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Description of key information

READ-across information from MMA:
rat, 2 years: negative (NTP, 1986)
mouse, 2 years: negative (NTP, 1986)
rat, 2 years: negative (Borzelleca et al. 1964)

Key value for chemical safety assessment

Additional information

Data availability

Data in animals and in humans are not available for MAA. Data are only available for the highest volume ester of the category, MMA and this has been reviewed in the EU ESR on this substance. However, it can be concluded that all members of the category, including MAA, are not mutagenic or genotoxic, hence, further testing is not necessary and the available data are sufficient for assessment.

Animal data


The EU ESR on MMA concluded: “An early 2-year chronic study on dogs and rats treated orally with MMA revealed no adverse effect other than a lower body weight gain in high-dose dogs and elevated kidney weights in high-dose female rats (Borzelleca et al., 1964). In this study two male and two female dogs received gelatine capsules with 10, 100 and 1000 ppm MMA dissolved in corn oil. The high- dose was reduced to 500 ppm on day 2, 0 ppm on day 3-13 and 300 ppm on day 14 due to vomiting, and then increased to 1200 ppm at week 5 and to 1400 ppm at week 7 to 1500 ppm at week 9. 25 male and 25 female rats were administered with 6, 60 and 2000 ppm MMA in the drinking water, the low and medium doses increased to 7 and 70 ppm after five months.

These studies on dogs and rats revealed no increase of neoplastic lesions. However the reliability of these studies is limited due to their non-conformance to current carcinogenicity test guidelines (e.g., histopathological examination was performed on a limited number of organs).”


EU ESR on MMA concluded: “Groups of 50 male F344/N rats were exposed to methyl methacrylate (purity > 99 %; containing 0.04 mg/l equivalent to 10 ppm monomethylethyl ether of hydroquinone as an inhibitor of polymerization) by inhalation at 0, 2.1, 4.2 mg/l (equivalent to 500 or 1000 ppm), female F344/N rats at 0, 1.0 or 2.1 mg/l (equivalent to 250 or 500 ppm) and male and female B6C3F1 mice at 2.1 or 4.2 mg/l (equivalent to 500 or 1000 ppm), 6 hours a day, 5 days a week for 102 weeks (NTP, 1986; Chan et al., 1988). Animals were killed at 111-112 weeks (rats) or 113-114 weeks (mice) of age. No significant differences of the survival rates were observed between any groups of rats and mice. During most of the second year of the study, the mean body weights of treated male mice and high-dose female mice were 10-18 % lower than those of the controls. The marginal increase in the incidence of mononuclear-cell leukaemia observed in female rats (control 11/50; low-dose 13/50; high-dose 20/50) fell within the range of values seen in historical controls. Both in mice and rats no treatment-related tumours were observed.”

No treatment-related increases in tumour incidence occurred in Golden hamsters with groups of 53-56 males and 56-59 females exposed to 0, 25, 100 or 400 ppm (0, 102.5, 410 or 1640 mg/m³) MMA 6 h/d, 5 d/wk for 78 weeks (no interim sacrifice). At the high-dose, body weight decreased and mortality increased in high dose males (Rohm and Haas, 1979c, cited from Chan et al. 1994; Lomax et al., 1997). After week 60, males exposed to 400 ppm and to 25 ppm had significantly lower body weight during some weeks. There were no clinical signs or haematological effects attributable to exposure to methyl methacrylate at either the 52- or 78- week sampling times. No gross haematological changes indicative for a possible exposure-related effect were observed.”

Human data

EU ESR on MMA concluded: “A retrospective mortality study has been conducted among workers exposed to the vapour phase of methyl methacrylate, low percentages of ethyl acrylate (EA) and volatile by-products of the methyl methacrylate and EA polymerization process in acrylic sheet manufacture in twoplants. Detailed analyses of colorectal cancer mortality were performed for each of the three cohorts (cohort I: 3934 white males employed between 1933 and 1945; cohort II: 6548 white males hired between 1946 and 1986; cohort III: 3381 white males hired between 1943 and 1982). Exposure was estimated on the basis of a job-specific semi-quantitative rating scale. Mortality from colon cancer was significantly increased in cohort I and non-significantly increased in cohort III. The risk for colon cancer was highest in the most exposed workers, who worked extensively in the early 1940s. No regular increase according to years elapsed since first exposure or intensity of exposure was observed for colon cancer. The rate for rectal cancer was increased in cohort I (Walker et al., 1991; IARC, 1994). Some evidence of increased death rate from respiratory cancer or non-malignant respiratory disease were reported for cohort III (Rohm and Haas, 1987).


Another retrospective mortality study (Collins et al., 1989) included a cohort of 2671 male workers employed between 1951 (1957 respectively) and 1974 in two acrylic fibre production plants. Exposed to methyl methacrylate were only 1561 men of the cohort at mean concentrations below or equal to 1 ppm. A small excess of respiratory cancer was reported. There was no significant increase in the number of cancer deaths.


In the cohort study of Tomenson (1994) colorectal cancer was as expected (17 observed deaths versus 16.9 expected) and respiratory cancer mortality was lower than expected (SMR=93). Mortality due to stomach cancer was increased by approximately one third.


The epidemiologic data on humans do not provide consistent evidence on the carcinogenic effect in humans. The studies did not allow a strong association of increased tumour rates in a distinct organ or several organs to MMA as the responsible agent.”

Since the completion of the EU ESR on MMA the Tomenson (1994) internal company report was published as Tomenson et al., 2000 and a summary review of the available epidemiology (cancer mortality) studies published by Tomenson et al., 2005. These publications confirm the conclusion of the ESR.


References for MMA not copied into the MAA dataset:

IARC (1994). Methyl methacrylate. In: IARC Monographs on the evaluation of carcinogenic risks to humans. Vol. 60: Some industrial chemicals. IARC, Lyon, 445-474.

Rohm and Haas (1987). Mortality study ofplant employees (1943-1982). Prepared by Maher KV and DeFonso R, Rohm and Haas,,

Tomenson JA (1994).A cohort study of employees in Perspex plants.ICI Acrylics, Wilton Centre, Middlesborough, Cleveland .

Tomenson JA, Bonner SM, Edwards JC, Pemberton MA, Cummings TF, Paddle GM, 2000, Study of two cohorts of workers exposed to methyl methacrylate in acrylic sheet production. Occup. Environ. Med., 57(12): 810-817

Walker AM, Cohen AJ, Loughlin JE, Rothman KJ, DeFonso LR (1991).Mortality from cancer of the colon or rectum among workers exposed to ethylacrylate and methyl methacrylate. Scand. J. Work Environ. Health.17, 7-19.

Justification for classification or non-classification

In the case of MAA the ESR concluded “There are no data on carcinogenicity from methacrylic acid itself; from methyl methacrylate data, there is no concern on carcinogenic properties of methacrylic acid.As there is no concern for mutagenic or genotoxic potential for the other esters of the category there is equally no concern for carcinogenicity.

Therefore, MAA is not classified for carcinogenicity according to CLP (1272/2008/EEC) and UN-GHS requirements.