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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Short description of key information on bioaccumulation potential result: 
No key study on toxicokinetics was identified. However, some studies were considered as weight of evidence for uptake, excretion and metabolism

Key value for chemical safety assessment

Bioaccumulation potential:
no bioaccumulation potential
Absorption rate - oral (%):

Additional information

Several data were available in the literature considering the toxicokinetics of 1,6-hexamethylene diamine (HMD) including the metabolism and the routes of excretion.

In human volunteers, HMD orally administered is rapidly excreted (within 10 h) in urine as parent compound and N-acetyl-1,6-hexamethylene diamine metabolites. The fast acetylators excreted more HMD than the slow acetylators (Brorson et al., 1990). The available human data show considerable inter-individual variation in the elimination of the 6-aminohexanoic acid metabolite and that the elimination of HMD was based on wether the individuals were fast or slow acetylators.

Moreover, data suggested that heterozygous antitrypsin carriers might be more susceptible to the effects of inhaled amines, including HMD as detailed in section 7.9.3 (Berode et al, 1988).

Following oral administration of HMD-1,6-[14C]dihydrochloride (HMD salt) to male rats, about 20% of the administered dose was recovered as CO2 after 72 h while urinary and fecal excretion accounted for 47% and 27% of the administered radioactivity, respectively (David and Heck, 1983). Based on these results (nearly) complete absorption is assumed for the oral uptake in rats.

By partially purifed mammalian liver aldehyde oxidase, metabolism of HMD into 6-aminohexanoic acid and caprolactam occurredvia3,4,5,6-tetrahydro-2H-azepine (Subramanyam et al., 1989). In vitro incubation of HMD with purified pig kidney diamine oxidase lead to a rate oxidation of 41 % of cadaverine oxidation (Bardsley, 1970).