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EC number: 231-748-8 | CAS number: 7719-09-7
- 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
Exposure related observations in humans: other data
Administrative data
- Endpoint:
- exposure-related observations in humans: other data
- Adequacy of study:
- key study
Data source
Reference
- Reference Type:
- review article or handbook
- Title:
- Schwefeldioxid [MAK Value Documentation in German language, 1974, 1981, 1998, 2000, 2013]
- Author:
- Anonymous
- Year:
- 2 013
- Bibliographic source:
- Wiley-VCH Verlag GmbH & Co. KGaA, Published Online: 31 JAN 2012 DOI: 10.1002/3527600418.mb744609d0008
Materials and methods
- Endpoint addressed:
- other: MAK value documentation
- Principles of method if other than guideline:
- review
Test material
- Reference substance name:
- Sulphur dioxide
- EC Number:
- 231-195-2
- EC Name:
- Sulphur dioxide
- Cas Number:
- 7446-09-5
- Molecular formula:
- O2S
- IUPAC Name:
- oxosulfane oxide
Constituent 1
Results and discussion
- Results:
- Sulfur dioxide irritates at concentrations of 5-10 ml/m³ (non-adapted persons) particularly the mucous membranes of the upper respiratory tract, at higher concentrations the eyes and mucous membranes, and with increased breathing the deeper airways. The irritation is caused by the hydration of sulfur dioxide on the moist mucous membranes, due to the formation of sulfurous acid (H2SO3).
The MAK value is based however not primarily to the irritating effect, but was from tudies with- probably hyperreactive - subjects in which during physical activity at concentrations from 0.6 to 2 ml/m³ a bronchoconstriction was found (Andersen et al 1974. Bedi et al 1984. Islam et al in 1992.; Koenig et al. 1982, Beermann et al. 1984, 1986; Rondinelli et al. 1987 Stacy et al. , 1981; Snell and Luchsinger, 1969).
In workers exposed to mean concentrations of 0.67 ml sulphur dioxide/m³, no changes in lung function parameters were observed, could be a habituation effect. Exposures of up to a 2-hour period with concentrations up to 0.5 ml/m3 caused in healthy volunteers no changes of the lung function.
In a study with 790 people, the concentration of 1 ml/m³ caused on 98% of the test persons not to decline in the FEV1 of more than 20% (Nowak et al. 1997). Since the people have been exposed at a respiratory minute volume of 40 I, it can be assumed that under workplace conditions with a lower respiratory minute volume (10 m³ per 8 hours, equivalent to 21 liters per minute), the proportion of workers who responds at 1 ml/m³ with bronchoconstriction will be below 2%.
TLV. The subjects in the study by Nowak et al. (1997) were exclusively exposed through the mouth. In a typical workplace respiratory minute volume of 21 l / min, about 60% is breathed through the nose (Bennett et al. 2003).
With nasal breathing, 90% of the sulfur dioxide from the air flow through the nose
is removed and didn’t reach the lungs (Speizer and Frank 1966). Also in dogs
has been shown that sulfur dioxide in the nose is removed more effectively than in the mouth.
In asthmatics it was shown, that during hyperventilation an airway obstruction on lower SO2 concentration is caused than at rest (Linn et al 1983. Sheppard et al. 1981).
The concentration is not alone determinative of the obstruction, but also the inhaled amount or depth of breathing. On nasal breathing with a respiratory minute volume of 21 l/min a lower amount of SO2 reach the lungs compared with mouth with a respiratory minute volume of 40 l/min.
Therefore, the MAK value is fixed at 1 ml/m³.
STEL. The short-term value-category I and the excess factor 1 are maintained.
Teratogenic effect.
In reproductive toxicity studies in mice and rabbits, at weak maternally toxic concentrations no evidence of teratogenic effects of sulfur dioxide were detected.
Naturally, about 750 mg sulphate/l urine (Supplement 1998) are excreted. Assuming a urine volume of 1.5 liters/day, a total amount of 1125 mg sulfate are excreted.
During a working day at an exposition corresponding to the TLV value with a tidal volume of 10 m³, about 27 mg of SO2 were adsorbed. Under the assumption of complete oxidation this corresponds to 40.5 mg sulfate and thus 1/30 of the daily excreted amount of sulphate. Thus, the daily absorbed amount of sulphate and the excreted sulphate in the urine increased only by 1/30 (3.33%). Therefore, sulfur dioxide remains the pregnancy group C.
Any other information on results incl. tables
Sulfur dioxide irritates at concentrations of 5-10 ml/m³ (non-adapted persons) particularly the mucous membranes of the upper respiratory tract, at higher concentrations the eyes and mucous membranes, and with increased breathing the deeper airways. The irritation is caused by the hydration of sulfur dioxide on the moist mucous membranes, due to the formation of sulfurous acid (H2SO3). The MAK value is based however not primarily to the irritating effect, but was from tudies with- probably hyperreactive - subjects in which during physical activity at concentrations from 0.6 to 2 ml/m³ a bronchoconstriction was found (Andersen et al 1974. Bedi et al 1984. Islam et al in 1992.; Koenig et al. 1982, Beermann et al. 1984, 1986; Rondinelli et al. 1987 Stacy et al. , 1981; Snell and Luchsinger, 1969). In workers exposed to mean concentrations of 0.67 ml sulphur dioxide/m³, no changes in lung function parameters were observed, could be a habituation effect. Exposures of up to a 2-hour period with concentrations up to 0.5 ml/m3 caused in healthy volunteers no changes of the lung function. In a study with 790 people, the concentration of 1 ml/m³ caused on 98% of the test persons not to decline in the FEV1 of more than 20% (Nowak et al. 1997). Since the people have been exposed at a respiratory minute volume of 40 I, it can be assumed that under workplace conditions with a lower respiratory minute volume (10 m³ per 8 hours, equivalent to 21 liters per minute), the proportion of workers who responds at 1 ml/m³ with bronchoconstriction will be below 2%. TLV. The subjects in the study by Nowak et al. (1997) were exclusively exposed through the mouth. In a typical workplace respiratory minute volume of 21 l / min, about 60% is breathed through the nose (Bennett et al. 2003). With nasal breathing, 90% of the sulfur dioxide from the air flow through the nose is removed and didn’t reach the lungs (Speizer and Frank 1966). Also in dogs has been shown that sulfur dioxide in the nose is removed more effectively than in the mouth. In asthmatics it was shown, that during hyperventilation an airway obstruction on lower SO2 concentration is caused than at rest (Linn et al 1983. Sheppard et al. 1981). The concentration is not alone determinative of the obstruction, but also the inhaled amount or depth of breathing. On nasal breathing with a respiratory minute volume of 21 l/min a lower amount of SO2 reach the lungs compared with mouth with a respiratory minute volume of 40 l/min. Therefore, the MAK value is fixed at 1 ml/m³. STEL. The short-term value-category I and the excess factor 1 are maintained. Teratogenic effect. In reproductive toxicity studies in mice and rabbits, at weak maternally toxic concentrations no evidence of teratogenic effects of sulfur dioxide were detected. Naturally, about 750 mg sulphate/l urine (Supplement 1998) are excreted. Assuming a urine volume of 1.5 liters/day, a total amount of 1125 mg sulfate are excreted. During a working day at an exposition corresponding to the TLV value with a tidal volume of 10 m³, about 27 mg of SO2 were adsorbed. Under the assumption of complete oxidation this corresponds to 40.5 mg sulfate and thus 1/30 of the daily excreted amount of sulphate. Thus, the daily absorbed amount of sulphate and the excreted sulphate in the urine increased only by 1/30 (3.33%). Therefore, sulfur dioxide remains the pregnancy group C.
Applicant's summary and conclusion
- Executive summary:
Sulfur dioxide irritates at concentrations of 5-10 ml/m³ (non-adapted persons) particularly the mucous membranes of the upper respiratory tract, at higher concentrations the eyes and mucous membranes, and with increased breathing the deeper airways. The irritation is caused by the hydration of sulfur dioxide on the moist mucous membranes, due to the formation of sulfurous acid (H2SO3). The MAK value is based however not primarily to the irritating effect, but was from tudies with- probably hyperreactive - subjects in which during physical activity at concentrations from 0.6 to 2 ml/m³ a bronchoconstriction was found (Andersen et al 1974. Bedi et al 1984. Islam et al in 1992.; Koenig et al. 1982, Beermann et al. 1984, 1986; Rondinelli et al. 1987 Stacy et al. , 1981; Snell and Luchsinger, 1969). In workers exposed to mean concentrations of 0.67 ml sulphur dioxide/m³, no changes in lung function parameters were observed, could be a habituation effect. Exposures of up to a 2-hour period with concentrations up to 0.5 ml/m3 caused in healthy volunteers no changes of the lung function. In a study with 790 people, the concentration of 1 ml/m³ caused on 98% of the test persons not to decline in the FEV1 of more than 20% (Nowak et al. 1997). Since the people have been exposed at a respiratory minute volume of 40 I, it can be assumed that under workplace conditions with a lower respiratory minute volume (10 m³ per 8 hours, equivalent to 21 liters per minute), the proportion of workers who responds at 1 ml/m³ with bronchoconstriction will be below 2%. TLV. The subjects in the study by Nowak et al. (1997) were exclusively exposed through the mouth. In a typical workplace respiratory minute volume of 21 l / min, about 60% is breathed through the nose (Bennett et al. 2003). With nasal breathing, 90% of the sulfur dioxide from the air flow through the nose is removed and didn’t reach the lungs (Speizer and Frank 1966). Also in dogs has been shown that sulfur dioxide in the nose is removed more effectively than in the mouth. In asthmatics it was shown, that during hyperventilation an airway obstruction on lower SO2 concentration is caused than at rest (Linn et al 1983. Sheppard et al. 1981). The concentration is not alone determinative of the obstruction, but also the inhaled amount or depth of breathing. On nasal breathing with a respiratory minute volume of 21 l/min a lower amount of SO2 reach the lungs compared with mouth with a respiratory minute volume of 40 l/min. Therefore, the MAK value is fixed at 1 ml/m³. STEL. The short-term value-category I and the excess factor 1 are maintained. Teratogenic effect. In reproductive toxicity studies in mice and rabbits, at weak maternally toxic concentrations no evidence of teratogenic effects of sulfur dioxide were detected. Naturally, about 750 mg sulphate/l urine (Supplement 1998) are excreted. Assuming a urine volume of 1.5 liters/day, a total amount of 1125 mg sulfate are excreted. During a working day at an exposition corresponding to the TLV value with a tidal volume of 10 m³, about 27 mg of SO2 were adsorbed. Under the assumption of complete oxidation this corresponds to 40.5 mg sulfate and thus 1/30 of the daily excreted amount of sulphate. Thus, the daily absorbed amount of sulphate and the excreted sulphate in the urine increased only by 1/30 (3.33%). Therefore, sulfur dioxide remains the pregnancy group C.
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