Glycollic acid

Repeated dose toxicity: inhalation

Administrative data

Endpoint:

short-term repeated dose toxicity: inhalation

Type of information:

experimental study

Adequacy of study:

supporting study

Reliability:

2 (reliable with restrictions)

Data source

Reference

Reference Type:

study report

Title:

Unnamed

Year:

1983

Report date:

1983

Materials and methods

Principles of method if other than guideline:

Groups of 10 rats were exposed to 0, 0.23, 0.72, and 2.0 mg/L in air for 6 hrs/day, 5 days/week for 2 weeks. At the end of the exposure period and after a 14-day recovery period, blood and urine samples were collected for clinical analysis and rats were sacrificed for pathological examination.

GLP compliance:

no

Limit test:

no

Test material

Test material information

Constituent 1

Reference substance name:

Glycollic acid

EC Number:

201-180-5

EC Name:

Glycollic acid

Cas Number:

79-14-1

Molecular formula:

C2H4O3

IUPAC Name:

2-hydroxyacetic acid

Details on test material:

Glycolic acid 70% solution

Test animals

Species:

rat

Strain:

other: Crl:CD®

Sex:

male

Administration / exposure

Route of administration:

inhalation: aerosol

Type of inhalation exposure:

nose only

Vehicle:

air

Analytical verification of doses or concentrations:

yes

Duration of treatment / exposure:

Exposure was for 6 hours per day, 5 days per week for 2 weeks. Due to deteriorating condition in the high dose group, these rats were only dosed on eight occasions.

Frequency of treatment:

five days/week for two weeks followed by a 14 day observation period.

Doses / concentrations

Remarks:

Doses / Concentrations:
0.20, 0.70 and 2.0 mg/L
Basis:
nominal conc.

No. of animals per sex per dose:

10

Control animals:

yes, concurrent no treatment

Results and discussion

Effect levels

Dose descriptor:

NOAEL

Effect level:

0.23 mg/L air (nominal)

Sex:

male

Target system / organ toxicity

Critical effects observed:

not specified

Any other information on results incl. tables

Mortality: Exposure of the 2.0 mg/L treatment was stopped after the 8th exposure. Seven of the rats at this treatment were sacrificed in extremis: one after the 8th exposure, four the following day, and one each on the 11th and 12th days after the eighth exposure. A single rat died in the 0.72 mg/L treatment 13 days after the 10th exposure.

Clinical signs: No clinical signs or weight gain differences were seen between the control and 0.23 mg/L animals. Rats in the 0.72 and 2.0 mg/L treatments experienced significant and severe weight loss throughout the exposure and recovery periods. Symptoms of toxicity included laboured breathing, lung noise, ruffled and discoloured fur, red and clear nasal and ocular discharges.

Clinical chemistry: Measurements made at the end of the exposure period showed no compound-related changes in rats exposed to 0.23 mg/L. Changes were noted in the 0.72 and 2.0 mg/L treatments. Rats exposed to 2.0 mg/L had decreased concentrations of serum protein, increased serum activities of glutamic-pyruvic transaminase and glutamic-oxaloacetic transaminase, and decreases in urine volume and pH. These changes were interpreted as evidence of compound related effects on the integrity and function of hepatic tissue. However the effects were all reversible following the 14 day recovery period.

Gross necropsy: Gross pathological examination following the exposure period revealed no compound-related changes in rats exposed to 0.23 and 0.72 mg/L. Rats exposed to 2.0 mg/L showed distended G. I. tract, small spleen and small thymus. Similar effects were seen in rats at all test levels 14 days after exposure. Microscopic examination showed mild, diffuse hepatocellular degeneration in one rat in the 0.23 mg/L treatment, 9 rats in the 0.72 and 7 rats at 2.0 mg/L. A comparison of organ and body weights between control and rats at 0.243 mg/L showed no changes. Effects were seen in rats exposed to 0.72 and 2.0 mg/L. Fourteen days later, rats exposed to 0.72 mg/L had significantly lower lung, kidney, liver and thymus weights than control rats. Rats exposed to 2.0 mg/L had significantly lower kidney weights. On an organ/body weight basis, rats exposed to 0.72 mg/L had elevated testes weights.

Applicant's summary and conclusion

Conclusions:

Based on parameters evaluated in this study, the 0.72 and 2.0 mg/l treatments are definite and dose-dependent effect levels with the primary effects on survival and on hepatic integrity. The only effect seen at 0.23 mg/L was very mild diffuse hepatocellular degeneration in one of ten rats, 14 days post exposure. Based on the steepness of the dose-response curve (disappearance of mortality, weight loss and clinical signs with concentration) this level is practically a no-effect level. NOAEL = 0.23 mg/L for repeated administration by inhalation exposure.

Executive summary:

Groups of 10 rats were exposed to 0, 0.23, 0.72, and 2.0 mg/L in air for 6 hrs/day, 5 days/week for 2 weeks. At the end of the exposure period and after a 14-day recovery period, blook and urine samples were collected for clinical analysis and rats were sacrificed for patological examination. Based on parameters evaluated in this study, the 0.72 and 2.0 mg/l treatments are definite and dose-dependent effect levels with the primary effects on survival and on hepatic integrity. The only effect seen at 0.23 mg/L was very mild diffuse hepatocellular degeneration in one of ten rats, 14 days post exposure. Based on the steepness of the dose-response curve (disappearance of mortality, weight loss and clinical signs with concentration) this level is practically a no-effect level. NOAEL = 0.23 mg/L for repeated administration by inhalation exposure.