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EC number: 222-823-6 | CAS number: 3622-84-2
- Life Cycle description
- Uses advised against
- Endpoint summary
- Appearance / physical state / colour
- Melting point / freezing point
- Boiling point
- Density
- Particle size distribution (Granulometry)
- Vapour pressure
- Partition coefficient
- Water solubility
- Solubility in organic solvents / fat solubility
- Surface tension
- Flash point
- Auto flammability
- Flammability
- Explosiveness
- Oxidising properties
- Oxidation reduction potential
- Stability in organic solvents and identity of relevant degradation products
- Storage stability and reactivity towards container material
- Stability: thermal, sunlight, metals
- pH
- Dissociation constant
- Viscosity
- Additional physico-chemical information
- Additional physico-chemical properties of nanomaterials
- Nanomaterial agglomeration / aggregation
- Nanomaterial crystalline phase
- Nanomaterial crystallite and grain size
- Nanomaterial aspect ratio / shape
- Nanomaterial specific surface area
- Nanomaterial Zeta potential
- Nanomaterial surface chemistry
- Nanomaterial dustiness
- Nanomaterial porosity
- Nanomaterial pour density
- Nanomaterial photocatalytic activity
- Nanomaterial radical formation potential
- Nanomaterial catalytic activity
- Endpoint summary
- Stability
- Biodegradation
- Bioaccumulation
- Transport and distribution
- Environmental data
- Additional information on environmental fate and behaviour
- Ecotoxicological Summary
- Aquatic toxicity
- Endpoint summary
- Short-term toxicity to fish
- Long-term toxicity to fish
- Short-term toxicity to aquatic invertebrates
- Long-term toxicity to aquatic invertebrates
- Toxicity to aquatic algae and cyanobacteria
- Toxicity to aquatic plants other than algae
- Toxicity to microorganisms
- Endocrine disrupter testing in aquatic vertebrates – in vivo
- Toxicity to other aquatic organisms
- Sediment toxicity
- Terrestrial toxicity
- Biological effects monitoring
- Biotransformation and kinetics
- Additional ecotoxological information
- Toxicological Summary
- Toxicokinetics, metabolism and distribution
- Acute Toxicity
- Irritation / corrosion
- Sensitisation
- Repeated dose toxicity
- Genetic toxicity
- Carcinogenicity
- Toxicity to reproduction
- Specific investigations
- Exposure related observations in humans
- Toxic effects on livestock and pets
- Additional toxicological data
Immunotoxicity
Administrative data
Description of key information
The most sensitive endpoint available today to assess chemical induced alteration to the immune system is used to evaluate BBSA for immunosuppression in the murine B6C3F1 model. Immunosuppression of BBSA was evaluated by examining the antibody plaque-forming cell (PFC) response to sheep red blood cells (SRBC). The antibody plaque-forming cell assay quantifies production of specific antibody through enumeration of antibody-producing cells following immunization with sheep red blood cells. This is based upon the antibody response to SRBC, a T-dependent antigen that requires functional integration of several cell populations including macrophages, T-helper cells, and B cells. Alterations in function or numbers of any of these populations may result in a suppressed immune response to pathogens. No suppression of the immune response was noticed after a 28 day dermal exposure with BBSA to the mice. In addition results showed in the LD group an increase in the IgM response in the spleen. However the biological significance of this finding is questionable due to the lack of change in spleen cellularity and absence of dose response. Furthermore immunophenotyping of the lymph node resulted in no marked changes in immune cell markers in the lymph node. Due to a technical issue, evaluation of the splenic immune markers could not be conducted. These results demonstrate that dermal exposure to BBSA, did not induce immunotoxicity in a murine model.
Key value for chemical safety assessment
Effect on immunotoxicity: via oral route
Link to relevant study records
- Endpoint:
- immunotoxicity: short-term dermal
- Remarks:
- 28 day
- Type of information:
- experimental study
- Adequacy of study:
- key study
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- study well documented, meets generally accepted scientific principles, acceptable for assessment
- Principles of method if other than guideline:
- In this study the potential for hypersensitivity and immune suppression was evaluated following dermal exposure to NBBS using a murine model.
- GLP compliance:
- not specified
- Limit test:
- no
- Species:
- mouse
- Strain:
- B6C3F1
- Sex:
- female
- Details on test animals or test system and environmental conditions:
- B6C3F1 mice are commonly uszed to evaluate potential immunotoxicioty and were used to evaluate the IgM response to sheep red blood cells (SRBC).
- Route of administration:
- dermal
- Vehicle:
- acetone
- Details on exposure:
- 25 µl per dorsal surface of each ear.
Groups of mice (5/group) were exposed on one of the three concentrations of test agents or acetone vehicle over a 28- d period for each mouse. - Analytical verification of doses or concentrations:
- not specified
- Duration of treatment / exposure:
- Groups of mice (5/group) were exposed on one of the three concentrations of test agents or acetone vehicle over a 28- d period for each mouse.
- Frequency of treatment:
- B6C3F1 mice were exposed over a 28-d period dermally (25µl per dorsal surface of each ear). This exposure schedule is based on immune-toxicity guidelines set forth by the NTP.
- Dose / conc.:
- 25 other: %
- Dose / conc.:
- 50 other: %
- Dose / conc.:
- 100 other: %
- No. of animals per sex per dose:
- Five female animals per dose group
- Control animals:
- yes, concurrent vehicle
- Details on study design:
- THe primary IgM response to sheep red blood cells (SRBC) was enumerated using a modified hemolytic plaque-forming cell (PFC) assay of Jerne and Nordin (1963). B6C3F1 mice were exposed over a 28-d period dermally( 25µl per dorsal surface of each ear). This exposure schedule is based on immune-toxicity guidelines set forth by the NTP. Groups of mice(5/group) were exposed to one of three concentrations of test agents or acetone vehicle over a 28-d period for each mouse.Results were expressed as specific activity (IgM PFC per 10E6 spleen cells) and total activity (IgM PFC per spleen).
- Observations and clinical examinations performed and frequency:
- Systemic toxicity was evaluated weekly by clinical observation and change in body weight. The plaque-forming cell assay was conducted. Results were expressed as specific activity (IgM per 10E6 spleen cells) and total activity (IgM PFC spleen).
- Sacrifice and pathology:
- Animals were euthanized by CO2 inhalation 24 h after the final exposure, weighed, and examined for gross pathology. Blood was collected in ethylenediamine tetraacetic acid (EDTA)-coated vacutainer tubes following transection of the abdominal aorta, and hematological analysis was conducted . The liver, spleen, kidney,and thymus were removed, cleaned of connective tissue,and weighed. Spleen and DLN cell suspensions were prepared by mechanical disruption of tissues between frosted microscope slides in phosphate-buffered saline (PBS) and counted on a cellometer( Nexcelom).
- Humoral immunity examinations:
- Immunoglobulin IgM response was evaluated to shep red blood cells.
- Other functional activity assays:
- Immune cell phenotyping
Animals were euthanized by CO2 inhalation 24 h after the final exposure, weighed, and examined for gross pathology. Blood was collected in ethylenediamine tetraacetic acid (EDTA)-coated vacutainer tubes following transection of the abdominal aorta, and hematological analysis was conducted (see later description). The liver, spleen, kidneys, and thymus were removed, cleaned of connective tissue, and weighed. Spleen and DLN cell suspensions were prepared by mechanical disruption of tissues between frosted microscope slides in phosphate-buffered saline (PBS) and counted on a cellometer (Nexcelom). Cells
(1–2 × 106) were aliquoted into a 96-well U-bottom plate and washed in staining buffer (PBS + 1% bovine serum albumin + 0.1% sodium azide). Cells were resuspened in staining buffer containing anti-mouse CD16/32 antibody (clone 2.4G2) for blocking of Fc receptors (BD Biosciences). Cells were next resuspended in staining buffer containing a cocktail of fluorochrome-conjugated antibodies specific for cell surface antigens: CD45-Allophycocyanin (clone 30-F11), CD3e-V500 (500A2), CD4-Allophycocyanin-H7 (GK1.5), CD8a-PE-CF594 (53-6.7), CD45R/B220-Alexa Fluor 700 (RA3-6B2), NK1.1-FITC (PK136) (BD Biosciences), CD11c-eFluor 450 (N418), and CD11b-PerCP-Cyanine5.5 (M1/70) (eBioscience). Cells were washed in staining buffer and fixed in Cytofix buffer (BD Biosciences). Within 24 h, cells were resuspended in staining buffer and analyzed on an LSR II flow cytometer (BD Biosciences). Data analysis was performed with FlowJo 7.6.5 software (TreeStar, Inc.). Leukocytes were first identified by their expression of CD45, and the cells were further identified as follows: CD4 T cells (CD4+ CD3+), CD8 T cells (CD8+ CD3+), B cells (B220+ CD3-), NK cells (NK1.1+, CD3-), and dendritic cells (CD11b+ CD11c+). - Other examinations:
- Selected hematological parametrs were evaluated using a Hemavet 950 automatic hematology analyzer (Frew Scientific , Waterbury , CT). Endpoints analyzed included peripheral erythrocyte and leukocyte counts, leukocyte differentials (lyùphocyres, nonocytes, basophols, and eosinophils), platelet counts, hematocrit, hemoglobin levels, mean corpuscular hemoglobin (MCH) and hemoglobin concentration (MCHC), mean corpuscular volume (MCP), mean platelet volume (MCV) and platelet distribution width.
- Positive control:
- Cyclophosphamide (CP) control for plaque -forming cell assay.
- Statistics:
- Data were first tested for homogeneity using the Bartlett's chi-squared test.If data were homogeneous, a one way analysis of variance (ANOVA) was conducted. If ANOVA showed significance at p<0.05 or less, Dunnett's multiple range t-test was used to compare treatment groups with the control group. For dose-response studies, linear trend analysis (linear trend test) was performed to detrmine whether BBSA had exposure concentration-related effects for specific endpoints. Differences were considered to be significant if p<0.05 compaire to vehicle controls. Statistical analysis using Graph Pad prism version 5.0( San Diego, Ca).
- Clinical signs:
- no effects observed
- Description (incidence and severity):
- Mice exposed to the positive control, cyclophosphamide (CP), showed a significantly reduced specific spleen IgM response and total IgM response compared to vehicle control.
In mice exposed to BBSA no suppression of IgM response to SRBC was observed. Mice exposed to the lowest concentration of BBSA 525 %) demonstrated a significantincrease of PFC/spleen. (87 % compaired with vehicle treated mice), suggesting an elevation in IgM antibody response to SRBC. However the biological significance of this finding is questionable due to the lack of change in spleen cellularity and absence of dose response. - Dermal irritation (if dermal study):
- no effects observed
- Mortality:
- no mortality observed
- Body weight and weight changes:
- no effects observed
- Description (incidence and severity):
- A significant elevation in kidney and liver weight as observed. However this was due to the extreme high not relevant exposure dose (25; 50, 100 % of BBSA), in contrast to the body weight which was not changed.
- Food consumption and compound intake (if feeding study):
- no effects observed
- Food efficiency:
- no effects observed
- Water consumption and compound intake (if drinking water study):
- no effects observed
- Ophthalmological findings:
- no effects observed
- Haematological findings:
- no effects observed
- Clinical biochemistry findings:
- no effects observed
- Urinalysis findings:
- not examined
- Behaviour (functional findings):
- not examined
- Immunological findings:
- no effects observed
- Description (incidence and severity):
- Mice exposed to the positive control, cyclophosphamide (CP), showed a significantly reduced specific spleen IgM response and total IgM response compared to vehicle control.
In mice exposed to BBSA no suppression of IgM response to SRBC was observed. Mice exposed to the lowest concentration of BBSA 525 %) demonstrated a significantincrease of PFC/spleen. (87 % compaired with vehicle treated mice), suggesting an elevation in IgM antibody response to SRBC. However the biological significance of this finding is questionable due to the lack of change in spleen cellularity and absence of dose response. - Organ weight findings including organ / body weight ratios:
- effects observed, treatment-related
- Gross pathological findings:
- not specified
- Neuropathological findings:
- not examined
- Histopathological findings: non-neoplastic:
- not examined
- Histopathological findings: neoplastic:
- not examined
- Humoral immunity examinations:
- no effects observed
- Description (incidence and severity):
- Dermal exposure to BBSA did not suppress the IgM response to SRBC.
- Specific cell-mediated immunity:
- no effects observed
- Non-specific cell-mediated immunity:
- no effects observed
- Remarks on result:
- not determinable due to absence of adverse toxic effects
- Remarks:
- No suppression of the immune response was noticed after a 28 day dermal exposure with BBSA to the mice
- Critical effects observed:
- no
- Conclusions:
- The purpose of this stuidy was to evaluate the potential for immune suppression following dermal exposure to BBSA using a murine model. To estimate the immunosuppressive potential of BBSA , assays that assessed immunotoxicity were performed, including the immunoglobulin (Ig) M response to cell-dependent antigen sheep red blood cells( SRBC),using the plaque-forming cell (PFC) assay and immune cell phenotyping phenotyping. 28-d treatment with BBSA did not induce immunotoxicity in a murine model.
- Executive summary:
The most sensitive endpoint available today to assess chemical induced alteration to the immune system is used to evaluate BBSA for immunosuppression in the murine B6C3F1 model. Immunosuppression of BBSA was evaluated by examining the antibody plaque-forming cell (PFC) response to sheep red blood cells (SRBC). The antibody plaque-forming cell assay quantifies production of specific antibody through enumeration of antibody-producing cells following immunization with sheep red blood cells. This is based upon the antibody response to SRBC, a T-dependent antigen that requires functional integration of several cell populations including macrophages, T-helper cells, and B cells. Alterations in function or numbers of any of these populations may result in a suppressed immune response to pathogens. No suppression of the immune response was noticed after a 28 day dermal exposure with BBSA to the mice. In addition results showed in the LD group an increase in the IgM response in the spleen. However the biological significance of this finding is questionable due to the lack of change in spleen cellularity and absence of dose response. Furthermore immunophenotyping of the lymph node resulted in no marked changes in immune cell markers in the lymph node. Due to a technical issue, evaluation of the splenic immune markers could not be conducted. These results demonstrate that dermal exposure to BBSA, did not induce immunotoxicity in a murine model.
Reference
Endpoint conclusion
- Endpoint conclusion:
- no adverse effect observed
Effect on immunotoxicity: via inhalation route
Endpoint conclusion
- Endpoint conclusion:
- no study available
Effect on immunotoxicity: via dermal route
Endpoint conclusion
- Endpoint conclusion:
- no adverse effect observed
- Study duration:
- subacute
- Species:
- mouse
Additional information
Justification for classification or non-classification
Based on the results and according to the EC criteria for classification and labelling requirements for dangerous substances and preparations (Guidelines in Commission Directive 93/21/EEC) and CLP regulation (EC No. 1272/2008 of 16 December 2008), N-butylbenzenesulphonamide is not classified for immunotoxicity.
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