Registration Dossier

Data platform availability banner - registered substances factsheets

Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.

The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.

Diss Factsheets

Administrative data

Link to relevant study record(s)

Description of key information

Key value for chemical safety assessment

Bioaccumulation potential:
no bioaccumulation potential

Additional information




No relevant data for propan-1 -ol is available.


For dermal absorption, only in vitro data from an IVPT ist available (Alinaghi et al., 2022) indicating that propan-1-ol penetrates human skin better than ethanol and less better than higher unbranched primary alcohols.


Following single oral administration of 174 mg 14C-propan-1-ol as an aqueous solution concentration to Wistar rats by gavage, propan-1 -ol concentration in blood peaked one hour after administration with a total recovery rate of about 77% measured 72 hours after dosage. About 71.6% of the radioactivity was eliminated in expired air, 4.7% via the urine and 0.4% in faeces. Six hours after oral dosing following distribution of radioactivity in tissues of rats was found (μmol of the dose/g tissue) : blood (0.4), brain (0.2), heart (0.3), kidney (0.7), liver (1.3) (Fahelbum and James, 1979).

In female Wistar rats gavaged with 50 mmol (3005 mg) propan-1-ol/ kg bw, blood serum concentration peaked one hour after administration. A peak value of about 1842 mg/l at about 1.6 h was derived. Thereafter blood levels decreased rapidly to below detection limits at 5 hours after administration with a metabolism rate of 510 mg/kg/h (Beaugé et al. 1979).

Peak blood levels of 320, 480 and 510 mg/l were seen ten minutes (e.g. the first collection point) after orally dosing mice (intubation) with 1000, 2000 and 4000 mg/kg, respectively. Twenty minutes after administration, levels were 290, 420, and 480 mg/l, respectively. Propan-1-ol was below detection limits 40 minutes after applying the lowest dose and 80 minutes after applying the two higher doses. An elimination half-life of 57 min was approximated (Maickel and Nash 1985).

 In a metabolism study, propan-1-ol of unknown substance purity was administered by gavage to chinchilla rabbits (3 animals/dose, no data on sex, about 3kg) at a dose level of 2400 mg/animal (800 mg/kg bw). Urinary elimination of propan-1 -ol as glucoronides was insignificant indicating a very low conjugation with glucoronic acid. Only 0.9% of administered dose could be recovered as glucoronides (Kamil et al. 1953).


Following inhalation exposures of rats to 2000 ppm propanol, propanol concentrations in blood peaked (136 μM) 10 min following exposure. Subsequent propionic acid concentrations in blood peaked (~10 μM) at 25 min (Smith et. al, 2020).



Using rat liver preparations, Hedlund et al (1969) demonstrated the rapid oxidation of propyl alcohol to propionaldehyde; mitochondrial oxidation rates of propionaldehyde were approximately comparable to acetaldehyde when incubated at a substrate concentration of 4.4 mM. 40 mmol n-propanol are metabolised per hour per gram rat liver. Liver homogenates from male and female rats oxidized propanol at equal rates and Plapp et al (2015) showed that 1-propanol was eliminated in rats in vivo with zero-order kinetics at doses of 10 mmol/kg.

Propan-1-ol was rapidly oxidized to its corresponding aldehyde by the human and rat liver alcohol dehydrogenase (ADH), more specifically by the Class I isozymes, and to a lesser extent - predominantly in chronic exposure - by the NADPH-dependent microsomal ethanol oxidizing system (MEOS) involving cytochrome P450 (Cytochrome P450 isozyme 3a, isolated from hepatic microsomes of rabbits). Propionaldehyde was then converted to propionic acid which was conjugated with coenzyme A (CoA). In man and animals propionyl-CoA is carboxylated to methylmalonyl-CoA, this is followed by transcarboxylation to succinyl-CoA, which subsequently enters the tricarboxylic cycle to be metabolized to carbon dioxide and water ((Ehrig et al., 1988; Sinclair et al., 1990; Morgan et al., 1982; (Halarnkar and Blomquist, 1989; Rietbrock and Abshagen, 1971; EU RAR, 2008)

Beaugé et al. (1979) reported a rate of metabolism of 510 mg/kg/h which was calculated from an elimination curve consisting of five measurements of blood propanol levels in rats exposed to a single oral (intubation) dose of 3000 mg/kg. Intrahepatic fatty acid metabolism was clearly altered by administration of propan-1-ol. Orally dosed animals were injected i.p. with albumin-bound palmitic acid (2.5 μCi/kg) 1 h before sacrifice. The administration of propan-1-ol results in a large increase of 1-14C-palmitate incorporation into serum triacylglycerols.


PBPK modelling

Smith JN et al. (2020) developed a PBPK model for the propyl metabolic series in rats and humans for application to risk assessment. The model predicts rapid clearance of propyl acetate, higher levels of propanol from propyl acetate inhalation compared to propanol inhalation in rats but not humans, and low concentrations of propionic acid in blood following exposures to propyl acetate or propanol.




From the available data it can be concluded that dermal absorption occurs. Considering the physicochemical properties (molecular weight 60 g/mol, complete water solubility and a log Pow of 0.34) absorption through the skin can be assumed. In absence of valid quantitative assessments, a dermal absorption of 100% is assumed as a worst case estimation.

Different studies demonstrate that the compound is readily absorbed from the GI tract. Based on the available data an oral absorption of 100% is assumed as a worst case estimation.

There is limited data on the toxicokinetics of propan-1-ol concerning exposure by inhalation. However, inhalative absorption of propan-1 -ol can be estimated based on comparison with data on other short-chain alcohols. Given inhalatory absorption rats for methanol range from 60 - 80%. Studies on ethanol yield to absorption rates ranging from 40 - 75%, whereas for propan-2 -ol and butan-1 -ol the uptake of the substance via inhaltion has shown to be approximately 40 - 50%. Taking into account the indicated high uncertainties in the inhalatory absorption figure an inhalation absorption rate of 75% is proposed as a reasonable worse case assumption for risk characterisation purposes 1.


1 (WHO working group, 1997. Environmental Health Criteria Vol. 196; Perkins, R.A., 1995. A Pharmacokinetic model of inhaled methanol in humans and camparison to methanol disposition in mice and rats. Environ Health Perspect 103, 726 -733.; Pedersen, L.M., 1987. Biological Studies in human exposure to and poisoning with organic solvents: Kinetics, haemotology, and serum chemistry. Phamacol Toxicol, 61, Suppl. III: 1-38; Fiserova-Bergerova, V., 1986. Determination and prediction of tissue-gas partition coefficients. Int Arch Occup Environ Health, 58: 75-87; Kruhoffer, P.W., 1983. Handling of inspired vaporized ethanol in the airways and lungs (with comments on forensic aspects). Forensic Science International, 21; 1-17; Johanson, G., 1991. Modelling of respiratory exchange of polar solvents. Ann Occup Hyg, 35: 323-339; Johanson, G. (1991): Modelling of respiratory exchange of polar solvents. Ann Occup Hyg, 35: 323-339; WHO working group, 1987. Environmental Health Criteria Vol. 65; WHO working group, 1990. Environmental Helath Criteria Vol. 103.)