Registration Dossier
Registration Dossier
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EC number: 231-977-3 | CAS number: 7783-06-4
Immunotoxicity
Administrative data
- Endpoint:
- immunotoxicity
- Adequacy of study:
- disregarded due to major methodological deficiencies
- Reliability:
- 4 (not assignable)
- Rationale for reliability incl. deficiencies:
- other: Secondary source
Data source
Referenceopen allclose all
- Reference Type:
- publication
- Title:
- Effect of hydrogen sulfide on bacterial inactivation in the rat lung
- Author:
- Rogers RE and Ferin J
- Year:
- 1 981
- Bibliographic source:
- Arch. Environ. Health, 36(5), 261-264
- Reference Type:
- publication
- Title:
- Effect of in vitro exposure to hydrogen sulfide on rabbit alveolar macrophages cultured on gas-permeable membranes
- Author:
- Robinson AV
- Year:
- 1 982
- Bibliographic source:
- Environ. Res. 27(2):491-500
- Reference Type:
- secondary source
- Title:
- TOXICOLOGICAL REVIEW OF HYDROGEN SULFIDE (CAS No. 7783-06-4). In Support of Summary Information on the Integrated Risk Information System (IRIS)
- Author:
- U.S. Environmental Protection Agency
- Year:
- 2 003
- Bibliographic source:
- EPA/635/R-03/005. www.epa.gov/iris
Materials and methods
Test material
- Reference substance name:
- Hydrogen sulphide
- EC Number:
- 231-977-3
- EC Name:
- Hydrogen sulphide
- Cas Number:
- 7783-06-4
- Molecular formula:
- H2S
- IUPAC Name:
- hydrogen sulfide
Constituent 1
Results and discussion
Applicant's summary and conclusion
- Executive summary:
The effects of H2S on lung bacterial defense has been investigated. Male Long-Evans rats were exposed to 45 ppm (636 mg/m3) H2S for 2, 4, or 6 hr followed by bacterial challenge to Staphylococcus epidermidis. In control animals, most of the bacteria was inactivated by the 6-hour postchallenge sacrifice time. Rats exposed to H2S for 2 hours responded similarly to controls. However, rats exposed to H2S for 4 and 6 hours had 6.5- and 52-fold greater percent bacteria remaining, respectively, compared to controls. The investigators suggest that an H2S-induced absence of bacterial inactivation may explain secondary pneumonias in humans subsequent to acute or subacute H2S exposure. The effect of bacterial inactivation was hypothesized by the investigators to be due to alveolar macrophage inactivation. The hypothesis is supported by Robinson (1982) who demonstrated that rabbit alveolar macrophages lost the phagocytic ability in vitro when exposed to 54 ppm (75 mg/m3) H2S for 24 hours.
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