Aluminium tributanolate

Repeated dose toxicity: oral

Administrative data

Endpoint:

sub-chronic toxicity: oral

Type of information:

experimental study

Adequacy of study:

supporting study

Reliability:

4 (not assignable)

Rationale for reliability incl. deficiencies:

abstract

Remarks:

abstract from reliable source

Data source

Reference

Reference 1

Reference Type:

secondary source

Title:

U.S. EPA. 1986. Butanol: Rat oral subchronic toxicity study.

Author:

US EPA

Year:

1986

Bibliographic source:

In Integrated Risk Information System (IRIS) U.S. Environmental Protection Agency Chemical Assessment Summary National Center for Environmental Assessment 1 n-Butanol; CASRN 71-36-3 ffice of Solid Waste, Washington, DC

Reference 2

Reference Type:

secondary source

Title:

n-Butanol (CAS No. 71-36-3) JACC No. 41

Author:

ECETOC

Year:

2003

Bibliographic source:

European Centre for Ecotoxicology and Toxicology of Chemicals 4 Avenue E. Van Nieuwenhuyse (Bte 6), B-1160 Brussels, Belgium.

Materials and methods

Test guideline

Qualifier:

no guideline followed

GLP compliance:

not specified

Test material

Test material information

Constituent 1

Reference substance name:

Butan-1-ol

EC Number:

200-751-6

EC Name:

Butan-1-ol

Cas Number:

71-36-3

Molecular formula:

C4H10O

IUPAC Name:

butan-1-ol

Results and discussion

Effect levels

Dose descriptor:

NOAEL

Effect level:

125 mg/kg bw/day (nominal)

Based on:

test mat.

Sex:

male/female

Basis for effect level:

other: CNS effects

Target system / organ toxicity

Critical effects observed:

yes

Lowest effective dose / conc.:

500 mg/kg bw/day (nominal)

System:

central nervous system

Organ:

not specified

Treatment related:

yes

Applicant's summary and conclusion

Executive summary:

Four groups of male and female CD rats (30/sex/group) were administered daily (not further specified; 5 or 7 d/wk) by gavage 0, 30, 125 or 500 mg nBA/kgbw/d for either 6 or 13 weeks.  Body weight and food consumption were recorded weekly.  Any signs of mortality and overt toxicity were noted twice a day.  Ophthalmic examination was conducted prior to treatment and during week 13 before final necropsy.  Clinical pathology of urine and blood was investigated, prior to study initiation, in a separate group of 10 male and 10 female rats, during week 6 in all surviving rats scheduled for interim kill and during week 13 in the first 10 male and 10 female rats scheduled for final necropsy.  Ten male and ten female rats from each group were necropsied on study days 43 to 44 and the remaining animals on study days 92 to 93.  Gross pathology of all animals was assessed and organs from animals necropsied on study days 92 to 93 were weighed.  A complete histopathological investigation was made of all animals of the control and high-dose groups.  In the low and mid-dose groups, histopathology included the liver, kidney, and heart from all animals and all gross lesions.  All animals found dead or killed in extremis were also microscopically examined.  No dose-related differences were observed between treatment or control rats in body or organ weight changes, food consumption or mortality, gross pathology, and histopathological and ophthalmic evaluations.  Ataxia and hypoactivity (lasting less than 1 h) were observed 2 to 3 minutes after dosing in both sexes of the high-dose group (500/mg/kgbw/d) during the final 6 weeks of dosing.  Such ataxia and hypoactivity are typically seen following high oral doses of alcohols.  The rapid induction/remission of these effects and the reported increased incidence after the interim kill may be due to the fact that personnel were able to collect post-dose observations more quickly since fewer animals required dosing.  nBA was not expected to persist or accumulate over time.  No treatment-related signs were observed in the 30 or 125 mg/kgbw/d treatment groups, the latter value being the no-observed adverse effect level