Hazardous substance assessment: Hydrogen peroxide

Identification

Chemical name:

Hydrogen peroxide

CAS #:

7722-84-1

Chemical composition:

H₂O₂

Synonyms:

Hydrogen peroxide
Hydrogen peroxide solution
Hydrogen dioxide

UN #:

UN2014 (20 to 60% aqueous solution); UN2015 (>60% aqueous solution or pure form); UN2984 (8 to <20% aqueous solution)

Pictogram(s):

Figure 1 - Text Equivalent

The symbol within the pictogram is an exclamation mark. This symbol indicates that hazardous products with this pictogram can cause certain health effects for example:

• skin irritation
• eye irritation
• skin sensitization

Figure 2 - Text Equivalent

The symbol within the pictogram, which applies to pure hydrogen peroxide or a 6% or above aqueous solution of hydrogen peroxide, shows a container dripping liquid onto a piece of metal and another container dripping liquid onto a hand. This symbol indicates that hazardous products with this pictogram can:

• damage or destroy metal
• cause irreversible damage to the skin (for example, burns, blisters, scarring)
• produce tissue damage in the eye or vision loss that is irreversible or not fully reversible within 21 days

Figure 3 - Text Equivalent

The symbol within the pictogram, which applies to pure hydrogen peroxide or a 42.5% or above aqueous solution of hydrogen peroxide, shows an "o" with flames on top of it and a line underneath it. The "o" is for oxygen, and the flames indicate that hazardous products with this pictogram present a fire or explosion hazard if they are not stored and handled properly.

WHMIS classification

Health hazards:

• Acute Toxicity (Oral) – Category 4
• Skin Corrosion – Category 1 (pure hydrogen peroxide or a 36% or above aqueous solution)
• Serious Eye Damage – Category 1 (pure hydrogen peroxide or a 6% or above aqueous solution)

Physical hazards:

• Oxidizing Liquids – Category 1 (pure hydrogen peroxide or a 69.7% or above aqueous solution); Oxidizing Liquids – Category 2 (50 to 63.2% aqueous solution); Oxidizing Liquids – Category 3 (42.5 to 47.3% aqueous solution)

Health hazards

Acute Toxicity (Oral):

Category 4

Oral median lethal dose (LD₅₀): 417.6 milligrams per kilogram of body weight (mg/kg-bw) (male rats)^{Footnote 1}.

In an Organisation for Economic Co-operation and Development Test Guideline (OECD TG) 401-compliant (Acute Oral Toxicity) study in Crl:CD BR rats (5 per sex and dose) gavaged once with a 70% by weight aqueous solution of hydrogen peroxide at a dose of solution of 500, 1 000 or 1 500 mg/kg-bw in males or of 500, 750 or 1 000 mg/kg-bw in females, the LD₅₀ of the solution in males was 1 026 mg/kg-bw and in females was 693.7 mg/kg-bw^{Footnote 1}. The LD₅₀ of pure hydrogen peroxide, based on its 70% concentration in the solution, would accordingly be 718.2 and 485.6 mg/kg-bw in males and females, respectively. Clinical signs of toxicity were observed in all dose groups, and included lethargy, immobility, irregular respiration and hunched posture. In all dose groups, degenerative ulceration and regenerative hyperplasia of the pyloric antrum of the stomach were also reported^{Footnote 1}.

An acute oral toxicity study compliant with United States Environmental Protection Agency (US EPA) guidelines in Sprague-Dawley rats (10 per sex and dose) gavaged once with a 35% hydrogen peroxide aqueous solution at a dose of solution of 630, 794, 1 000, 1 260, 1 588 or 2000 mg/kg-bw in males or of 794, 1 000, 1 260 or 1 588 mg/kg-bw in females reported an LD₅₀ of solution in males and females of 1 193 mg/kg-bw and 1 270 mg/kg-bw, respectively. The LD₅₀ of pure hydrogen peroxide, based on its 35% concentration in the solution, would accordingly be 417.6 and 444.5 mg/kg-bw in males and females, respectively. Clinical signs observed included tremors, decreased locomotion, prostration, recumbency, lacrimation, chromodacryorrhea and oral discharge. Gross internal abnormalities in animals found dead included hemorrhagic stomachs, intestines filled with blood, blood-filled bladders and stomach and livers containing white foci^{Footnote 1}.

A study similar in design to OECD TG 401 in Sprague-Dawley rats (5 per sex) gavaged with a 10% hydrogen peroxide solution at a dose of solution of 5 000 mg/kg-bw reported only 1 female death and an LD₅₀ greater than 5 000 mg/kg-bw. Clinical signs included decreased or blackened feces, decreased locomotion, hypersensitivity to touch, hematuria, lacrimation, recumbency, cyanosis, ataxia, chromorhinorrhea, nasal discharge and abdominogenital staining. The necropsy findings included hemorrhagic, blood-filled stomachs and intestines and reddened lungs in the female rat that died^{Footnote 1}.

The available data meet classification criteria for Acute Toxicity (Oral) - Category 4 [subsection 8.1.1(1) of the HPR].

Acute Toxicity (Dermal):

Does not meet criteria

Dermal LD₅₀: 6 440 mg/kg-bw (male rabbits)^{Footnote 1}.

A study similar in design to OECD TG 402 (Acute Dermal Toxicity) and in accordance with US EPA guidelines in New Zealand White rabbits (10 per sex and dose) exposed dermally to 2 000 mg/kg-bw of a 35% hydrogen peroxide aqueous solution under occlusive conditions for 24 hours reported no mortality nor gross internal lesions. All animals exposed demonstrated local skin irritation, eschar and exfoliation^{Footnote 1}.

A study similar in design to OECD TG 402 in male rabbits (4 per dose) exposed dermally to a dose of 6 500 or 13 000 mg/kg-bw of a 70% hydrogen peroxide solution reported an LD₅₀ of solution of 9 200 mg/kg-bw. The LD₅₀ of pure hydrogen peroxide, based on its 70% concentration in the solution, would accordingly be 6 440 mg/kg-bw. All animals in the high-dose group died. Massive edema and corroded skin at the application sites were reported^{Footnote 1}.

The available data do not meet the classification criteria for a category of Acute Toxicity (Dermal).

Acute Toxicity (Inhalation – Gases):

Not applicable

Hydrogen peroxide is not a gas. The classification criteria for Acute Toxicity (Inhalation – Gases) do not apply to this substance.

Acute Toxicity (Inhalation – Vapours):

Does not meet criteria

Inhalation median lethal concentration (LC₅₀): >0.17 milligrams per litre (mg/L) (4-hours) (rats)^{Footnote 1}.

In a study equivalent in design to OECD TG 403 (Acute Inhalation Toxicity) and compliant with good laboratory practices (GLP), Sprague-Dawley rats (5 per sex) exposed whole-body for 4 hours to the maximum attainable vapour concentration of hydrogen peroxide of 0.17 mg/L, produced by bubbling air through a 50% hydrogen peroxide solution, showed no mortality or significant signs of toxicity (LC₅₀ greater than 0.17 mg/L)^{Footnote 1}.

A non-guideline acute inhalation study in rats exposed once to hydrogen peroxide vapour for 4 hours reported an LC₅₀ of 2 mg/L. The study summary provides insufficient details for use in classification^{Footnote 1}.

The available data do not meet the classification criteria for a category of Acute Toxicity (Inhalation - Vapours).

Acute Toxicity (Inhalation – Dusts and Mists):

Does not meet criteria

Inhalation LC₅₀: >0.232 mg/L (4-hours) (male mice)^{Footnote 1}.

In a non-guideline, GLP-compliant study, no mortality was reported in Swiss male mice (4 per dose) exposed nose-only once to an aerosol of an aqueous 70% hydrogen peroxide solution at a hydrogen peroxide concentration in air of up to 1 856 milligrams per cubic metre (mg/m³) for 30 minutes. On a 4-hour exposure basis, the LC₅₀ of hydrogen peroxide would exceed 0.232 mg/L. The concentrations at which a 50% reduction in respiratory rate and minute volume was observed were 665 and 696 mg/m³, respectively. Also, 2 animals from the lowest- and highest-concentration exposure groups showed local degenerative changes of the liver^{Footnote 1}.

The available data do not meet the classification criteria for a category of Acute Toxicity (Inhalation – Dusts and Mists).

Skin Corrosion / Irritation:

Category 1 (pure hydrogen peroxide or a 36% or above aqueous solution)

Humans: A retrospective review of all exposures reported to the Utah Poison Control Center over a 36-month reporting period identified 325 cases reported related to hydrogen peroxide exposure. The 3 main dermatologic findings, as a percentage of cases, were paresthesia (60%), whiteness (56%), and blistering (16%). The most common outcome of exposure was minor transient effects to the skin. There were no permanent sequelae from these dermal exposures^{Footnote 2}.

Animals: Several skin irritation and corrosion studies in animals have been performed on hydrogen peroxide with varying degrees of skin effects depending on the concentration.

In a Draize skin irritation study, a New Zealand White rabbit was exposed for 3 minutes, 1 hour or 4 hours to 0.5 millitres (mL) of a 50% hydrogen peroxide solution under semi-occlusive conditions. After a 3-minute exposure, mean scores over 24, 48 and 72 hours were 2 out of 4 for erythema and 1 out of 4 for edema. Effects were fully reversible by day 7 after patch removal. After a 1-hour exposure, mean scores over 24, 48 and 72 hours were 2 out of 4 for erythema and 1.33 out of 4 for edema. Blanching was observed at 1 hour and superficial necrosis at 72 hours after patch removal. Sloughing and necrosis were observed at 7 days and scar tissue at 14 days after patch removal. After a 4-hour exposure, mean scores over 24, 48 and 72 hours were 2.67 out of 4 for erythema and 1.33 out of 4 for edema. Sloughing of the skin and necrosis were observed at 7 days and sloughing and scar tissue at 14 days after patch removal^{Footnote 3}. In the same study, when a 70% hydrogen peroxide solution was applied to the shaved intact skin of a New Zealand White rabbit for 3 minutes, blanching was observed at 3 minutes, sloughing at 24 hours, superficial necrosis at 24, 48 and 72 hours, necrosis, fissuring and sloughing at 7 days and scar tissue at 14 days after patch removal^{Footnote 3}. Skin corrosion was thus observed after a 1- or 4-hour exposure to a 50% hydrogen peroxide solution or after 3 minutes to a 70% hydrogen peroxide solution.

A study similar in design to OECD TG 404 (Acute Dermal Irritation/Corrosion) and that was GLP-compliant reported similar results with a 0.5-mL application of a 49.2% hydrogen peroxide aqueous solution to 2 sites of an anesthetized female New Zealand White rabbit for 4 hours under semi-occlusive conditions. Severe erythema, moderate edema and gray areas were noted on both test sites at 24 hours and moderate erythema, slight edema, gray areas and ataxia at 48 hours after patch removal. The histopathologic examination of exposure sites indicated severe irritation that would have resulted in ulceration and necrosis^{Footnote 1}.

A skin irritation study compliant with US EPA guidelines and GLP was conducted in 6 New Zealand White rabbits (3 per sex) exposed to 0.5 mL of a 35% hydrogen peroxide aqueous solution for 4 hours under occlusive conditions on shaved intact skin. The study reported mean erythema scores out of 4 over 24, 48 and 72 hours following patch removal of 1.33 in 2 animals, 1.17 in 2 animals, 0.5 in 1 animal and 0.33 in 1 animal. The study reported mean edema scores out of 4 over 24, 48 and 72 hours following patch removal of 0.33 in 5 animals and 0 in 1 animal. Erythema was reversible by day 5 and edema by 48 hours after patch removal in all animals. Brown areas appeared over test sites at 48 hours after patch removal, and progressed to desquamation in some animals by day 6; desquamation persisted in 2 animals at study termination (day 14)^{Footnote 1}. At a 35% concentration, hydrogen peroxide does not meet classification criteria for a category of this hazard class.

An OECD TG 404-compliant study was conducted in 6 New Zealand White rabbits (3 per sex) exposed to 0.5 mL of a 10% hydrogen peroxide aqueous solution for 4 hours on shaved intact skin under semi-occlusive conditions. The study reported mean erythema scores out of 4 over 24, 48 and 72 hours following patch removal of 0.33 in 1 animal and 0 in 5 animals. The study reported mean edema scores out of 4 over 24, 48 and 72 hours following patch removal of 0 in all 6 animals. All irritant effects resolved within 48 hours of patch removal^{Footnote 1}. At a 10% concentration, hydrogen peroxide does not meet classification criteria for a category of this hazard class.

Solutions containing hydrogen peroxide at a concentration of 3, 6 or 8% caused mild skin effects in rabbits when exposed dermally under occlusive conditions for 24 hours, and were not considered irritating to the skin. No other study details were reported^{Footnote 2}.

The available data meet classification criteria for Skin Corrosion – Category 1 for solutions containing hydrogen peroxide at a concentration of 36% or greater [subsection 8.2.2(2) of the HPR].

Serious Eye Damage / Eye Irritation:

Category 1 (pure hydrogen peroxide or a 6% or above aqueous solution)

Human: Topical application of solutions containing hydrogen peroxide at a concentration of 1 to 3% in the human eye, used historically as an antibacterial agent, did not cause significant ocular injury. Application of solutions containing hydrogen peroxide at a concentration of 5 to 10% caused cloudiness in the cornea, severe pain, and intraocular inflammation^{Footnote 2}. In a retrospective review of 325 exposures to hydrogen peroxide reported to the Utah Poison Control Center over a 36-month reporting period, 8% concerned the eye, with symptoms reported including burning (65% of ocular cases), redness (50% of ocular cases), and blurry vision (19% of ocular cases). The typical outcome was a minor, transient effect, and there were no permanent sequelae^{Footnote 2}. A case of a female adult exposed to a soft contact lens that had been stored in a 3% hydrogen peroxide solution identified eye irritant effects, including hyperaemia, tearing, eyelid spasm, discomfort and punctate keratopathy^{Footnote 2}.

Animals: An study similar in design to OECD TG 405 (Acute Eye Irritation/Corrosion) in 6 albino rabbits exposed ocularly to 0.1 mL of a 3% hydrogen peroxide solution, without an eye wash, reported mean scores over 24, 48 and 72 hours post-instillation of 0 in all animals for corneal opacity, iritis, conjunctival redness and chemosis. At the concentration tested, the test substance was not considered to be irritating^{Footnote 1}.

An OECD TG 405-compliant study in 4 female New Zealand White rabbits exposed ocularly to 0.1 mL of an aqueous solution containing hydrogen peroxide at a concentration of 5%, with 2 animals receiving an eye wash and the other 2 not, reported mean scores over 24, 48 and 72 hours post-instillation across all animals of 0 out of 4 for corneal opacity, 0 out of 2 for iritis, 1.25 out of 3 for conjunctival redness and 0 out of 4 for chemosis. Mean scores per animal were not reported. Conjunctival redness had fully resolved at 72 hours post-instillation. At the concentration tested, the test substance was considered only slightly irritating to the eye^{Footnote 1}.

In a study similar in design to OECD TG 405, 0.1 mL of a 6% hydrogen peroxide solution was instilled into the right eye of 6 New Zealand White rabbits. An eye wash was conducted for 3 of the rabbits; the eyes of the other 3 were unwashed. The mean scores over 24, 48 and 72 hours post-instillation across all animals were 1 out of 2 for corneal opacity, 1 out of 1 for iritis and 1.5 out of 2 for conjunctival redness. A mean score for chemosis was not provided but it was noted to be slight or mild in unwashed eyes and slight or moderate in washed eyes. Irritant effects were fully reversible in animals that had not received an eye wash by day 7 and in those that had received an eye wash by day 21 post-instillation. In 1 animal that had received an eye wash, moderate to severe corneal damage was observed. Although irritant effects had reversed by day 21 in this animal, healing of the eye, as evidenced by corneal vascularization, was still observed^{Footnote 1Footnote 3}. The results of the study meet classification criteria for Eye Irritation - Category 2. Sub-categorization was not undertaken due to the unclear score maxima.

An OECD TG 405-compliant study was conducted in 4 male New Zealand White rabbits to which 0.1 mL of an 8% aqueous hydrogen peroxide solution was instilled into the right eye of each animal. In 2 animals, eyes were washed 20 to 30 seconds after instillation, whereas in the other 2 no wash was performed. In the 2 rabbits with washed eyes, mean scores over 24, 48 and 72 hours post-instillation were 3 out of 4 for corneal opacity in both animals, 0.33 or 1 out of 2 for iritis, 2.67 or 3 out of 3 for conjunctival redness and 1.33 or 2.33 out of 4 for chemosis. In the 2 rabbits with unwashed eyes, mean scores over 24, 48 and 72 hours post-instillation were 0.33 or 0.67 out of 4 for corneal opacity, 0.33 out of 2 for iritis in both animals, 0.83 or 2.67 out of 3 for conjunctival redness and 0.67 or 2 out of 4 for chemosis. Effects at day 21 post-instillation had not fully reversed, and included slight corneal opacity and mild conjunctivitis in some animals^{Footnote 1}. The results of the study meet the classification criteria for Serious Eye Damage – Category 1 [subsection 8.3.2(1) of the HPR].

An OECD TG 405-compliant study was conducted in 4 female New Zealand White rabbits ocularly exposed to 0.1 mL of a 10 % hydrogen peroxide aqueous solution. The eyes of 2 rabbits were unwashed whereas those of the other 2 were washed with water 20 to 30 seconds after instillation. Animals were examined for 7 days and scoring was conducted using the Draize protocol. In the 2 animals that received an eye wash, mean scores over 24, 48 and 72 hours post-instillation were 3.67 out of 4 for corneal opacity in both animals, 1.67 out of 2 for iritis in both animals, 3 out of 3 for conjunctival redness in both animals and 2.67 or 3 out of 4 for chemosis. In the 2 animals with unwashed eyes, mean scores over 24, 48 and 72 hours post-instillation were 3.33 or 3.67 out of 4 for corneal opacity, 0.67 or 1.67 out of 2 for iritis, 3 out of 3 for conjunctival redness in both animals and 2.67 or 3 out of 4 for chemosis. Within 24 hours, severe corneal opacities, iritis and conjunctivitis were observed in the eyes of all animals treated. In addition, 3 rabbits had conjunctival hemorrhages. Although gradual improvement was seen in eye effects until study termination (day 7), corneal opacities and conjunctivitis were still present in all eyes at that time point and iritis was still present in 1 unwashed and 1 washed eye^{Footnote 1}. The corneal opacity and iritis scores meet the classification criteria for Serious Eye Damage – Category 1.

In a Draize test, 0.1 mL of 35% hydrogen peroxide solution was administered into the eyes of 9 rabbits. Eye irritation was scored at 1, 24, 48 and 72 hours post-instillation, and at day 4 and every 3 days thereafter until day 22. At 1 hour following instillation, eyes in all exposed animals had corneal opacities, iritis, and moderate conjunctivitis. All of the rabbits had hemorrhages on the conjunctiva, blanching of the conjunctiva, hemorrhagic iritis, bubbles under the cornea, blanching of the cornea or corneal ulcerations. Some signs of severe irritation continued to be observed until day 7 post-instillation. Pannus developed in all rabbits on day 7, which was not resolved at study termination (day 22). Rinsing the eyes shortly after exposure had no significant impact on the eye effects observed^{Footnote 1Footnote 2Footnote 4}. In consideration of the severity of effects and the lack of complete resolution within 21 days, the results of the study meet the classification criteria for Serious Eye Damage – Category 1.

In 2 other Draize tests, 0.1 mL of solutions containing hydrogen peroxide at a concentration of 5 or 10% were instilled into the eyes of 4 rabbits. Eyes were washed in 2 of the rabbits. The 5% solution of hydrogen peroxide was only minimally irritating, with a Draize maximum average score (MAS) of 3 out of 110 at 24 hours post-instillation. For the 10% concentration, Draize MAS of 107 and 108 out of 110 for unwashed and washed eyes, respectively, were observed at 24 hours post-instillation. At study termination for the 10% concentration (day 7), eye effects were still evident, with Draize MAS of 41 and 50 out of 110 for unwashed and washed eyes, respectively. Exposure to hydrogen peroxide at a concentration of 10% was considered to be corrosive to the eyes^{Footnote 1Footnote 4}.

In a test in accordance with section 191.12 of a regulation of the Federal Hazardous Substances Act, 0.1 mL of 2 test materials, either a 6% aqueous hydrogen peroxide solution or a 6% aqueous hydrogen peroxide solution with 5% ammonium sulfate, was placed in the right eye of 6 albino rabbits per material. Eyes were scored at 1, 2, 3 and 13 days post-instillation. In animals exposed to the 6% aqueous hydrogen peroxide solution, the exposed eyes of 3 had severe, irreversible corneal damage, of 2 had moderate, reversible corneal damage and of another had no corneal damage^{Footnote 5}.

The available data meet the classification criteria for Serious Eye Damage – Category 1 for solutions containing hydrogen peroxide at a concentration of 6% or greater [subsection 8.3.2(1) of the HPR].

Respiratory Sensitization:

No data available

No data are available to determine whether hydrogen peroxide meets the classification criteria for a category or subcategory of Respiratory Sensitization.

Skin Sensitization:

Does not meet criteria

Humans: In a survey of patch tests conducted for allergens in the hairdressing industry in the United Kingdom over a 2 to 6 year period, results from 8 testing centres were negative (0 out of 525 tests) for hydrogen peroxide in hairdressers and clients^{Footnote 6}. In a review, cases of allergenicity were reported for 2 women, one who worked as a hairdresser and one who was a homemaker, who had positive skin reactions to a 3% hydrogen peroxide solution. The review also noted that 156 other individuals, who worked as hairdressers, were patch tested and found to be negative to a 3% hydrogen peroxide solution^{Footnote 2}. A review of Finnish human patch tests conducted in patients between 1975 and 1997 did not report any positive reactions to hydrogen peroxide^{Footnote 2Footnote 7}.

Animals: In a guinea pig maximization test (GPMT) conducted using a modification of the Magnusson-Kligman method, 5 animals were each induced with 6 intradermal injections of 0.1 mL of a 0.1% hydrogen peroxide solution over a 2-week period while another group of 5 animals were each induced with 6 drops a 3% hydrogen peroxide solution on abraded skin. Following a single challenge with the 0.1 or 3% hydrogen peroxide solution previously used for induction, no positive reactions were reported^{Footnote 2}.

In a local lymph node assay, mice (3 per concentration) induced with an aqueous solution of hydrogen peroxide at a concentration of 0.34, 2, 5, 7.5 or 10% weight by volume in a vehicle of acetone/glycerol/water (8:1:1 ratio by volume) demonstrated stimulation indices of 0.66, 0.84, 1.1, 1.4 and 1.9, respectively. Hydrogen peroxide was classified as non-sensitizing to the skin at the concentrations tested^{Footnote 8}.

The available data do not meet the classification criteria for a category or subcategory of Skin Sensitization.

Germ Cell Mutagenicity:

Does not meet criteria

In vivo: In a tooth bleaching study, 30 participants with central incisors shade A1 or darker were selected. A lip and cheek retractor was used to prevent contact of the bleaching gel with the cheek, lips and tongue of each participant. The gingival tissue of the teeth to be bleached was isolated with a light-polymerized resin dam, and a 35% hydrogen peroxide aqueous gel was administered to the teeth during 3 applications of 15 minutes each over the course of a 45-minute application period. Each participant received 2 bleaching sessions with a 1-week interval in between. Exfoliated gingival cells from the oral mucosa and upper lip lining epithelial cells were collected at baseline and 1 month after the in-office bleaching procedure. The frequency of micronuclei (MN) per 1 000 exfoliated cells did not increase from baseline following bleaching and was within the normal range for oral mucosa^{Footnote 1}.

An OECD TG 474-compliant (Mammalian Erythrocyte Micronucleus Test) study was conducted in Swiss OF1/ICO:OF1 mice (5 per sex, dose and post-exposure period) exposed once via intraperitoneal injection to an aqueous hydrogen peroxide solution at a hydrogen peroxide dose of 0, 250, 500 or 1 000 mg/kg-bw. The concentrations of hydrogen peroxide administered in the treated groups were 1, 2 and 4%, respectively. The post-exposure period was 24 or 48 hours. In all groups treated with the hydrogen peroxide solution, the mean values of micronucleated polychromatic erythrocytes (MPE) per 1 000 polychromatic erythrocytes (PE) were similar to those of the vehicle control for the respective post-exposure period. Exposure to hydrogen peroxide at the doses tested did not induce cytogenetic damage in bone marrow cells of mice^{Footnote 1Footnote 2}.

In another micronucleus study, harvested bone marrow from catalase-deficient C57BL/6NCr1BR mice (10 per sex) exposed to hydrogen peroxide in drinking water for 2 weeks at a concentration of 6 000 parts per million (ppm) did not demonstrate a statistically significant increase in the frequency of MPE compared to that of the negative control group^{Footnote 2}.

An unscheduled DNA synthesis (UDS) study in 5 male Wistar rats administered a dose of hydrogen peroxide of 25 or 50 mg/kg-bw (0.1 or 0.2% solution, respectively) by intravenous infusion over 30 minutes provided negative results^{Footnote 2}.

In a pre-screening study for carcinogenicity, a 70% hydrogen peroxide solution was applied to the skin of female Sencar mice (10 per dose) at a dose of 10, 100 or 200 micromoles (µmol) of hydrogen peroxide in 200 microlitres (µL) of ethanol 2 times per week for 4 weeks. The respective hydrogen peroxide concentrations in the vehicle were 0.2, 1.6 and 3.2%. No detectable cellular proliferation or in vivo mutagenicity in treated skin was observed in mice sacrificed at day 2 or 4 after the last administration^{Footnote 2}.

In vitro: In bacterial reverse mutation assays, exposure to a 3% hydrogen peroxide solution was not mutagenic to S. typhimurium strains TA 1535, TA 1537, TA 1538 or TA 98 nor to E. coli strain WP2 uvrA with or without S9-mix metabolic activation. An increase in histidine-independent revertants compared to the negative control was observed in S. tymphimurium strain TA 100, both with and without activation^{Footnote 9}.

In an L5178Y mouse lymphoma assay compliant with the then OECD TG 476 (Genetic Toxicology: In vitro Mammalian Cell Gene Mutation Tests), exposure to a 30% hydrogen peroxide solution was mutagenic at the thymidine kinase (TK) locus in mouse lymphoma cells in the absence of S9-mix metabolic activation but was not mutagenic in the presence of such activation^{Footnote 10}.

In an OECD TG 473-compliant (In Vitro Mammalian Chromosomal Aberration Test) study in Chinese hamster ovary cells, exposure to an aqueous hydrogen peroxide solution caused substantial increases in the percentage of cells with chromosomal aberrations and in the number of aberrations per cell at one or more test concentrations in the presence and absence of S9-mix metabolic activation. In the activated system, the increases exhibited a clear dose-response relationship^{Footnote 1}.

While there are some in vitro studies with positive results, hydrogen peroxide does not meet the classification criteria for a category or subcategory of Germ Cell Mutagenicity in consideration of the available negative results from in vivo studies.

Carcinogenicity:

Does not meet criteria

Hydrogen peroxide is classified as Group 3 (not classifiable as to its carcinogenicity to humans) by the International Agency for Research on Cancer (IARC) and as A3 (a confirmed animal carcinogen with unknown relevance to humans) by the American Conference of Governmental Industrial Hygienists (ACGIH)^{Footnote 11Footnote 12}. The National Toxicology Program (NTP) has not classified the carcinogenicity of hydrogen peroxide to date.

A non-guideline study in catalase-deficient C57BL/6J mice (50 per sex and concentration) exposed via drinking water to hydrogen peroxide at a concentration of 0.1 or 0.4% for 100 weeks and involving a complete autopsy at study termination reported a dose-dependent increase in the incidences of erosions and ulcers in the glandular stomach and of duodenal nodules. Localized duodenal carcinomas were found only in treated mice (5% and 1% in the high- and low-exposure groups, respectively, whereas none among the controls). The findings for other tumours were unremarkable. A limitation of the study is that only 2 exposure levels were used^{Footnote 2}.

A follow-up carcinogenicity study by the same group, albeit only involving a limited autopsy (stomach and duodenum), was conducted on 3 strains of mice (C57BL/6N, DBA/2N, BALB/cAnN) also exposed to a 0.1 or 0.4% concentration of hydrogen peroxide in drinking water. In C57BL mice treated for 120 days, over 67% had forestomach lesions while in those treated for 60 days, over 80% had duodenal lesions. After treatment ceased, the duodenal lesions mostly regressed or disappeared completely. When treated for 420 to 740 days, duodenal cancer was noted only in treated but not control mice, specifically in 1 and 5% of mice treated with a 0.1 or 0.4% hydrogen peroxide concentration, respectively. The C57BL mice were noted to be more sensitive to the nodulogenic effect of hydrogen peroxide than the other 2 strains. In both the original and follow-up carcinogenicity studies, it was noted that the duodenal cancers did not metastasize^{Footnote 2}.

In an oral carcinogenicity study involving exposure of F344 rats (50 per sex and concentration) to hydrogen peroxide in drinking water at a concentration of 0.3 or 0.6% for 78 weeks, no significant differences between treated and control rats were observed in the organs that bore tumours, the incidences of these tumours, or the stage at which they developed. Most male rats bore tumours, particularly of the Leydig cells and of the endocrine system. No tumours of the gastrointestinal tract were noted in any of the rats. Like the mouse studies, a limitation of this rat study was the use of only 2 exposure concentrations. Exposure to hydrogen peroxide at the concentrations tested was concluded to be not carcinogenic to rats^{Footnote 2}.

In a non-guideline study of intestinal tumour-promoting effects in male F344 rats exposed to hydrogen peroxide in drinking water at a concentration of 1.5% for 10 or 21 weeks, with or without intraperitoneal injections of methylazoxymethanol acetate, no carcinogenic effects in the gastrointestinal tract were reported in the 3 rats exposed only to hydrogen peroxide^{Footnote 2}.

A non-guideline study was conducted in 9 male Syrian hamsters exposed in their buccal cavity to a 30% hydrogen peroxide solution, via painting 2 times per week on the left buccal mucosa, for 22 weeks. The study revealed hyperkeratosis and hyperplasia in all 9 animals, with hyperchromatic cells and mild dysplasia additionally in 4 of them, but no tumours at the application site^{Footnote 2}.

While the available evidence suggests that hydrogen peroxide has a weak potential to induce local carcinogenic effects, the available data are insufficient for classification purposes.

The available data do not meet the classification criteria for a category or subcategory of Carcinogenicity.

Reproductive Toxicity:

Does not meet criteria

A non-guideline reproductive toxicity study was conducted in male albino mice (12 per concentration) exposed to a concentration of 0.33, 1 or 3% of hydrogen peroxide in drinking water for up to 28 days. The experiment was discontinued for the high-exposure group after 5 days of exposure due to a refusal to drink and a 20% loss of body weight. The other 2 exposure groups were each divided into 4 subgroups of 3 animals each; some subgroups involved mating with females. All the female mice mated to the treated males became pregnant and bore healthy offspring in litters of normal size. In pregnant mice that drank drinking water containing hydrogen peroxide at a concentration of 1% until near term, a delay in parturition was observed compared to control dams, however the effect was small and inconsistent. The concentration, morphology and motility of epididymal spermatozoa in treated male mice after 3 weeks of exposure was normal. The study also exposed 3 albino rabbits to hydrogen peroxide in drinking water at a concentration of 0.33, 1 or 3% for 6 weeks. Like the male mice, no detectable abnormalities in the sperm of the 3 rabbits were observed. Overall, no adverse effects on sexual function or fertility were reported in either species of this study, although it was limited by a lack of male controls^{Footnote 2}.

In another study, male and female rats were administered hydrogen peroxide daily by gavage at a dose of 10 to 20% of the oral LD₅₀ (which was unspecified) for 45 days. At the highest dose, the estrous cycle was modified in females and the mobility of spermatozoa was reduced in males, although without an effect on the weight of the testes^{Footnote 2}.

In another study, male and female rats received daily a dose of 0.005, 0.05, 0.5, 5 or 50 milligrams per kilogram of body weight per day (mg/kg-bw/day) of hydrogen peroxide by gavage for 6 months, and were subsequently mated. Variations of the estrous cycle in females were observed during treatment with a dose of 50 or 0.5 mg/kg-bw/day of hydrogen peroxide, but not with 5 mg/kg-bw/day. At a dose of 50 mg/kg-bw/day, reduced mobility of spermatozoa in males was observed. No differences were found in the morphology and weight of the testes. Among the high-dose females, only 3 of 9 produced litters, as compared to 7 of 9 in the control group. The litter size and the body weight gain of the offspring of these high-dose females were also reduced relative to those of control females^{Footnote 2}.

In a developmental toxicity study, powdered feed was mixed with aqueous solutions of hydrogen peroxide to achieve a dietary hydrogen peroxide concentration of 0.02, 0.1, 2 or 10% and was administered to groups of 5 to 8 pregnant Wistar rats for 1 week. The fetuses were removed on day 20 for examinations. In addition, separate groups of 2 to 3 rats per exposure level were similarly treated but the rats were allowed to go through normal delivery, with follow-up of their offspring for 4 weeks. In the first experiment, maternal toxicity as indicated by decreased weight gain and food consumption of the dams was observed at the highest exposure level. Fetal resorptions were increased and fetal body weight was decreased, with most fetuses being near death. None of the fetuses of any exposure group had external malformations. Hemorrhaging of the eye, parietal region of the brain, cardiopulmonary region and torso was observed, and increased in a dose-dependent manner from a hydrogen peroxide concentration of 0.1 to 10%. A dose-dependent increase in skeletal hyperplasia was also observed from 2 to 10%. In the second experiment, all the neonates of the highest exposure group died within 1 week post-partum and had low body weights; the number of live births was also lower at this exposure level. No significant adverse effects in the fetuses at any other exposure level were observed. Overall, although some developmental effects occurred in the study, the authors proposed that they may have resulted from a breakdown of essential nutrients in the feed by hydrogen peroxide^{Footnote 2}.

The available data do not meet the classification criteria for a category or subcategory of Reproductive Toxicity.

Specific Target Organ Toxicity – Single Exposure:

Does not meet criteria

Oral Route of Exposure:

Humans: Several incidences of human poisonings by aqueous hydrogen peroxide solutions causing oxygen embolism have been reported but the doses ingested were not usually provided^{Footnote 2}.

Ingestion of a large volume of a 3% hydrogen peroxide solution caused death in a 16-month-old boy at an approximate hydrogen peroxide dose of 600 mg/kg-bw. In another case report, ingestion of a 35% hydrogen peroxide solution caused severe brain damage in an 84-year-old man (approximate hydrogen peroxide dose of 150 mg/kg-bw)^{Footnote 2}.

Animals: In an OECD TG 401-compliant study in Crl:CD BR rats (5 per sex and dose) gavaged once with a 70% by weight aqueous solution of hydrogen peroxide at a dose of solution of 500, 1000 or 1500 mg/kg-bw in males or of 500, 750 or 1000 mg/kg-bw in females, the LD₅₀ of the solution in males was 1 026 mg/kg-bw and in females was 693.7 mg/kg-bw. Clinical signs of toxicity were observed in all dose groups, and included lethargy, immobility, irregular respiration and hunched posture. In all dose groups, degenerative ulceration and regenerative hyperplasia of the pyloric antrum of the stomach were also reported^{Footnote 1}.

An acute oral toxicity study compliant with US EPA guidelines in Sprague-Dawley rats (10 per sex and dose) gavaged once with a 35% hydrogen peroxide aqueous solution at a dose of solution of 630, 794, 1 000, 1 260, 1 588 or 2000 mg/kg-bw in males or of 794, 1 000, 1 260 or 1 588 mg/kg-bw in females reported an LD₅₀ of solution in males and females of 1 193 mg/kg-bw and 1 270 mg/kg-bw, respectively. Clinical signs observed included tremors, decreased locomotion, prostration, recumbency, lacrimation, chromodacryorrhea and oral discharge. Gross internal abnormalities in animals found dead included hemorrhagic stomachs, intestines filled with blood, blood-filled bladders and stomach and livers containing white foci^{Footnote 1}.

A study similar in design to OECD TG 401 in Sprague-Dawley rats (5 per sex) gavaged with a 10% hydrogen peroxide solution at a dose of solution of 5 000 mg/kg-bw reported only 1 female death and an LD₅₀ greater than 5 000 mg/kg-bw. Clinical signs included decreased or blackened feces, decreased locomotion, hypersensitivity to touch, hematuria, lacrimation, recumbency, cyanosis, ataxia, chromorhinorrhea, nasal discharge and abdominogenital staining. The necropsy findings included hemorrhagic, blood-filled stomachs and intestines and reddened lungs in the female rat that died^{Footnote 1}.

Dermal Route of Exposure:

Humans: Transient skin effects following exposure to hydrogen peroxide solutions have been reported, such as paresthesia, whiteness, and blistering; no permanent dermal sequelae were reported. In a case report involving irrigation of an infected wound with a 3% hydrogen peroxide solution, a hydrogen peroxide dose as low as 15 mg/kg-bw caused transient shock and coma, considered likely to be the result of systemic embolization of oxygen microbubbles. Other cases of oxygen embolism have similarly been reported in surgical patients following such irrigation^{Footnote 2}. As this embolism results from exposure of an open wound, the effect is not considered relevant for typical workplace exposures.

Animals: In an acute dermal toxicity study (method not well described), in which a 10% or 28% hydrogen peroxide solution was dermally applied to mice, corresponding to a respective hydrogen peroxide dose of 1 400 or greater than 8 000 mg/kg-bw, signs of systemic toxicity were reported at 1 400 mg/kg-bw, including excitation and inhibition, ataxia, tremor and paresis of the limbs, and an increased respiration rate. These signs were reported as having developed 5 to 10 minutes after application. At the dose greater than 8 000 mg/kg-bw, mortality was reported^{Footnote 2}.

Inhalation Route of Exposure:

Humans: In a study conducted to examine the acute effects of exposure to hydrogen peroxide vapours in humans, 11 healthy volunteers were exposed on 3 separate occasions to a hydrogen peroxide concentration of 0, 0.5 or 2.2 ppm for 2 hours. Each exposure was at least 1 week apart. Exposure to hydrogen peroxide vapours was slightly irritating to nasal and throat airways and slightly increased nasal airway resistance at a concentration of 2.2 ppm but not at 0.5 ppm. Exposure-related effects were not observed on pulmonary function, nasal volume, breathing or blinking frequency or on inflammation and coagulation biomarkers^{Footnote 13}. The irritation in this study was borderline and was not clearly correlated with the nasal airway resistance.

Animals: In an oronasal sensory irritation study (compliance with guidelines and GLP not specified), male OF1 mice (8 per concentration) were exposed to vapours of hydrogen peroxide at an airborne concentration of 0.035, 0.055, 0.15 or 0.30 mg/L, for 1 hour. Exposure to hydrogen peroxide resulted in a concentration-dependent decrease in the respiratory rate at all tested concentrations. The concentration that would result in a 50% decrease in the respiratory rate of mice (RD₅₀) was estimated to be 0.157 mg/L^{Footnote 14}. The decrease in respiratory rate was described as indicative of sensory irritation and was not accompanied by an examination of local cytotoxicity.

The available oral, dermal and inhalation data do not meet the classification criteria for a category of Specific Target Organ Toxicity – Single Exposure.

Specific Target Organ Toxicity – Repeated Exposure:

Does not meet criteria

Oral Route of Exposure: In an OECD TG 408-compliant study, C57BL/6NCrlBR mice (15 per sex and dose) exposed to hydrogen peroxide in drinking water at a concentration of 0, 100, 300, 1 000 or 3 000 ppm for 90 days showed no treatment-related mortality or clinical signs at the concentrations tested. At the highest tested concentration, mice of both sexes demonstrated significant reductions in body weight accompanied by significantly reduced food and water consumption. Food and water consumption was also reduced, to a lesser extent, at a concentration of 300 and of 1 000 ppm. Minimal non-neoplastic hyperplasia of the duodenal mucosa was observed at a concentration of 300 ppm and above for males and of 1 000 ppm and above for females. No treatment-related gross lesions were noted at necropsy^{Footnote 1}. The 300-ppm concentration would result in a dose within guidance values, assuming a mouse body weight of 25 grams and a water consumption rate of 5 mL per day. However, the effect at that concentration was minimal and likely an adaptive response to the irritant nature of the substance.

In a non-guideline study, male Wistar rats (12 per dose) were gavaged 6 days per week with a 5% hydrogen peroxide solution at a dose of 0, 56.2, 168.7 or 506.0 mg/kg-bw/day for 12 weeks. No mortality was reported. A dose-dependent decrease in liver enzymes was noted starting at the low dose. At the medium and high doses, increases of segmented neutrophils and monocytes were observed along with a decrease in lymphocytes. At the high dose, decreased body weight gain, accompanied by decreased feed intake and feed efficacy, was observed along with decreases in erythrocyte count, hematocrit and hemoglobin concentrations. Relative weights of the lungs, spleen, adrenal gland and testis were increased at the high dose but were not accompanied by treatment-related histopathological findings in these organs. At the high dose, local effects on the gastric and intestinal mucosa were also observed^{Footnote 2}. Although the low dose was within guidance values, the adversity of the clinical chemistry change is unclear at that dose.

In another non-guideline study, male Wistar rats (9 to 12 per dose) were gavaged daily with a diluted solution of hydrogen peroxide (0.06 to 0.6%) at dose of 0, 6, 10, 20, 30 or 60 mg/kg-bw/day for 40 or 100 days. No mortality was reported. At the top dose, significantly reduced body weight gain was observed after day 20 of treatment, a slightly higher spleen weight at day 40 (resolved by study termination) and decreases in hematocrit and plasma proteins at study termination. At the top and second highest doses, significant decreases in plasma catalase were also observed at study termination. Differences in liver and kidney weights were not observed^{Footnote 2}. Although the doses at which effects were observed were within guidance values, the adversity of the body weight, clinical chemistry and hematological changes is unclear.

Dermal Route of Exposure: A non-guideline dermal (and inhalation) toxicity study was conducted in rats with shaved fur that were exposed whole-body to hydrogen peroxide for 2 to 4 months, using an exposure regimen of 5 hours per day and 5 days per week, at a concentration of 0.1 to 10.1 mg/m³. At 1 mg/m³, increases in the activities of several epidermal enzymes were reported and a significant dysfunction of the horny layer of the skin^{Footnote 1}. Due to poor study design and limited details, this study does not inform the classification evaluation.

Inhalation Route of Exposure:

Humans: A study of pulmonary function, which included measurements of forced vital capacity (FVC), forced expiratory volume (FEV), and peak expiratory flow (PEF), was performed for 3 to 5 years on all employees of a hydrogen peroxide production facility. There was no evidence of adverse effects at the exposure concentrations occurring at that time^{Footnote 2}. A handful of other inhalation studies in occupational settings with limited study details available have also reported no significant signs of toxicity^{Footnote 2}.

In study of 110 workers at 4 hydrogen peroxide production plants, no significant exposure-related decline in lung function parameters (FVC or PEF) was reported. Dermal effects from accidental contact had been reported at 2 plants, hair bleaching in 1 plant and 1 case of acute throat irritation^{Footnote 2}.

A worker health surveillance study was conducted at 1 company where workers were exposed to hydrogen peroxide vapours during aseptic packaging of fruit juices. Complaints were received from 6 machine operators and maintenance workers of eye and airway irritation, headaches, temporary loss of olfaction, skin effects and hair bleaching. A questionnaire administered identified that half of workers working with 2 packaging machines that had been causing high exposures had experienced eye and airway irritation and symptoms of asthma. Medical records identified 3 workers as having exhibited recurring bronchitis-sinusitis. Case reports of 2 patients identified them as having experienced bronchoconstriction. The authors concluded that repeated exposures to hydrogen peroxide vapours at a high concentration resulted in irritation and inflammation of the airway mucosa, increased susceptibility to respiratory infections and potential irritant-induced asthma^{Footnote 2}.

Animals: In an OECD TG 412-compliant (Subacute Inhalation Toxicity: 28-Day Study) study, Wistar-derived rats (5 per sex and concentration) were exposed whole-body to a vapour of hydrogen peroxide at a concentration of 2.88, 14.6 or 33 mg/m³ (2.03, 10.3 and 23.3 ppm, respectively) for 6 hours per day, 5 days per week for 28 days. At the intermediate and high concentrations, clinical signs consistent with respiratory tract irritation were observed, including reddened nose, nose stains and abnormal respiratory noise, with the onset, incidence and severity related to the concentration and repetition of exposure. At these concentrations, slight necrosis of the anterior regions of the nasal cavity and rhinitis were observed. At the high concentration, lower body weight gain and food consumption were observed in males compared to controls and minor changes in albumin and total protein blood levels were found in both sexes^{Footnote 1}. Both concentrations at which effects were observed are within guidance values for this hazard class.

In non-guideline studies with limited details available, 23 rats were exposed whole-body to a hydrogen peroxide vapour at a concentration of 93 mg/m³ (67 ppm) and groups of 10 mice to a concentration of 79 mg/m³ (57 ppm) or 107 mg/m³ (77 ppm). Exposures occurred for 6 hours per day, 5 days per week for 7 weeks. No significant signs of toxicity were reported other than nasal discharge, edematous feet, irritation of skin in the groin and hair loss. Pathological and histopathological studies of the lungs, trachea, liver, kidneys, spleen and cornea did not reveal significant changes^{Footnote 2}.

In an OECD TG 413-compliant (Subchronic Inhalation Toxicity: 90-day Study) study, Wistar rats (10 per sex and concentration) were exposed nose-only to a vapour of hydrogen peroxide at a concentration of 1.5, 3.6 or 10.3 mg/m³ (1.02, 2.51 and 7.08 ppm, respectively) for 6 hours per day, 5 days per week for 13 weeks. The study reported no treatment-related adverse effects at any tested concentration^{Footnote 1}.

Although an irritant response was observed in some repeated-exposure inhalation toxicity studies, the response was considered to be related to the acute toxicity (corrosivity) of hydrogen peroxide. As hydrogen peroxide meets the classification criteria for Skin Corrosion – Category 1 and Serious Eye Damage – Category 1, classification in a category of Specific Target Organ Toxicity – Repeated Exposure is considered superfluous.

Aspiration Hazard:

No data available

No human data are available and this substance is not a liquid hydrocarbon.

Biohazardous Infectious Materials:

Not applicable

Hydrogen peroxide is not a microorganism, protein or nucleic acid.

Physical hazards

Explosives:

Not evaluated*

* Explosives are excluded from the Hazardous Products Act and its regulations. Explosives are regulated under the Explosives Act. For more information, visit Natural Resources Canada .

Flammable Gases:

Not applicable

Hydrogen peroxide is not a gas. The classification criteria for Flammable Gases do not apply to this substance.

Aerosols:

Not evaluated

Classification of a hazardous product in the Aerosols hazard class is product dependent.

Oxidizing Gases:

Not applicable

Hydrogen peroxide is not a gas. The classification criteria for Oxidizing Gases do not apply to this substance.

Gases Under Pressure:

Not applicable

Hydrogen peroxide is not a gas. The classification criteria for Gases Under Pressure do not apply to this substance.

Flammable Liquids:

Does not meet criteria

High-concentration hydrogen peroxide has been identified as a candidate for monopropellant thruster systems for spacecraft. Its mechanism of action involves the generation of hot gas following its exothermic decomposition in the presence of a catalyst which, when expelled, generates thrust^{Footnote 15}. High-concentration hydrogen peroxide can also be used as an oxidizer in bipropellant thruster systems, where the products of its exothermic decomposition result in ignition of a fuel^{Footnote 16}. Hydrogen peroxide does not undergo combustion in either of these uses.

The available data do not meet the classification criteria for a category of Flammable Liquids.

Flammable Solids:

Not applicable

Hydrogen peroxide is not a solid. The classification criteria for Flammable Solids do not apply to this substance.

Self-reactive Substances and Mixtures:

Excluded from classification

Pure hydroxide peroxide is excluded from classification as aqueous solutions containing hydrogen peroxide at a concentration of 40% or higher meet the classification criteria for a category of Oxidizing Liquids [paragraph 7.8.1(1)(c) of the HPR].

Pyrophoric Liquids:

Does not meet criteria

Although hydrogen peroxide can be used in propellants for thruster systems, the mechanisms of action do not involve its combustion^{Footnote 15Footnote 16}.

The available data do not meet the classification criteria for a category of Pyrophoric Liquids.

Pyrophoric Solids:

Not applicable

Hydrogen peroxide is not a solid. The classification criteria for Pyrophoric Solids do not apply to this substance.

Self-heating Substances and Mixtures:

Does not meet criteria

There is no evidence that hydrogen peroxide self-heats via reaction with air and without an energy supply. Rather, hydrogen peroxide has been noted to self-decompose in the presence of catalysts or at high temperatures^{Footnote 17}.

The available data do not meet the classification criteria for a category of Self-heating Substances and Mixtures.

Substances and Mixtures which, in Contact with Water, Emit Flammable Gases:

Excluded from classification

The chemical structure of hydrogen peroxide does not contain metals or metalloids. Furthermore, hydrogen peroxide is soluble in water and forms a stable mixture, with its solubility denoted to be "very high"^{Footnote 18}. Therefore, hydrogen peroxide is excluded from classification [paragraphs 7.12.1(1)(a) and (c) of the HPR].

Oxidizing Liquids:

Category 1 (pure hydrogen peroxide or a 69.7% or above aqueous solution); Category 2 (50 to 63.2% aqueous solution); Category 3 (42.5 to 47.3% aqueous solution)

A study performed in accordance with test O.2 of sub-section 34.4.2 of Part III of the United Nations (UN) Manual of Tests and Criteria was undertaken on 1:1 mixtures of powdered cellulose and solutions of hydrogen peroxide at a concentration of 34.4, 37.6, 40.0, 42.5, 45.0, 47.3 or 50.0% by mass. The mean pressure rise time over 5 trials from 690 to 2 070 kilopascals (kPa) above atmospheric pressure was 908 milliseconds (ms) for the mixture with the 50.0% hydrogen peroxide solution, less than that of a 1:1 mixture of powdered cellulose and the reference substance sodium chlorate at a concentration of 40% in solution (1 276 ms). The mean pressure rise times were 3 272, 2 336 and 1 516 ms for the mixtures with the 42.5, 45.0 or 47.3% hydrogen peroxide solutions, less than that of a 1:1 mixture of powdered cellulose and the reference substance nitric acid at a concentration of 65% in solution (3 904 ms). The mean pressure rise times were 8 176, 5 528 and 4 552 ms for the mixtures with the 34.4, 37.6 or 40.0% hydrogen peroxide solutions, exceeding those of both mixtures of reference substances^{Footnote 1}. Hydrogen peroxide at a concentration of 50% or of 42.5 to 47.3% meets classification criteria for Oxidizing Liquids – Category 2 and Oxidizing Liquids – Category 3, respectively.

Another study performed in accordance with test O.2 of sub-section 34.4.2 of Part III of the UN Manual of Tests and Criteria was undertaken on a 1:1 mixture of powdered cellulose and a solution of hydrogen peroxide at a concentration of 69.7% by mass. The mean pressure rise time over 5 trials from 690 to 2 070 kPa above atmospheric pressure for this mixture was 23 ms, less than that of a 1:1 mixture of powdered cellulose and the reference substance perchloric acid at a concentration of 50% in solution (123 ms)^{Footnote 1}. Hydrogen peroxide at a concentration of 69.7% meets the classification criteria for Oxidizing Liquids – Category 1.

Another study performed in accordance with test O.2 of sub-section 34.4.2 of Part III of the UN Manual of Tests and Criteria was undertaken on a 1:1 mixture of powdered cellulose and a solution of hydrogen peroxide at a concentration of 59.7%. The mean pressure rise time over 5 trials from 690 to 2 070 kPa above atmospheric pressure for this mixture was 136 ms, greater than that of a 1:1 mixture of powdered cellulose and the reference substance perchloric acid at a concentration of 50% in solution (91 ms) but less than that of a 1:1 mixture of powdered cellulose and the reference substance sodium chlorate at a concentration of 40% in solution (758 ms)^{Footnote 1}. Hydrogen peroxide at a concentration of 59.7% meets the classification criteria for Oxidizing Liquids – Category 2.

Another study performed in accordance with test O.2 of sub-section 34.4.2 of Part III of the UN Manual of Tests and Criteria was undertaken on a 1:1 mixture of powdered cellulose and a solution of hydrogen peroxide at a concentration of 63.2%. The mean pressure rise time over 5 trials from 690 to 2 070 kPa above atmospheric pressure for this mixture was 92 ms, greater than that of a 1:1 mixture of powdered cellulose and the reference substance perchloric acid at a concentration of 50% in solution (68 ms) but less than that of a 1:1 mixture of powdered cellulose and the reference substance sodium chlorate at a concentration of 40% in solution (321 ms)^{Footnote 1}. Hydrogen peroxide at a concentration of 63.2% meets the classification criteria for Oxidizing Liquids – Category 2.

The available data for an aqueous solution containing hydrogen peroxide at a concentration of 69.7% or above (or for pure hydrogen peroxide), of 50 to 63.2% or of 42.5 to 47.3% meet the classification criteria for Oxidizing Liquids – Category 1, Oxidizing Liquids – Category 2 and Oxidizing Liquids – Category 3, respectively [subsection 7.13.1(2) of the HPR].

Aqueous solutions containing hydrogen peroxide at a concentration of 40% or lower do not meet classification criteria for a category of Oxidizing Liquids.

Oxidizing Solids:

Not applicable

Hydrogen peroxide is not a solid. The classification criteria for Oxidizing Solids do not apply to this substance.

Organic Peroxides:

Not applicable

Although hydrogen peroxide contains a bivalent -O-O- structure, it is not organic.

The classification criteria for Organic Peroxides do not apply to this substance.

Corrosive to Metals:

Does not meet criteria

A study performed in accordance with sub-section 37.4 of Part III of the UN Manual of Tests and Criteria was undertaken on an aqueous solution containing hydrogen peroxide at a concentration of 49.5%. Following 7 days of exposure to the solution, samples of aluminum and carbon steel demonstrated no mass loss nor reduction of uniform thickness^{Footnote 1}.

The available data do not meet the classification criteria for a category of Corrosive to Metals.

Combustible Dusts:

Not applicable

Hydrogen peroxide is not a solid. The classification criteria for Combustible Dusts do not apply to this substance.

Simple Asphyxiants:

Not applicable

Hydrogen peroxide is not a gas. The classification criteria for Simple Asphyxiants do not apply to this substance.

Chemicals Under Pressure:

Not evaluated

Classification of a hazardous product in the Chemicals Under Pressure hazard class is product dependent.

Regulatory and other information

Regulatory information:

Hazardous substance assessments are prepared by Health Canada as educational and information resources. Under the HPA, suppliers of hazardous products must, upon the sale or importation of a hazardous product, provide a safety data sheet and label that meet the requirements set out in the HPR.

Other information:

The information and classifications contained in these hazardous substance assessments are based on publicly available sources, such as peer-reviewed literature or reports by international bodies. New information, including proprietary information, could have an impact on the classification of substances or hazardous products containing them. It is the responsibility of the supplier to ensure the accuracy, sufficiency and reliability of their hazardous product classifications.

Last updated:

2025

Prepared by:

Workplace Hazardous Materials Bureau, Health Canada