Reaction mass of sulphuric acid, hydrogen peroxide and peroxomonosulphuric acid

Endpoint summary

Description of key information

In accordance with Regulation (EC) 1907/2006, Annex I, the toxicokinetic behaviour of the multi-constituent substance has been assessed to the extent that can be derived from relevant available information.

Key value for chemical safety assessment

Bioaccumulation potential:

no bioaccumulation potential

Absorption rate - oral (%):

100

Absorption rate - dermal (%):

100

Absorption rate - inhalation (%):

100

Additional information

SULPHURIC ACID

 

Sulphuric acid readily dissociates, with any local toxicity resulting from the H⁺ion (pH change) rather than the liberation of sulphate ions. Following oral ingestion, the sulphate anion is readily absorbed and joins the pool of sulphate anions in the body, indistinguishable from sulphate derived from dietary sources. Once in the lungs, sulphate from sulphuric acid is rapidly absorbed into the blood. Due to its polarity, dermal absorption of sulphuric acid is likely to be low (unless penetration is enhanced by destruction of the skin barrier). Sulphate, a normal constituent in the blood and a metabolite of sulphur‑containing amino acids, is excreted in the urine.

 

ABSORPTION

 

Oral

Sulphuric acid ingested orally will be rapidly diluted and buffered by the contents of the GI tract (EFSA, 2012). Following acid dissociation, the sulphate anion will be absorbed and enter the body’s normal sulphate electrolyte pool. The local toxic effects of sulphuric acid are a result of pH change (excess H⁺) rather than an effect of the sulphate anion (ATSDR, 1998; Bassanet al. 2012; OECD, 2001).

 

Inhalation

Following inhalation exposure, sulphuric acid particles may be deposited in various regions of the respiratory tract. Distribution of deposited particles is dependent on particle size, physiological factors (e.g. breathing rate and breathing depth) and environmental conditions (particularly relative humidity as it is likely to affect aerosol size due to the hygroscopic nature of sulphuric acid) (HPA, 2011). Larger droplets (10-15 µ­m and above) deposit mainly in the nose while smaller droplets (1-10 µm) would reach deeper regions of the respiratory tract including the larynx, trachea and bronchi (SCOEL, 2007) and, presumably, the alveoli.

 

In humans, during a 5-15 minutes exposure through a face mask to 0.4-1 mg/m³mist with an average aerosol size of 1 µm, the retention of sulphuric acid mist averaged at 77% (ATSDR, 1998). In rats, guinea pigs and dogs, sulphuric acid-derived sulphur (aerosol sizes 0.4‑1.2 µm) was rapidly absorbed into the blood (“cleared from the pulmonary region within a half-time of 2-9 minutes” for all species) following lung deposition. Upper respiratory tract clearance was much slower (Dahlet al. 1983).

 

Dermal

No studies specifically regarding dermal absorption of sulphuric acid were identified. According to ECHA (2012), the low molecular weight (98 Daltons) and aqueous miscibility of sulphuric acid are considered favourable for dermal absorption. However, its polarity suggests that there would be little absorption via this route unless the acidity causes skin damage and breaching of the skin barrier (SCOEL, 2007). In the absence of any better data, the ECHA default assumption of 100% absorption has to be selected.

 

DISTRIBUTION and METABOLISM

 

Sulphate is a normal constituent of the blood, with concentrations of 0.8-1.2 mg/dL usually found in human serum. Sulphate is a normal metabolite of sulphur-containing amino acids and does not need to be further metabolised for urinary excretion (ATSDR, 1998).

 

EXCRETION

 

Excess sulphate is excreted as is in the urine (ATSDR, 1998). It is highly unlikely that sulphate anions would bioaccumulate (HPA, 2011).

 

References

 

ATSDR (1998). Agency for Toxic Substances and Diseases Registry. Toxicological profile for sulfur trioxide and sulfuric acid. Available fromhttp://www.atsdr.cdc.gov/toxprofiles/tp117.pdf

 

Bassan Aet al. (2012). Reports on toxicokinetics, toxicity and allergenicity data on substances to be evaluated as acceptable previous cargoes for edible fats and oils (NP/EFSA/CONTAM/2011/01) – Batches n. 1, 2 and 3. Scientific report submitted to EFSA. Supporting publications: EN-274. Available from /http://www.efsa.europa.eu/en/supporting/doc/274e.pdf.

 

Dahl ARet al. (1983). Clearance of sulfuric acid-introduced 35S from the respiratory tracts of rats, guinea pigs and dogs following inhalation or instillation. Fundamental and Applied Toxicology 3, 293-297.

 

ECHA (2012). Guidance on information requirements and chemical safety assessment. Chapter R.7c: Endpoint specific guidance. November 2012 (version 1.1).

 

EFSA (2012). Scientific Opinion on the evaluation of the substances currently on the list in the annex to Commission Directive 96/3/EC as acceptable previous cargoes for edible fats and oils – Part II of III. EFSA Journal, 10 (5), 2703. Available fromhttp://www.efsa.europa.eu/en/efsajournal/doc/2703.pdf

 

HPA (2011). Health Protection Agency. Compendium of Chemical Hazards. Sulphuric acid. Available fromhttp://www.hpa.org.uk/webc/HPAwebFile/HPAweb_C/1202115622008

 

OECD (2001). Organisation for Economic Co-operation and Development. SIDS Initial Assessment

Reports for Sulfuric Acid (CAS No: 7664-93-9) for 11th SIAM (January 2001). Available from

http://www.inchem.org/documents/sids/sids/7664939.pdf.

 

SCOEL (2007). Recommendation from the Scientific Committee on Occupational Exposure Limits for sulphuric acid. Available fromhttp://ec.europa.eu/social/keyDocuments.jsp?pager.offset=0&langId=en&mode=advancedSubmit&policyArea=82&subCategory=153&year=0&country=0&type=0&advSearchKey=SCOEL.

 

HYDROGEN PEROXIDE

 

Hydrogen peroxide is an endogenous metabolite in aerobic cells, with its concentration normally kept in equilibrium. Exogenous hydrogen peroxide, administered via the oral, inhalation or dermal routes, passes the absorption surfaces to enter the adjacent tissues and blood vessels, where it is rapidly degraded liberating oxygen and water. Metabolism occurs via catalase or glutathione peroxidase, dependent on the hydrogen peroxide concentration and location within the body. Considering the high degradation capacity for hydrogen peroxide in the blood, it is unlikely that it will be distributed systemically. As such, no bioaccumulation is likely. Liberated oxygen and water are expected to be eliminated via the lungs and urine, respectively.

 

ABSORPTION and DISTRIBUTION

Hydrogen peroxide is an endogenous metabolite in aerobic cells, with its concentration regulated through a balance of generation and degradation (EC, 2003). At high exposures, exogenous hydrogen peroxide is expected to be readily taken up by cells at the absorption surfaces (including the skin and mucous membranes), since the permeability coefficient is comparable with that of water (EC, 2003). It then enters the adjacent tissues and blood vessels where it is rapidly degraded to oxygen and water. It is, therefore, difficult to estimate the amount of unchanged substance available for absorption (EC, 2003; ECETOC, 1996). The liberation of gaseous oxygen has the potential to cause mechanical pressure injury or oxygen embolism if the liberated oxygen cannot freely escape (EC, 2003). The efficient breakdown of hydrogen peroxide prevents it from entering general circulation.Therefore, the endogenous steady state level of the substance in tissues is unlikely to be affected(EC, 2003; ECETOC, 1996; HERA, 2005) and the bioaccumulation potential is low (ECETOC, 1996).

 

METABOLISM

Hydrogen peroxide is metabolised to water and oxygen via two metabolising enzymes, catalase and glutathione peroxide (EC, 2003; DF, 2011). At high substrate concentrations decomposition occurs mainly via catalase, whereas at low substrate concentrations the action of glutathione peroxide dominates. Enzyme activity of catalase is high in the intestine, liver, kidneys, mucosae and other vascularised tissues, but low in the brain, lungs and heart (EC, 2003; ECETOC, 1996). Glutathione peroxidase activity is maximal in the stomach (EC, 2003). Due to the high catalase activity in red blood cells, exogenous hydrogen peroxide is efficiently removed from the blood (EU, 2003). In the presence of oxidisable metal ions such as Fe²⁺or Cu⁺, hydrogen peroxide may be converted to cytotoxic hydroxyl radicals via the Haber-Weiss or Fenton reaction (DF, 2011).

 

EXCRETION

Under normal conditions, the released oxygen is expected to transfer to the oxygen pool of the body and be eliminated via the lungs (DF, 2011; EC, 2003). Any water is presumably utilised or removed via the urine.

 

References

 

EC (2003). European Commission. European Chemicals Bureau. European Union risk assessment report: Hydrogen peroxide. EUR 20844 EN. Volume 38.

http://echa.europa.eu/documents/10162/a6f76a0e-fe32-4121-9d9d-b06d9d5f6852

 

ECETOC (1996). European Centre for Ecotoxicology and Toxicology of Chemicals. Hydrogen peroxide OEL criteria document. Special Report No.10.http://www.ecetoc.org/

 

DF (2011). Deutsche Forschungsgemeinschaft. MAK Value Documentations. The MAK-Collection for Occupational Health and Safety. Part 1: MAK Value documentations. Volume 26. Edited by Greim H. Wiley-VCH Publishers.

 

HERA (2005). Human & Environmental Risk Assessment on ingredients of household cleaning products. HERA – Hydrogen Peroxide Version 1.0 April 2005.http://www.heraproject.com/files/36-F-05-Shor_H2O2_version1.pdf

 

PEROXOMONOSULPHURIC ACID

 

In the absence of specific data on the ADME of peroxomonosulphuric acid, its physicochemical properties were assessed for insights into likely ADME characteristics. Since peroxomonosulphuric acid will rapidly breakdown to yield sulphuric acid and active oxygen, its ADME behaviour is likely to reflect those of sulphuric acid and hydrogen peroxide. Following oral ingestion, peroxomonosulphuric acid is expected to dissociate to liberate a sulphate anion, which will be readily absorbed and join the pool of sulphate anions in the body, indistinguishable from sulphate derived from dietary sources. Any OH^-and H⁺ions released, subsequently form oxygen and water. Once in the lungs, sulphate from peroxomonosulphuric acid is expected to be rapidly absorbed into the blood. Due to its polarity, dermal absorption of peroxomonosulphuric acid is likely to be low (unless penetration is enhanced by destruction of the skin barrier). Sulphate, a normal constituent in the blood and a metabolite of sulphur‑containing amino acids, is excreted in the urine. Liberated oxygen and water are expected to be eliminated via the lungs and urine, respectively.

 

ABSORPTION

 

Oral

Peroxomonosulphuric can be presumed to act similarly to sulphuric acid and be rapidly diluted and buffered by the contents of the GI tract. The acid would dissociate to form peroxysulphate ions that will be rapidly transformed to active oxygen and to sulphate anions that will be absorbed and enter the body’s normal sulphate electrolyte pool. Consequently, any H⁺cations and OH^-anions released are likely to rapidly form oxygen and water, as in the case of hydrogen peroxide.

 

Inhalation

There are no studies specifically regarding absorption following inhalation of peroxomonosulphuric acid; however, it can be expected to act in a similar way to sulphuric acid. Any particles may be deposited in various regions of the respiratory tract. Distribution of deposited particles is dependent on particle size, physiological factors (e.g. breathing rate and breathing depth) and environmental conditions (particularly relative humidity as it is likely to affect aerosol size due to the hygroscopic nature of sulphuric acid) (HPA, 2011). Larger droplets (10-15 µ­m and above) deposit mainly in the nose while smaller droplets (1-10 µm) would reach deeper regions of the respiratory tract including the larynx, trachea and bronchi (SCOEL, 2007) and, presumably, the alveoli. In humans, during a 5-15 minutes exposure through a face mask to 0.4-1 mg/m³mist with an average aerosol size of 1 µm, the retention of sulphuric acid mist averaged at 77% (ATSDR, 1998). In the absence of any specific data to the contrary on peroxomonosulphuric acid, a default of 100% is suggested.

 

Dermal

There are no studies specifically regarding dermal absorption of peroxomonosulphuric acid or sulphuric acid. Based on ECHA (2012) guidance, the low molecular weight (114 Daltons) and presumed aqueous miscibility (based on sulphuric acid) would be favourable for dermal absorption. Like sulphuric acid, its polarity suggests little absorption via this route unless the acidity causes skin damage and breaching of the skin barrier. In the absence of any better data, the ECHA default assumption of 100% absorption has to be selected. 

 

DISTIBUTION and METABOLISM

If any peroxomonosulphuric acid is absorbed intact, it is likely to degrade rapidly to yield active oxygen and hydrogen and sulphate ions. Sulphate is a normal constituent of the blood, with concentrations of 0.8-1.2 mg/dL usually found in human serum. Sulphate is a normal metabolite of sulphur-containing amino acids and does not need to be further metabolised for urinary excretion (ATSDR, 1998).

 

EXCRETION

Excess sulphate is excreted as is in the urine (ATSDR, 1998). It is highly unlikely that sulphate anions would bioaccumulate (HPA, 2011). Under normal conditions, any oxygen released is expected to transfer to the oxygen pool of the body and be eliminated via the lungs (DF, 2011; EC, 2003). Any water is presumably utilised or removed via the urine.

 

References

 

ATSDR (1998). Agency for Toxic Substances and Diseases Registry. Toxicological profile for sulfur trioxide and sulfuric acid. Available fromhttp://www.atsdr.cdc.gov/toxprofiles/tp117.pdf

 

DF (2011). Deutsche Forschungsgemeinschaft. MAK Value Documentations. The MAK-Collection for Occupational Health and Safety. Part 1: MAK Value documentations. Volume 26. Edited by Greim H. Wiley-VCH Publishers.

 

EC (2003). European Commission. European Chemicals Bureau. European Union risk assessment report: Hydrogen peroxide. EUR 20844 EN. Volume 38.

http://echa.europa.eu/documents/10162/a6f76a0e-fe32-4121-9d9d-b06d9d5f6852

 

ECHA (2012). Guidance on information requirements and chemical safety assessment. Chapter R.7c: Endpoint specific guidance. November 2012 (version 1.1).

 

HPA (2011). Health Protection Agency. Compendium of Chemical Hazards. Sulphuric acid. Available fromhttp://www.hpa.org.uk/webc/HPAwebFile/HPAweb_C/1202115622008

 

SCOEL (2007). Recommendation from the Scientific Committee on Occupational Exposure Limits for sulphuric acid. Available fromhttp://ec.europa.eu/social/keyDocuments.jsp?pager.offset=0&langId=en&mode=advancedSubmit&policyArea=82&subCategory=153&year=0&country=0&type=0&advSearchKey=SCOEL.

 

NANOSTRIP 2X

 

Nanostrip 2X is a three-constituent product, containing sulphuric acid (~87%), peroxomonosulphuric acid (~10%) and hydrogen peroxide (~3 %).In the absence of specific data regarding the ADME of Nanostrip 2X, its physicochemical properties and the ADME behaviour of the individual components have been assessed. Sulphuric acid readily dissociates to liberate sulphate ions, which are readily absorbed and join the pool of sulphate anions in the body. Peroxomonosulphuric acid acts similarly anddissociates to form peroxysulphate ions that will be rapidly transformed to active oxygen and to sulphate anions. The low vapour pressure of Nanostrip 2X indicates that the opportunity for exposure by inhalation is likely to be low.If sulphuric acid or peroxomonosulphuric acid do reach the lungs, the liberated sulphate will be rapidly absorbed into the blood. The liquid state and aqueous miscibility of Nanostrip 2X would favour dermal absorption. However, due to the polarity, dermal absorption of both sulphuric and peroxomonosulphuric acids is likely to be low (although penetration would be enhanced by destruction of the skin barrier). Sulphate, a normal constituent in the blood and a metabolite of sulphur‑containing amino acids, is excreted in the urine.It is highly unlikely that sulphate anions would bioaccumulate. On exposure via oral, inhalation or dermal routes, hydrogen peroxide is likely to be absorbed and enter the adjacent tissues and blood vessels, where it rapidly degrades, liberating active oxygen and water. Any metabolism of the intact substance occurs via catalase or glutathione peroxidase. Considering the rapid and extensive degradation of hydrogen peroxide in the blood, systemic distribution is not feasible; no bioaccumulation is likely. Liberated oxygen and water are expected to be eliminated via the lungs and urine, respectively.

 

ABSORPTION

Oral

Ingested sulphuric acid will be rapidly diluted and buffered by the contents of the GI tract (EFSA, 2012) to liberate sulphate anions. Peroxomonosulphuric acid will dissociate, forming peroxysulphate ions that will be rapidly transformed to active oxygen and to sulphate anions. The sulphate anions will be absorbed and enter the body’s normal sulphate electrolyte pool (ATSDR, 1998; Bassanet al. 2012; OECD, 2001).Exogenous hydrogen peroxide will pass the absorption surfaces to enter the adjacent tissues and blood vessels, where rapid degradation to active oxygen and water occurs(EC, 2003; ECETOC, 1996; HERA, 2005).In the absence of any better data, the ECHA default assumption of 100% absorption has to be selected.

 

Inhalation

Following inhalation exposure, sulphuric acid and (presumably) peroxomonosulphuric acid particles may be deposited in various regions of the respiratory tract. Distribution of deposited particles will depend on particle size, physiological factors (e.g. breathing rate/depth) and environmental conditions (particularly relative humidity as it is likely to affect aerosol size due to the hygroscopic nature of sulphuric acid) (HPA, 2011). Larger droplets (10-15 µ­m and above) deposit mainly in the nose while smaller droplets (1-10 µm) would reach deeper regions of the respiratory tract including the larynx, trachea and bronchi (SCOEL, 2007) and, presumably, the alveoli. In the absence of any better data, the ECHA default assumption of 100% absorption has to be selected.

 

In humans, during a 5-15 minutes exposure through a face mask to 0.4-1 mg/m³mist with an average aerosol size of 1 µm, the retention of sulphuric acid mist averaged at 77% (ATSDR, 1998). In rats, guinea pigs and dogs, sulphuric acid-derived sulphur (aerosol sizes 0.4‑1.2 µm) was rapidly absorbed into the blood (“cleared from the pulmonary region within a half-time of 2-9 minutes” for all species) following lung deposition. Upper respiratory tract clearance was much slower (Dahlet al. 1983).

 

Inhaled hydrogen peroxide is expected to be readily taken up by cells of the mucous membranes, entering the adjacent tissues and blood vessels, and rapidly degrading to oxygen and water (EC, 2003).

 

Nanostrip 2X has a vapour pressure of >0.313 Pa at 25 °C, which is below the 0.5 kPa threshold considered by ECHA (2012) to display low volatility. Therefore, the opportunity for vapour inhalation is low.

 

Dermal

No studies specifically regarding dermal absorption of sulphuric acid or peroxomonosulphuric acid were identified. According to ECHA (2012), the low molecular weights (98 and 114 Daltons, respectively) and aqueous miscibility would favour dermal absorption. However, the polarity suggests that there would be little absorption via this route unless the acidity causes skin damage and breaching of the skin barrier (SCOEL, 2007).

 

When in contact with skin, hydrogen peroxide passes the surface cellsto enter adjacent tissues, where it is rapidly degraded to active oxygen and water (EC, 2003).

 

The liquid state and aqueous miscibility of Nanostrip 2X would tend to assist penetration into the stratum corneum and subsequently the epidermis, favouring absorption (ECHA, 2012). In the absence of any better data, the ECHA default assumption of 100% absorption has to be selected.

 

DISTRIBUTION and METABOLISM

If any sulphuric acid or peroxomonosulphuric acid is absorbed intact, they are likely to degrade rapidly to yield hydrogen ions, sulphate ions and active oxygen. Sulphate is a normal constituent of the blood, with concentrations of 0.8-1.2 mg/dL usually found in human serum. Sulphate is a normal metabolite of sulphur-containing amino acids and does not need to be further metabolised for urinary excretion (ATSDR, 1998). Any hydrogen peroxide present has the ability to pass through cell membranes since the permeability coefficient is comparable with that of water (EC, 2003). It is metabolised to water and active oxygen via two metabolising enzymes, catalase and glutathione peroxide (DF, 2011; EC, 2003; ECETOC, 1996). Due to the high catalase activity in red blood cells, exogenous hydrogen peroxide is efficiently removed from the blood (EC, 2003).

 

EXCRETION

Excess sulphate is excreted (as is) in the urine (ATSDR, 1998) and is highly unlikely to bioaccumulate (HPA, 2011). In view of the high degradation capacity, the same applies to hydrogen peroxide. Under normal conditions, any oxygen released is expected to transfer to the oxygen pool of the body and be eliminated via the lungs (DF, 2011; EC, 2003). Any water is presumably utilised or removed via the urine.

 

References

 

ATSDR (1998). Agency for Toxic Substances and Diseases Registry. Toxicological profile for sulfur trioxide and sulfuric acid. Available fromhttp://www.atsdr.cdc.gov/toxprofiles/tp117.pdf

 

Bassan Aet al. (2012). Reports on toxicokinetics, toxicity and allergenicity data on substances to be evaluated as acceptable previous cargoes for edible fats and oils (NP/EFSA/CONTAM/2011/01) – Batches n. 1, 2 and 3. Scientific report submitted to EFSA. Supporting publications: EN-274. Available fromhttp://www.efsa.europa.eu/en/supporting/doc/274e.pdf.

 

Dahl ARet al. (1983). Clearance of sulfuric acid-introduced 35S from the respiratory tracts of rats, guinea pigs and dogs following inhalation or instillation. Fundamental and Applied Toxicology 3, 293-297.

 

DF (2011). Deutsche Forschungsgemeinschaft. MAK Value Documentations. The MAK-Collection for Occupational Health and Safety. Part 1: MAK Value documentations. Volume 26. Edited by Greim H. Wiley-VCH Publishers.

 

EC (2003). European Commission. European Chemicals Bureau. European Union risk assessment report: Hydrogen peroxide. EUR 20844 EN. Volume 38.

http://echa.europa.eu/documents/10162/a6f76a0e-fe32-4121-9d9d-b06d9d5f6852

 

ECETOC (1996). European Centre for Ecotoxicology and Toxicology of Chemicals. Hydrogen peroxide OEL criteria document. Special Report No.10.http://www.ecetoc.org/

 

ECHA (2012). Guidance on information requirements and chemical safety assessment. Chapter R.7c: Endpoint specific guidance. November 2012 (version 1.1).

 

EFSA (2012). Scientific Opinion on the evaluation of the substances currently on the list in the annex to Commission Directive 96/3/EC as acceptable previous cargoes for edible fats and oils – Part II of III. EFSA Journal, 10 (5), 2703. Available fromhttp://www.efsa.europa.eu/en/efsajournal/doc/2703.pdf

 

HERA (2005). Human & Environmental Risk Assessment on ingredients of household cleaning products. HERA – Hydrogen Peroxide Version 1.0 April 2005.http://www.heraproject.com/files/36-F-05-Shor_H2O2_version1.pdf

 

HPA (2011). Health Protection Agency. Compendium of Chemical Hazards. Sulphuric acid. Available fromhttp://www.hpa.org.uk/webc/HPAwebFile/HPAweb_C/1202115622008

 

OECD (2001). Organisation for Economic Co-operation and Development. SIDS Initial Assessment

Reports for Sulfuric Acid (CAS No: 7664-93-9) for 11th SIAM (January 2001). Available from

http://www.inchem.org/documents/sids/sids/7664939.pdf.

 

SCOEL (2007). Recommendation from the Scientific Committee on Occupational Exposure Limits for sulphuric acid. Available fromhttp://ec.europa.eu/social/keyDocuments.jsp?pager.offset=0&langId=en&mode=advancedSubmit&policyArea=82&subCategory=153&year=0&country=0&type=0&advSearchKey=SCOEL.