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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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:
respiratory sensitisation: in vivo
Type of information:
experimental study
Adequacy of study:
key study
Reliability:
1 (reliable without restriction)
Rationale for reliability incl. deficiencies:
other: Reliable without restrictions. Well-presented study, with relevant measurement of chemical concentrations

Data source

Reference
Reference Type:
study report
Title:
Unnamed
Year:
2007

Materials and methods

Test guideline
Qualifier:
according to guideline
Guideline:
other: exacerbation and development of bronchial asthma.
GLP compliance:
not specified

Test material

Constituent 1
Chemical structure
Reference substance name:
Aluminium sulphate
EC Number:
233-135-0
EC Name:
Aluminium sulphate
Cas Number:
10043-01-3
Molecular formula:
Al.3/2H2O4S; General formula Al2(OH)x(SO4)(3-x/2), with x=0 and x=3 and x ranging from 0 to 3.
IUPAC Name:
Aluminium sulphate
Details on test material:
- Name of test material (as cited in study report):Aluminium sulfate

Test animals

Species:
mouse
Strain:
Balb/c
Sex:
female
Details on test animals or test system and environmental conditions:
Pregnant female BALB/c mice were exposed to aerosolized leachate of residual oil fly ash (ROFA, 50 mg/ml, 30 min) at 5, 3, and 1 d before delivery.
Offspring were treated once at 3 d of age with ovalbumin (OVA, 5 mug) and alum (ip), an intentionally suboptimal dose for sensitization, exposed to aerosolized OVA (1%, 10 min) at 12-14 d or 32-35 d of age, and evaluated 2 d after the final exposure.

Test system

Route of induction exposure:
other: Intraperitoneal
Route of challenge exposure:
inhalation
Vehicle:
other: aerosolized leachate of residual oil fly ash
Concentration:
(1% aluminium sulphate)
Details on study design:
Pregnant female BALB/c mice were exposed to aerosolized leachate of residual oil fly ash (ROFA, 50 mg/ml, 30 min) at 5, 3, and 1 d before delivery. Offspring were treated once at 3 d of age with ovalbumin (OVA, 5 mug) and aluminium sulphate (ip), an intentionally suboptimal dose for sensitization, exposed to aerosolized OVA (1%, 10 min) at 12-14 d or 32-35 d of age, and evaluated 2 d after the final exposure.

Results and discussion

Results:
The offspring of ROFA-exposed mothers (ROFA group) revealed increasing airway hyperresponsiveness (higher enhanced pause [Penh] to methacholine challenge) and elevated substantial numbers of eosinophils in the bronchoalveolar lavage flued (BALF).
Histopathology revealed prominent inflammation in the lungs of ROFA group and showed increased allergen-specific IgE and IgG1 levels. Their cultured splenocytes showed an enhanced interleukin (IL)-4/interferon (IFN)-gamma cytokine, indicating Th2 skewed immunity.

Applicant's summary and conclusion

Interpretation of results:
sensitising
Conclusions:
Data indicate that exposure of pregnant female mice to an air pollutant aerosol increased asthma susceptibility in their offspring.
Executive summary:

Air pollution contributes to both exacerbation and development of bronchial asthma. Studies showed that coexposure to air pollution directly promotes sensitization to inhaled allergen in neonatal mice. The aim of this study was to investigate whether prenatal exposure to air pollution could also increase susceptibility to development of asthma in early life.

 Pregnant female BALB/c mice were exposed to aerosolized leachate of residual oil fly ash (ROFA, 50 mg/ml, 30 min) at 5, 3, and 1 d before delivery. Offspring were treated once at 3 d of age with ovalbumin (OVA, 5 mug) and alum (ip), an intentionally suboptimal dose for sensitization, exposed to aerosolized OVA (1%, 10 min) at 12-14 d or 32-35 d of age, and evaluated 2 d after the final exposure. The offspring of ROFA-exposed mothers (ROFA group) revealed increasing airway hyperresponsiveness (higher enhanced pause [Penh] to methacholine challenge) and elevated substantial numbers of eosinophils in the bronchoalveolar lavage flued (BALF).

 Histopathology revealed prominent inflammation in the lungs of ROFA group and showed increased allergen-specific IgE and IgG1 levels. Their cultured splenocytes showed an enhanced interleukin (IL)-4/interferon (IFN)-gamma cytokine, indicating Th2 skewed immunity.

 Data indicate that exposure of pregnant female mice to an air pollutant aerosol increased asthma susceptibility in their offspring.