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Toxicological information

Carcinogenicity

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Description of key information

Acrylic acid showed no evidence of carcinogenicity in a 2-year drinking water study in Wistar rats up to the highest dose tested of 78 mg/kg bw/day. In two dermal carcinogenicity studies in three mice strains (C3H/HeJ, C3H/HeN Hsd BR and Hsd:(ICR)BR), the frequency of skin tumours was not elevated compared to the vehicle controls.

Key value for chemical safety assessment

Additional information

In a valid carcinogenicity study according to OECD TG 451 (BASF AG, 1989; Hellwig et al., 1993) Wistar rats were administered doses of 120, 400 or 1200 ppm (corresponding to approx. 8, 27, and 78 mg/kg bw/d, respectively) acrylic acid (purity: 99 %, stabilized with 200 ppm hydroquinone monomethylether) in drinking water for 26 months (males) or 28 months (females). Except for a slightly reduced water consumption in high-dose males and females no treatment-related clinical, hematological changes were detected in comparison with the controls. The extensive histopathological examination of the preserved tissues revealed that in all three treatment groups, the non-neoplastic tissue changes did not differ from those of the controls. The incidence and organ distribution of tumours found in the groups treated with acrylic acid was not significantly different from those of the controls.

 

In addition, there are several studies which did not fulfill the requirements of guideline testing protocols for regulatory purposes but give valuable additional information on acrylic acid.

 

In a dermal carcinogenicity study no tumours of the skin or subcutis were induced in treated mice or in the vehicle controls (Intercompany Acrylate Study Group, 1982). A group of 40 C3H/HeJ male mice received 25 µL applications of acrylic acid as 1.0 % (v/v) dilutions in acetone. A negative control group received acetone only. The substances were applied to the skin of the back three times a week for lifetime. Histological examination was performed on the dorsal skin of all treated mice and on gross lesions. The mortality rate was not affected by treatment (mean survival time in the acrylic acid group 515 days, in the acetone group 484 days). No signs of skin irritation were observed. While one mouse in the acrylic acid group had evidence of epidermal hyperplasia, no neoplasms were found in the skin or subcutis of the acrylic acid-treated mice or in the negative controls.

 

In another dermal carcinogenicity study 25 or 100 µL of 1 % (v/v) acrylic acid in acetone was administered to two strains of mice (C3H/HeN Hsd BR and Hsd:(ICR)BR) during 21 months (3 times/week). Histopathology was done on the skin, some internal organs and unusual gross lesions. No treatment-related signs of skin irritation, toxicity, clinical signs or skin tumours were observed. There was no treatment-related effect on body weight gain or mortality rate. 7/50 female C3H-mice of the 100 µL acrylic acid treated group revealed a significantly increased frequency of lymphosarcomas compared to the acetone control group (BAMM 1990, 1991). However, statistically significant increases in lymphosarcoma frequency were not seen in the C3H males or either sex of the ICR mice. Lymphosarcomas are commonly seen in most strains of mice which are 18-24 months of age (Frith and Wiley, 1981) and their relation to the treatment was considered to be uncertain.

 

 

Conclusion

 

There is no evidence that acrylic acid administered orally to rats or applied dermally to mice is carcinogenic.

 

Justification for classification or non-classification

EU classification according to Annex VI of Directive 67/548/EEC: no classification required

GHS classification (GHS UN rev.3, 2009): no classification required