Registration Dossier

Administrative data

Link to relevant study record(s)

Description of key information

Short description of key information on bioaccumulation potential result: 
The acute toxicity data reported elsewhere in this file show comparable LD/LC50 values across a range of species and administration routes, suggesting similarities in uptake following oral, parenteral, dermal and inhalational administration as well as interspecies similarity in lethality. Elevated blood levels of allyl alcohol were reported 15 minutes after intragastric administration to rats (peak blood levels occurring about 15-45 minutes later). Such rapid absorption following ingestion is compatible with reports of human poisoning, where death occurred within 2 hours of ingestion. Allyl alcohol is metabolised in the liver, where alcohol dehydrogenase mediated conversion to acrolein occurs. Formation of this major metabolite is reported to be the principal cause of the observed hepatotoxicity of allyl alcohol; acrolein is excreted mainly in the urine after glutathione conjugation.

Key value for chemical safety assessment

Bioaccumulation potential:
low bioaccumulation potential

Additional information

Dunlap et al (1958) reported a range of LD50 values (mg/kg):

- rabbit intragastric 71, percutaneous 89

- mouse intragastric 96, intraperitoneal 60

- rat intragastric 99 and 105, intraperitoneal 42

- rat inhalation 1h 120-206, 4h 19-32, 8h 9-15 (converted from ppm exposure to mg/kg inhaled dose using ECHA R.8 default values and reported bodyweights).

Kodama and Hine (1958) reported elevated blood levels of allyl alcohol in rats 15 minutes after intragastric administration at 120 mg/kg, with peak blood levels (mean value >10 ug/ml) occurring about 15-45 minutes later. Such rapid absorption is compatible with reports of human poisoning after ingestion: Toennes et al (2002) and NTP (1993) described individual cases of death after 90 or 120 minutes.

Although Kodama and Hine (1958) postulated a direct hepatotoxic effect of allyl alcohol by disruption of cellular membranes, subsequent work by various researchers has shown the major mechanism of hepatotoxicity to be ADH-mediated conversion to acrolein; following this conversion in the liver, acrolein elimination occurs via glutathione conjugation (Patel, Wood and Leibman, 1980; Hormann, Moore and Rikans, 1989; NTP 1993; ORNL/US DoE 2008). The primary metabolic pathway for hepatic transformation of allyl alcohol in rats, documented in several review papers, has been defined as conversion to acrolein, principally followed by conjugation and urinary excretion of the toxic acrolein in the form of hydroxypropylmercapturic acid (although other pathways of acrolein elimination are also known: Carpanini et al 1978; Nordiska Expertgruppen fur Gransvardesdokumentation 1986; NTP 2006). Confirmation of metabolism to acrolein in man has been provided by the measurement of acrolein (7.2 mg/l) in the blood, bile and urine of a man fatally poisoned by ingestion of allyl alcohol, cause of death being presumed as acrolein-induced cardiotoxicity (Toennes et al 2002).