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Diss Factsheets

Administrative data

Key value for chemical safety assessment

Genetic toxicity in vitro

Description of key information

Several studies available.

Endpoint conclusion
Endpoint conclusion:
no adverse effect observed (negative)

Genetic toxicity in vivo

Description of key information

Several studies available.

Endpoint conclusion
Endpoint conclusion:
no adverse effect observed (negative)

Additional information

Short description of key information:
Multiple in vitro genetic toxicity studies are available, covering several types of bacterial mutation assays, mammalian cell chromosome aberration assays, sister chromatid exchange assays, a HPRT assay, a Comet assay and mouse lymphoma assays. In vivo studies are available in insects (drosphila), amphibians (micronucleus test) and rodents (DNA strand breaks, chromosome aberrations and micronuclei). See entries in 7.6.1 and 7.6.2 for guideline specifications.

In Chinese hamster V79 ovary cells, a dose-related increase in sister chromatid exchanges was observed without S9 but not with S9 but no induction of chromosome aberrations was observed after treatment with or without S9.

All other in vitro assays were negative except the mouse lymphoma test, which was positive only at cytotoxic concentrations under acidic pH shift conditions. Below cytotoxic concentrations, the response was negative.

Therefore, and as concluded by the EU RAR (2005), this effect is deemed to be due to the pH shift and not considered as a positive test outcome. It is well known that changes in pH may lead to increased mutation frequencies, but neither of the two mutation assays with mouse lymphoma cells did include appropriate controls for the possible influence of changes in pH under the test conditions used, thereby hampering the evaluation of the relevance of the test results.

The results from all valid in vivo assays, covering multiple endpoints in various organs are mostly negative. One study, considered invalid because of poor reporting, mentioned an increase in chromosomal aberrations, but, in accordance with the EU RAR (2005) this study was disregarded. JRC (2005) concluded that MCA is not a genotoxic substance.

According to NRC (2009), there is no evidence of genotoxic potential in bacterial mutagenicity studies, in vitro chromosomal aberration tests, and in vitro and in vivo primary DNA damage assays. Gene mutation tests in mammalian cells gave contradictory results, and in one study, increased chromosomal aberrations were found after intraperitoneal injection in mice.

One more recent study (Siddiqui et al., 2006) showed an increase in micronuclei and chromosome aberrations in rats at the highest ip dose tested of 12 mg/kg bw, a dose close to the ip LD50 of 16 mg/kg bw which had been found in the literature. However, the increases were only seen at the 24 h time point and not at 12 or 48 h, and no such increases were observed at the lower doses of 8 or 10 mg/kg bw. Moreover, rats dosed long-term with 60 mg/kg bw neutralized MCA did not show tumors.

According to MAK (2019): In more recent in vitro studies DNA-damaging effects were demonstrated by MCA which can be attributed to oxidative stress. Clastogenic effects were shown as double strand breaks in primary rat and mouse hepatocytes only at cytotoxic concentrations in vitro, but not in vivo. Induction of micronuclei in human lymphocytes in vitro and a positive result in the HPRT test can also be attributed to reactive oxygen species, because an alkylating effect of MCA is unlikely as suggested by the negative results in the Salmonella mutagenicity tests at non-cytotoxic concentrations. Induction of micronuclei in vivo at 12 mg/kg bw in rats (Siddiqui et al., 2006) is implausible because it means the potency of MCA would be half as high as that of the positive control cyclophosphamide; however, in rats no tumors occurred up to approx. 60 mg neutralized MCA/kg bw in long-term experiments. Therefore, there are doubts about the validity of the study. In addition, no clastogenicity was observed either in vitro or in vivo. Considering all data, MCA and its sodium salt are not classified for germ cell mutagenicity.

Endpoint Conclusion: No adverse effect observed (negative)


EU RAR (2005) - Monochloroacetic acid (MCAA) CAS No. 79 -11 -8, EINECS No. 201 -178 -4, European Union Risk Assessment Report, European Chemicals Bureau (ECB), Institute for Health and Consumer Protection, vol. 52

JRC (2005) - Monochloroacetic acid (MCAA) CAS No. 79 -11 -8, EINECS No. 201 -178 -4, Summary Risk Assessment Report, Joint Research Centre (JRC), European Commission, Institute for Health and Consumer Protection, Ispra, Italy

NRC (2009) - Monochloroacetic acid - Acute Exposure Guidelines for Selected Airborne Chemicals, Committee on Acute Exposure Guideline Levels, Committee on Toxicology Board on Environmental Studies and Toxicology Division on Earth and Life Studies National Research Council (NRC), The National Academic Press, Washington DC, USA, Volume 7, p. 135 -177

MAK (2019) - Monochloroacetic acid, Sodium monochloroacetate / Chloroacetic acid, Sodium 2-chloroacetate [Monochloressigsäure, Natriummonochloracetat] The MAK Collection for Occupational Health and Safety 2019, Vol 4, No 2, 769 -792


Justification for classification or non-classification

In vitro overall: negative

in vivo overall: negative.

Negative in 2 -year carcinogenicit studies in rats and mice.

Conclusion: not a genotoxic substance, MCA should not be classified for germ cell mutagenicity.