Distillation residue, butyl alcohols production, rectification

Endpoint summary

Description of key information

There are no studies available from the target substance. The composition of UVCB-substance mainly consists of primary alcohols derived as a still residue obtained from the rectification of butyl alcohols by using the naphtheno-evaporating procedure in propylene oxosynthesis. The surrogate substance, 2-ethylhexanol, was used. 
Rapid absorption, metabolism and excretion of 2-EH as oxidized metabolites predominantly in urine was observed following oral ingestion. Bioaccumulation is unlikely due to virtually complete excretion within 28 hrs.
 
Acute dermal toxicity study report exhibited that the target substance was fully absorbed, with no excessive irritation.

Key value for chemical safety assessment

Bioaccumulation potential:

no bioaccumulation potential

Additional information

There are no studies available made from the target substance. The composition of UVCB-substance mainly consists of primary alcohols derived as a still residue obtained from the rectification of butyl alcohols by using the naphtheno-evaporating procedure in propylene oxosynthesis. The surrogate substance, 2-ethylhexanol, was used. The target organs of 2-ethylhexanol in rodents are the liver, the kidney, the central nervous system and the mucosa of respiratory and gastrointestinal tracts, depending on the route of administration.

Toxicokinetics of 2-ethylhexanol was investigated by Albro, P. W. (1975). The test substance was efficiently absorbed following oral administration to rats. 14C associated with 2-ethyl[1-14C]-hexanol was rapidly excreted in respiratory CO2 (6-7%), faeces (8-9%) and urine (80-82%), with essentially complete elimination by 28 h after administration. There was no difference between the low or high dose (9 μg/kg bw and 278 mg/kg bw, resp.). The major metabolite is 2-ethylhexanoic acid, which appears in urine; alternatively it may also be further metabolized by either ß-oxidation or omega and omega-1 oxidation. Only 3% of the 2-ethylhexanol are excreted unchanged. 2-EH is a good substrate for mammalian dehydrogenases which leads to 2-ethylhexanoic acid which can be conjugated or further metabolized via partial ß-oxidation, or omega- and omega-1 oxidation, followed by conjugation (Albro, 1975). 2-EH inhibits the mitochondrial ß-oxidation of fatty acids in-vitro and in-vivo, which results in decreased levels of plasma ketones, and increased levels of hepatic total lipids and triglycerides. In contrast, the peroxisomal oxidation pathways are not inhibited by 2 -EH (Badr, 1990). Overall, 2-EH was rapidly absorbed, metabolized, and excreted mainly via urine within 28 hours following the oral administration to rats. Accumulation of 2-EH or its metabolites is unlikely to occur.