetyl chloride, may have an adverse effect on stratospheric ozone due to its long half-life (United Kingdom, 1996).

16.5Conclusions

17.Overall Conclusions and Recommendations

17.1Hazard classification

Results of studies in human volunteers and reports of workers exposed to trichloroethylene have indicated that trichloroethylene caused burning sensation of the skin with redness and rashes and burning and irritation of the corneal epithelium. Studies in animals, not conducted according to accepted test guidelines, reported skin irritation and corneal abrasions. Based on human evidence and results of animal studies trichloroethylene meets the classification for skin and eye irritation.

Positive results in tests in somatic cells in vivo such as:

single strand breaks in rat and mouse liver, kidney, lungs and stomach (Nelson & Bull 1988, Walles 1986);

increased number of mutants in cultures from liver and kidneys but not from lungs in a host-mediated assay in mice (Bronzetti et al (1978);

positive pink eyed unstable mutation test in mice (Schiestl et al, 1997)

Supported by:

mutations in VHL tumour suppressor gene in renal cancer cases (Bruning et al, 1997);

weak in vitro mutagen; and

mutagenicity of known metabolites.

Some of the studies have limitations (Schiestl et al, 1997; Bruning et al, 1997) and these have been noted in the report. However, looking at the overall data, the results of these studies raise concern regarding possible mutagenic effects of trichloroethylene.

Currently available data in animals and humans, as follows:

Well conducted epidemiological studies (Axelson et al, 1994; Spirtas et al, 1991 updated by Blair et al, 1998) have shown no association between exposure to trichloroethylene and renal cancer under the conditions of these studies.

However another well conducted study (Antilla et al, 1995) provided limited evidence of an association between cancer and trichloroethylene exposure.

Studies by Henschler et al (1995) and Vamvakas et al (Deutsche Forschungsgemeinschaft, 1996) have indicated an association between renal cancer in workers exposed to trichloroethylene.

Bruning et al (1997) in a preliminary study demonstrated that trichloroethylene caused somatic mutations of the VHL tumour supressor gene in renal cancer cases and concluded that a linkage existed between exposure to trichloroethylene and somatic mutation of the VHL gene.

Bruning et al (1996b) also reported renal tubular damage in patients who had been diagnosed with renal cell carcinoma and had undergone nephrectomy.

Kidney tumours observed in rats along with cytotoxicity.

Although it is noted that some of the the human studies provide limited data and have several methodological weaknesses, the findings in humans are supported by evidence in experimental animals, with tumours observed at the same site and the mechanism yet to be elucidated. Renal cytotoxicity has been observed in rats, however the mechanism is not clear.

Overall, for mutagenicity and carcinogenicity, the pattern of results observed is consistent with a chemical which is a weak mutagen and a weak carcinogen.

The European Union (EU) is also considering the classification of trichloroethylene. The EU Specialised Experts Group considered the mutagenic and carcinogenic potential of trichloroethylene at their meeting in June 1997.

For mutagenicity the Group considered that:
trichloroethylene was an in vitro mutagen;

the results from the in vivo studies were however, less clear;

based on the current data trichloroethylene could not be classified as a Category 3 mutagen.

further data was required to clarify in vivo mutagenic potential. As trichloroethylene was under the Existing Substances Risk Assessment Regulations (ESR) where additional studies can be requested, the Specialised Experts recommended that the Kligerman micronucleus study be repeated with some modifications. This was subsequently agreed by the superior EU body as the basis on which the EU will determine whether to classify trichloroethylene as a category 3 mutagen (a positive result to result in classification). The EU also noted other data in generation.

For carcinogenicity, a majority of the Specialised Experts recommended that:

trichloroethylene be classified as carcinogen category 2; R45 on the basis of clear data in one animal species (rat) with supportive evidence from epidemiology and genotoxicity studies;

The Specialised Experts recommended that as the genotoxicity of trichloroethylene was still in doubt it should be treated as a genotoxic carcinogen until proven otherwise and thresholds should not be anticipated to exist for cancer effects.

The above reflects the EU status as advised to NICNAS at the time of preparing this report. EU consideration of trichloroethylene has not been finalised.

During the final stages of preparation of this report, one applicant advised that additional laboratory work relevant to the question of mutagenicity and renal effects was expected to be completed by September 1998 (Dow Chemical, personal communication).

Considering the available information and that further data are being generated, the following recommendations are made to the National Occupational Health and Safety Commission.