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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Endpoint:
repeated dose toxicity: inhalation
Type of information:
other: hazard assessment report
Adequacy of study:
supporting study
Study period:
-2004
Reliability:
other: reliable hazard assessment report
Rationale for reliability incl. deficiencies:
other: see 'Remark'
Remarks:
The literature search for the CERI hazard assessment was conducted in April 2002 with the databases including CAS online, HSDB, IRIS, RTECS ,TOXLINE etc. The references were updated when additional information on data source and others were obtained. In April 2004, the status of the risk assessment of acetaldehyde by international organizations was confirmed and any new studies that were critical to determine NOAEL/LOAEL were included in the references.

Data source

Reference
Reference Type:
other: hazard assessment
Title:
Hazard Assessment Report Acetaldehyde
Author:
Chemicals Evaluation and Research Institute (CERI), Japan
Year:
2007
Bibliographic source:
http://www.cerij.or.jp/ceri_en/hazard_assessment_report/yugai_indx_en.htm

Materials and methods

Test material

Constituent 1
Chemical structure
Reference substance name:
Acetaldehyde
EC Number:
200-836-8
EC Name:
Acetaldehyde
Cas Number:
75-07-0
Molecular formula:
C2H4O
IUPAC Name:
acetaldehyde

Results and discussion

Target system / organ toxicity

Critical effects observed:
not specified

Any other information on results incl. tables

Table 1: Inhalative repeated dose data [cited from Chemicals Evaluation and Research Institute (CERI), Japan, Hazard assessment on Acetaldehyde 2007, http://www.cerij.or.jp/ceri_en/hazard_assessment_report/yugai_indx_en.htm]

 

Species/strain

/sex/age/num

berof animals

Period

Dose

Results

Reference

Mouse

ICR

4-5 weeks

17-18 animals

/group

5days

3hours/day

0, 324 mg/m3

(0, 180ppm)

324 mg/m3

Decrease in bactericidal activity of alveolar macrophages by 11.2%, no change in mortality by streptococcal infection

Aranyi

et al.,

1986

Rat

SD

Male

Age unknown

6 animals

/group

22days

750-2,500 mg/m3

No death following phased increases of exposure concentrations. The authors consider that the reason is due to metabolic adaptation.

Lamboeuf

et al. 1987;

Latgeet al.,

1987

Rat

Wistar

Male and

female

10 animals

/group

4 weeks

6 hours/day

5 days/week

0, 400, 1,000, 2,200, 5,000ppm

(0, 720, 1,800, 3,950, 9,000 mg/m3)

400ppmand above Degeneration of the nasal mucosa 1,000ppmand above

Male: suppression of body weight gain 2,200ppmand above Hyperplasia andmetaplasiaof the nasal mucosa, increase in mortality 5,000ppm

Male: increase in relative weight of lung, decrease in relative weight of liver

Female: suppression of body weight gain, decrease in relative weight of liver LOAEL: 400ppm(720 mg/m3)

Appelman

et al., 1982

Rat

Wistar

Male

10 animals

/group

4 weeks

6 hours/day

5 days/week

At basic concentrations of 0, 150, 500ppm(0, 270, 900 mg/m3)

(1) Continuous exposures of 6 hours/day at basic concentrations

(2) Exposures at 0, 110, 500ppmfor two periods of 3 hrs/day interrupted by a non-exposure period of 1.5 hrs

(3) An exposure profile as (2) superimposed with 5-min periods of six times the basic concentration with a frequency of four peak exposures per 3-hr period.

(1) 6-hr uninterrupted 500ppm: degeneration of the olfactory epithelium NOAEL: 150ppm(270 mg/m3)

(2) 6-hr interrupted 500ppm: degeneration of the olfactory epithelium

(3) 6-hr interrupted with peak (6 times the basic concentration) 500ppm:eyeirritation , nervously running around, suppression of body weight gain

Appelman

et al., 1986

Rat

Wistar

Male

12 animals

/group

5 weeks

8 hours/day

5 days/week

0, 243ppm(0, 437 mg/m3)

243ppm

Degradation of the olfactory epithelium, inflammation of the nasal mucosa, increases in residual volume and functional residual capacity in pulmonary function test

Saldiva

et al., 1985

Syrian

hamster

20animals

/group

13weeks

6hours/day

5days/week

0, 390, 1,340,

4,560ppm(0, 700, 2,400, 8,200 

mg/m3)

1,340ppm

Focal hyperplasia,metaplasiaof the respiratory tract

4,560ppm

Suppression of body weigh gain, rhinitis, nasal effusion, salivation, increased relative weights of lung, kidney and heart, degeneration, hyperplasia andmetaplasiaof respiratory and olfactory epithelium of nasal cavity, disappearance of sub epithelial gland of nasal cavity, severe degeneration, hyperplasia andmetaplasiaof the epithelium of nasal turbinate, and focal hyperplasia andmetaplasiaof the larynx, trachea and lung

NOAEL: 390ppm(in this assessment)

Kruysse

et al., 1975

 

Applicant's summary and conclusion