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EC number: 201-204-4
CAS number: 79-41-4
availability: For MAA a bacterial mutation test is available. For all
other required endpoints data from MMA are used by read-across.
mutation in bacteria
standardised bacterial mutation test according to NTP protocol,
methacrylic acid was
not mutagenic in S. typhimurium strains TA97, TA98, TA100, TA1535 and TA
1537 with and without metabolic activation (Zeiger et al. 1987).
Additionally, the esters of the category have been tested over a
relevant dose range in the Salmonella reverse mutation test (Ames test)
with and without metabolic activation by S9-mix. In no study was there
an indication of a mutagenic effect.
mutation in mammalian cells
no gene mutation studies available in mammalian cells. The EU ESR for
MAA (2002) concluded "Further testing on methacrylic acid is lacking.
However, taking into consideration the data on the structurally related
substance methyl methacrylate - which indicate that this substance does
not express a genotoxic potential in vivo - there is no need for further
testing." Supporting evidence can be drawn by category read-across from
a negative gene mutation test with EHMA (Harlan, 2009). Although the
dominant lethal assay of Anderson (1976) and micronucleus assay of Hachiya
(1982) with MMA are strictly speaking not gene mutation assays, the
absence of positive findings is also supporting the absence of concern
for genotoxicity of MAA.
in mammalian cells
analogy to MMA, has the potential for induction of mutagenic effects,
esp. clastogenicity; however, this potential seems to be limited to high
doses with strong toxic effects.
the in vitro data are therefore somewhat ambiguous the in-vivo study
data are used by read-across. Quote from the MMA ESR (ECB, 2002): “Two
chromosomal aberration tests were conducted by Anderson et al. (1976,
1979) investigating the effect of inhalation exposure to methyl
methacrylate for doses ranging from ca. 0.4 to 36.5 mg/L (100 to 9000
ppm). In both tests acute exposure was for 2 h (sampling 24 h after
treatment) and subacute exposure for 5 h a day on 5 consecutive days
(sampling 24 h after last treatment). Data on toxicity were not given.
Group sizes varied from 2 to 9; as far as possible 50 metaphases were
analysed per animal. The first study was negative for chromosomal
aberration frequencies when - as usual - gaps were excluded. Including
gaps and combining two acute experiments conducted independently some
increases in aberration frequency were statistically significant. ” This
is also due to a particularly low control rate in this experimental
segment. Compared to other, almost twofold higher control values in
other segments of the report, this finding appears to be of little
biological importance. Further from the MMA ESR (ECB, 2002): “In the
second study frequencies of chromosomal aberrations excluding gaps were
not given. Including gaps increases were recorded at some experimental
entries. Furthermore, combined data on chromosomal aberration
frequencies exclusively gaps from both studies were given, then weak
increases were obtained for 400 and 700 ppm in the acute study (not for
100, 1,000 or 9,000 ppm) and 9,000 ppm in the subacute study. Both
studies suffer from inadequate description; esp. the second study
demonstrates severe methodological problems, e. g., analysis of 50
metaphases was not possible for 10 out of 27 animals in the acute and 10
out 26 in the subacute test. Altogether, a clear conclusion cannot be
drawn from theses studies.
al. (1982) reported on a negative bone marrow micronucleus assay with
mice. In an acute test methyl methacrylate was given by gavage in doses
ranging from 1,130 to 4,520 mg/kg, in a subacute assay daily doses of
1,130 mg/kg were given on 4 consecutive days. All groups consisted of 6
animals; sampling was done 24 h after (last) administration. There was
no increase in the frequency of micronucleated polychromatic
erythrocytes. The percentage of reticulocytes from all bone marrow cells
was not affected data on general toxicity were not given. ”
has the potential for induction of mutagenic effects, esp.
clastogenicity; however, this potential seems to be limited to high
doses with strong toxic effects. Furthermore, the negative in vivo micronucleus
test - and to some extent the negative dominant lethal assay - indicates
that this potential is probably not expressed in vivo.”
it may be concluded from mammalian cell culture assays with methyl
methacrylate that MAA has the potential to be is a high-toxicity
clastogen (i. e. induction of chromosomal aberrations is bound to highly
toxic doses). Therefore the in vivo data for MMA are used to finally
assess the genotoxic potential.The
weight of evidence approach indicates that MMA is not mutagenic. MAA,
having a reduced reactivity at the double bond compared to MMA, is not
expected to be mutagenic.
acid was negative in a bacterial gene mutation test. Additional
information is gained by read-across from methyl methacrylate. From
mammalian cell culture assays it may be concluded that methyl
methacrylate is a high toxicity clastogen (i. e. induction of
chromosomal aberrations is bound to highly toxic doses). The effect is
not dependent on presence of S-9 mix. In vivo an oral mouse bone marrow
micronucleus test was negative for doses up to 4,520 mg/kg bw. No clear
conclusion could be drawn from bone marrow chromosomal aberration assays
with rats. A dominant lethal assay with male mice led to a negative
result. In vitro MMA has the potential for induction of mutagenic
effects, esp. clastogenicity; however, this potential seems to be
limited to high doses with strong toxic effects. Furthermore, the
negative in vivo micronucleus test and the negative dominant lethal
assay indicate that this potential is probably not expressed in vivo.
absence of the ester group in MAA reduces the reactivity of the double
bond in comparison to the esters.
methacrylic acid has not to be classified for its mutagenic potential
according to CLP (1272/2008/EEC) and UN-GHS requirements.
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