Ethanol

Respiratory sensitisation

Administrative data

Endpoint:

respiratory sensitisation: in vivo

Type of information:

experimental study

Adequacy of study:

supporting study

Reliability:

2 (reliable with restrictions)

Rationale for reliability incl. deficiencies:

other: Published study that contains sufficient details to judge it reliable with restrictions.

Data source

Reference

Reference Type:

publication

Title:

Impact of emerging pollutants on pulmonary inflammation in asthmatic rats: ethanol vapors and agglomerated TiO2 nanoparticles.

Author:

Scarino A, Noël A, Renzi PM, Cloutier Y, Vincent R, Truchon G, Tardif R, Charbonneau M.

Year:

2012

Bibliographic source:

Inhalation Toxicol. 24(8): 528–538

Materials and methods

Principles of method if other than guideline:

To investigate if exposure to inhaled ethanol vapors can modulate the rat pulmonary inflammatory response resulting from an allergic asthmatic reaction in Brown Norway rats.

GLP compliance:

not specified

Test material

Test material information

Constituent 1

Reference substance name:

Ethanol

EC Number:

200-578-6

EC Name:

Ethanol

Cas Number:

64-17-5

Molecular formula:

C2H6O

IUPAC Name:

ethanol

Test material form:

liquid

Test animals

Species:

rat

Strain:

Brown Norway

Sex:

male/female

Details on test animals or test system and environmental conditions:

TEST ANIMALS
- Age at study initiation: 6-8 weeks.
- Housing: Individually during exposure.
- No food or drink during exposure.

ENVIRONMENTAL CONDITIONS
- Photoperiod (hrs dark / hrs light): 12/12

Test system

Route of induction exposure:

inhalation

Route of challenge exposure:

inhalation

Vehicle:

unchanged (no vehicle)

Concentration:

3000ppm

No. of animals per dose:

8

Details on study design:

Chicken egg ovalbumin (OVA) was used to induce allergic asthma in two phases, i.e. sensitization and challenge. Animals were sensitized by s.c. injection of 1 mL solution containing 0.9% saline (w/v), 1 mg ovalbumin, and 3.5 mg aluminum hydroxide (adjuvant). Fourteen days later, animals were challenged for 15 min by inhalation with a freshly prepared 0.9% saline solution containing a specific OVA concentration. A compressor was used to vaporize OVA solution from the nebulizer to the cage (2 rats/exposure). OVA concentrations were selected to cause 30–40% of maximal pulmonary inflammation to leave sufficient capacity for enhancement of the effect in the presence of ethanol.

A. INDUCTION EXPOSURE
- No. of exposures:1
- Site: sub cutaneous

Ethanol exposure:
- Whole body inhalation exposure, 500L chamber. Concentration monitored (GC) every 10 mins.
- 6hrs/day for at least 22 days.

B. CHALLENGE EXPOSURE
- No. of exposures: 1
- Day(s) of challenge: 14
- Site: inhalation
- Bronchiolar lavage was performed in different groups of rats at 6, 24, 36, 48, and 72 h following OVA challenge, always immediately after the last ethanol exposure. Fixed white blood cells (WBC) were mixed 1:1 with methylene blue and then counted using a hemacytometer. The plasma concentrations of seven cytokines relevant to asthma inflammation (MCP-1, IL-1β, IL-4, IL-6, IL-10, INF-γ, and TNF-α)were measured using a cytokine kit). Lung histology was performed.

Results and discussion

Results:

Exposure to ethanol did not significantly affect leukocytes present in bronchiolar lavage after OVA challenge.

Applicant's summary and conclusion

Interpretation of results:

not sensitising

Executive summary:

A study was carried out to investigate if exposure to inhaled ethanol can modulate the rat pulmonary inflammatory response resulting from an allergic asthmatic reaction. Brown Norway rats were sensitized and challenged (15 min inhalation, 14 days later) with chicken egg ovalbumin (OVA). Leukocytes were counted in bronchoalveolar lavages (BAL) performed at 6, 24, 36, 48 and 72 h following the challenge and after ethanol exposures (3000 ppm, 6 h/day, daily). Exposure to ethanol did not significantly affect BAL leukocytes after OVA challenge leading to the conclusion that allergic pulmonary inflammation is not up-regulated by inhalation of ethanol.