Acrylaldehyde

Neurotoxicity

Description of key information

The available data do not indicate that the central nervous system or peripheral nervous system are targets of acrolein toxicity.

Additional information

Acrolein has been the subject of a risk assessment carried out under Community Regulation (EEC) No 793/93 (EU, 2001). However, neurotoxicity is no specific chapter in the EU Risk Assessment. The key information on neurotoxicity as stated correspond to the greatest extend to further assessments carried out under other international and national programmes published after finalisation of the EU Risk Assessment Report 2001 (World Health Organization, International Programme on Chemical Safety (IPCS), Concise International Chemical Assessment Document of Acrolein, CICADS 43 (WHO, 2002) and United States Agency for Toxic Substances and Desease Registry, Toxicological Profile for Acrolein (US ATSDR, 2007)):

1. European Union Risk Assessment Report of Acrolein (EU, 2001)

There is no specific chapter on neurotoxicity in the EU Risk assessment.

2. Agreement with further International Reports and Studies Published after Finalisation of the EU Risk Assessment Report 2001

Not applicable.

3. Substantial Disagreements in Comparison to further International Reports to European Union Risk Assessment Report 2001

Not applicable.

4. Additional Aspects in further International Reports

US ATSDR, 2007: No information was located regarding neurological effects of acrolein in humans. Symptoms of central nervous system depression were observed in rodents after oral exposure to acrolein, but only after lethal concentrations (Sprince et al. 1979). No such effects were observed in animals after inhalation exposure; the animals died from asphyxia caused by epithelial desquamation and, consequently, respiratory obstruction (Ballantyne et al. 1989; Catilina et al. 1966; Crane et al. 1986; Skog 1950). No behavioral changes were observed in animals exposed to acrolein by any route. Nonspecific histopathological effects  on the brains (remark: nonspecific inflammatory responses in sections of the brain of animals were found in subchronic inhalation studies (Feron et al. 1978; Kutzman et al. 1984, 1985; Lyon et al. 1970). No histopathological changes in neurological tissues were observed after oral exposure (Parent et al. 1991a, 1992a, 1992b). No studies regarding neurotoxicity of acrolein after dermal exposure were located. However, the available data do not indicate that the central nervous system is the major target of acrolein toxicity.” quotation from US ATSDR, 2007, 89-90 (information of remark from p40), identical information as quotation from US ATSDR in United States Environmental Protection Agency, HED Risk Assessment for Reregistration Eligibility Decision (RED) Document for Acrolein (US-EPA, 2008).

WHO 2002: “Limited data on neurotoxicity indicate a lack of morphological changes in the tracheal or pulmonary nerves of rats exposed by inhalation to up to 570 mg acrolein/m³ (249 ppm) for 10 min (Springall et al., 1990), no histopathological changes in the nerve cells of the nasal olfactory epithelium of mice exposed by inhalation to 3.9 mg acrolein/m³ (1.7 ppm) for 6 h/day for 5 days (Buckley et al., 1984), and no behavioural effects in rats exposed by inhalation to up to 9.2 mg acrolein/m³ (4.0 ppm) for 6 h/ day, 5 days/week, for up to 62 days (Kutzman et al., 1984).” Quotation from WHO, 2002, p27

5. Additional Information in Newer Studies, not Included in the European Union Risk Assessment Report 2001 or further Cited International Reports

None

Justification for classification or non-classification

The available data do not indicate that the central nervous system or peripheral nervous system are targets of acrolein toxicity.

Thus, acrolein does not comply with the classification requirements regarding neurotoxicity outlined in regulation (EC) 1272/2008 or the former directive on classification and labelling 67/548/EWG.