English Safety Data Sheet Database 中文版 MSDS

Catechol

CAS No. 120-80-9 | PubChem CID 289
Section 1. Identification
Chemical NameCatechol CAS No.120-80-9
Synonymscatechol;1,2-benzenediol; o-dihydroxybenzene Chinese Name邻苯二酚
Molecular FormulaC6H6O2 Molecular Weight110.11
UN No.2811 Data SourcePubChem (NIH/NLM)
GHS Hazard Classification
Signal Word DANGER
Pictograms GHS05 · Corrosive GHS06 · Acute Toxic GHS07 · Irritant GHS08 · Health Hazard
Hazard Statements H301H311H315H319H341H350H302H312H317H412H318H335H351H361H370H401H314H372H373H332
Precautionary Statements P203P262P264P264+P265P270P280P301+P316P302+P352P305+P351+P338P316P318P321P330P332+P317P337+P317P361+P364P362+P364P405P501P261P272P301+P317P317P333+P317P273P260P271P304+P340P305+P354+P338P308+P316P319P403+P233P301+P330+P331P302+P361+P354P363

Section 2. Hazards Identification

H301: Toxic if swallowed [Danger Acute toxicity, oral]

H311: Toxic in contact with skin [Danger Acute toxicity, dermal]

H315: Causes skin irritation [Warning Skin corrosion/irritation]

H319: Causes serious eye irritation [Warning Serious eye damage/eye irritation]

H341: Suspected of causing genetic defects [Warning Germ cell mutagenicity]

H350: May cause cancer [Danger Carcinogenicity]

P203, P262, P264, P264+P265, P270, P280, P301+P316, P302+P352, P305+P351+P338, P316, P318, P321, P330, P332+P317, P337+P317, P361+P364, P362+P364, P405, and P501 (click each P-code to see the statement)

H301 (16.4%): Toxic if swallowed [Danger Acute toxicity, oral]

H302 (83.6%): Harmful if swallowed [Warning Acute toxicity, oral]

H311 (16.4%): Toxic in contact with skin [Danger Acute toxicity, dermal]

H312 (83.6%): Harmful in contact with skin [Warning Acute toxicity, dermal]

H315 (> 99.9%): Causes skin irritation [Warning Skin corrosion/irritation]

H317 (12.6%): May cause an allergic skin reaction [Warning Sensitization, Skin]

H319 (94.6%): Causes serious eye irritation [Warning Serious eye damage/eye irritation]

H341 (16.4%): Suspected of causing genetic defects [Warning Germ cell mutagenicity]

H350 (11.4%): May cause cancer [Danger Carcinogenicity]

P203, P261, P262, P264, P264+P265, P270, P272, P280, P301+P316, P301+P317, P302+P352, P305+P351+P338, P316, P317, P318, P321, P330, P332+P317, P333+P317, P337+P317, P361+P364, P362+P364, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 2962 reports by companies from 34 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website.

H317 (100%): May cause an allergic skin reaction [Warning Sensitization, Skin]

H412 (100%): Harmful to aquatic life with long lasting effects [Hazardous to the aquatic environment, long-term hazard]

P261, P272, P273, P280, P302+P352, P321, P333+P317, P362+P364, and P501 (click each P-code to see the statement)

The GHS information provided by 1 company from 1 notification to the ECHA C&L Inventory.

H315 (100%): Causes skin irritation [Warning Skin corrosion/irritation]

H319 (100%): Causes serious eye irritation [Warning Serious eye damage/eye irritation]

P264, P264+P265, P273, P280, P302+P352, P305+P351+P338, P321, P332+P317, P337+P317, P362+P364, and P501 (click each P-code to see the statement)

P203, P280, P318, P405, and P501 (click each P-code to see the statement)

H317: May cause an allergic skin reaction [Warning Sensitization, Skin]

H318: Causes serious eye damage [Danger Serious eye damage/eye irritation]

H335: May cause respiratory irritation [Warning Specific target organ toxicity, single exposure; Respiratory tract irritation]

H351: Suspected of causing cancer [Warning Carcinogenicity]

H361: Suspected of damaging fertility or the unborn child [Warning Reproductive toxicity]

H370: Causes damage to organs [Danger Specific target organ toxicity, single exposure]

H401: Toxic to aquatic life [Hazardous to the aquatic environment, acute hazard]

P203, P260, P261, P262, P264, P264+P265, P270, P271, P272, P273, P280, P301+P316, P302+P352, P304+P340, P305+P354+P338, P308+P316, P316, P317, P318, P319, P321, P330, P332+P317, P333+P317, P361+P364, P362+P364, P403+P233, P405, and P501 (click each P-code to see the statement)

H314: Causes severe skin burns and eye damage [Danger Skin corrosion/irritation]

H372: Causes damage to organs through prolonged or repeated exposure [Danger Specific target organ toxicity, repeated exposure]

H373: May causes damage to organs through prolonged or repeated exposure [Warning Specific target organ toxicity, repeated exposure]

P203, P260, P261, P262, P264, P264+P265, P270, P271, P280, P301+P316, P301+P330+P331, P302+P352, P302+P361+P354, P304+P340, P305+P354+P338, P308+P316, P316, P317, P318, P319, P321, P330, P361+P364, P363, P403+P233, P405, and P501 (click each P-code to see the statement)

P203, P261, P262, P264, P264+P265, P270, P272, P280, P301+P316, P302+P352, P305+P351+P338, P316, P318, P321, P330, P332+P317, P333+P317, P337+P317, P361+P364, P362+P364, P405, and P501 (click each P-code to see the statement)

Section 4. First-Aid Measures

Fresh air, rest. Artificial respiration may be needed. Refer for medical attention.

Remove contaminated clothes. Rinse skin with plenty of water or shower. Refer for medical attention .

Rinse with plenty of water (remove contact lenses if easily possible). Refer immediately for medical attention.

Rinse mouth. Give one or two glasses of water to drink. Refer immediately for medical attention.

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.

SKIN: IMMEDIATELY flood affected skin with water while removing and isolating all contaminated clothing. Gently wash all affected skin areas thoroughly with soap and water. IMMEDIATELY call a hospital or poison control center even if no symptoms (such as redness or irritation) develop. IMMEDIATELY transport the victim to a hospital for treatment after washing the affected areas.

INHALATION: IMMEDIATELY leave the contaminated area; take deep breaths of fresh air. If symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth, throat, or chest) develop, call a physician and be prepared to transport the victim to a hospital. Provide proper respiratory protection to rescuers entering an unknown atmosphere. Whenever possible, Self-Contained Breathing Apparatus (SCBA) should be used; if not available, use a level of protection greater than or equal to that advised under Protective Clothing.

INGESTION: DO NOT INDUCE VOMITING. Phenols are very toxic poisons AND corrosive and irritating, so that inducing vomiting may make medical problems worse. IMMEDIATELY call a hospital or poison control center and locate activated charcoal, egg whites, or milk in case the medical advisor recommends administering one of them. If advice from a physician is not readily available and the victim is conscious and not convulsing, give the victim a glass of activated charcoal slurry in water or, if this is not available, a glass of milk, or beaten egg whites and IMMEDIATELY transport victim to a hospital. If the victim is convulsing or unconscious, do not give anything by mouth, assure that the victim's airway is open and lay the victim on his/her side with the head lower than the body. DO NOT INDUCE VOMITING. IMMEDIATELY transport the victim to a hospital. (NTP, 1992)

(General first aid procedures)

Eye: Irrigate immediately - If this chemical contacts the eyes, immediately wash (irrigate) the eyes with large amounts of water, occasionally lifting the lower and upper lids. Get medical attention immediately.

Skin: Water wash immediately - If this chemical contacts the skin, immediately wash the contaminated skin with water. If this chemical penetrates the clothing, immediately remove the clothing and wash the skin with water. If symptoms occur after washing, get medical attention immediately.

Breathing: Respiratory support

Swallow: Medical attention immediately - If this chemical has been swallowed, get medical attention immediately.

Section 5. Fire-Fighting Measures

Extinguish with dry chemicals, alcohol foam, or carbon dioxide. Water may be ineffective on fire. Cool exposed containers with water. (USCG, 1999)

Use water spray, dry powder, alcohol-resistant foam, carbon dioxide.

To fight fire, use water, carbon dioxide, dry chemical

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.

Advice for firefighters: Wear self contained breathing apparatus for fire fighting if necessary.

On combustion, forms irritating fumes.

Section 6. Accidental Release Measures

Excerpt from ERG Guide 154 [Substances - Toxic and/or Corrosive (Non-Combustible)]:

IMMEDIATE PRECAUTIONARY MEASURE: Isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids.

SPILL: Increase the immediate precautionary measure distance, in the downwind direction, as necessary.

FIRE: If tank, rail tank car or highway tank is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. (ERG, 2024)

Personal protection: particulate filter respirator adapted to the airborne concentration of the substance. Do NOT let this chemical enter the environment. Sweep spilled substance into covered containers. If appropriate, moisten first to prevent dusting. Carefully collect remainder. Then store and dispose of according to local regulations.

Sweep spilled substance into containers; if appropriate, moisten first to prevent dusting, then remove to safe place. Do NOT let this chemical enter the environment. Personal protection: P2 filter respirator for harmful particles.

Accidental Release Measures. Personal precautions, protective equipment and emergency procedures: Wear respiratory protection. Avoid dust formation. Avoid breathing vapours, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided. Methods and materials for containment and cleaning up: Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for disposal.

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal and plant life; and conformance with environmental and public health regulations.

Incineration: It should be combined with paper or other flammable material. An alternate procedure is to dissolve the solid in a flammable solvent and spray the solutions into the fire chamber.

Waste treatment methods. Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber. Contaminated packaging: Dispose of as unused product.

SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.

SRP: The scientific literature for the use of contact lenses by industrial workers is inconsistent. The benefits or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.

SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants. Ensure that the local ventilation moves the contaminant away from the worker.

SRP: Contaminated protective clothing should be segregated in a manner such that there is no direct personal contact by personnel who handle, dispose, or clean the clothing. The completeness of the cleaning procedures should be considered before the decontaminated protective clothing is returned for reuse by the workers. Contaminated clothing should not be taken home at the end of shift, but should remain at employee's place of work for cleaning.

The worker should immediately wash the skin when it becomes contaminated.

For more Preventive Measures (Complete) data for CATECHOL (11 total), please visit the HSDB record page.

Section 7. Handling and Storage

Avoid contact with solid and dust. Keep people away. Wear rubber overclothing (including gloves). Stop discharge if possible. Isolate and remove discharged material. Notify local health and pollution control agencies. (USCG, 1999)

Well closed. Separated from oxidants and food and feedstuffs. Keep in the dark. Ventilation along the floor. Store in an area without drain or sewer access.

Separated from strong oxidants, food and feedstuffs. Keep in the dark. Ventilation along the floor.

Conditions for safe storage, including any incompatibilities: Keep container tightly closed in a dry and well-ventilated place. Store under inert gas. Air and light sensitive.

Section 8. Exposure Controls / Personal Protection

15 [ppm]

170 [ppm]

990 [ppm]

5 ppm (20 mg/m³)

TWA 5 ppm (20 mg/m3) [skin]

none See Appendix G

See: IDLH INDEX

5.0 [ppm]

8 hr Time Weighted Avg (TWA): 5 ppm, skin.

Excursion Limit Recommendation: Excursions in worker exposure levels may exceed 3 times the TLV-TWA for no more than a total of 30 minutes during a work day, and under no circumstances should they exceed 5 times the TLV-TWA, provided that the TLV-TWA is not exceeded.

A3; Confirmed animal carcinogen with unknown relevance to humans.

5 ppm as TWA; (skin); A3 (confirmed animal carcinogen with unknown relevance to humans)

5 ppm [1985]

A harmful contamination of the air will not or will only very slowly be reached on evaporation of this substance at 20 °C.

The substance is irritating to the skin and respiratory tract. The substance is corrosive to the eyes. The substance may cause effects on the central nervous system. This may result in depression, convulsions and respiratory failure. Exposure could cause rise of blood pressure.

Repeated or prolonged contact may cause skin sensitization. This substance is possibly carcinogenic to humans. May cause heritable genetic damage to human germ cells.

Excerpt from NIOSH Pocket Guide for Catechol:

Skin: PREVENT SKIN CONTACT - Wear appropriate personal protective clothing to prevent skin contact.

Eyes: PREVENT EYE CONTACT - Wear appropriate eye protection to prevent eye contact.

Wash skin: WHEN CONTAMINATED - The worker should immediately wash the skin when it becomes contaminated.

Remove: WHEN WET OR CONTAMINATED - Work clothing that becomes wet or significantly contaminated should be removed and replaced.

Change: DAILY - Workers whose clothing may have become contaminated should change into uncontaminated clothing before leaving the work premises.

Provide: EYEWASH - Eyewash fountains should be provided in areas where there is any possibility that workers could be exposed to the substances; this is irrespective of the recommendation involving the wearing of eye protection. (NIOSH, 2024)

Wear appropriate personal protective clothing to prevent skin contact.

Wear appropriate eye protection to prevent eye contact.

Eyewash fountains should be provided in areas where there is any possibility that workers could be exposed to the substance; this is irrespective of the recommendation involving the wearing of eye protection.

Eye/face protection: Face shield and safety glasses Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).

For more Personal Protective Equipment (PPE) (Complete) data for CATECHOL (7 total), please visit the HSDB record page.

Important additional information about respirator selection

NO open flames. NO contact with oxidizing agents.

PREVENT DISPERSION OF DUST! IN ALL CASES CONSULT A DOCTOR!

Use local exhaust or breathing protection.

Protective gloves. Protective clothing.

Wear face shield or eye protection in combination with breathing protection.

Do not eat, drink, or smoke during work. Wash hands before eating.

Section 9. Physical and Chemical Properties

Solid; white; odorless. Sinks and mixes with water. (USCG, 1999)

Large Crystals; Other Solid

Colorless, crystalline solid with a faint odor; Note: Discolors to brown in air & light; [NIOSH]

COLOURLESS CRYSTALS WITH CHARACTERISTIC ODOUR. TURNS BROWN ON EXPOSURE TO AIR AND LIGHT.

Colorless, crystalline solid with a faint odor.

Colorless, crystalline solid with a faint odor. [Note: Discolors to brown in air & light.]

Monoclinic tablets, prisms from toluene ... its aqueous solutions soon turn brown

Colorless crystals, discolors to brown on exposure to air and light, especially when moist

Faint characteristic odor

Phenolic odor

Sweet and bitter taste

473 °F at 760 mmHg (sublimes) (NTP, 1992)

245.5 °C at 760 mm Hg; sublimes

BP: 221.5 °C at 400 mm Hg; 197.7 °C at 200 mm Hg; 176 °C at 100 mm Hg; 161.7 °C at 60 mm Hg; 134 °C at 20 mm Hg; 118.3 °C at 10 mm Hg; 104 °C at 5 mm Hg ... Volatile with steam

245.5 °C

245 °C @760 [mm Hg]

221 °F (NTP, 1992)

104.6 °C

261 °F (NTP, 1992)

260 °F (127 °C) (Closed cup)

127.2 °C (open cup)

127 °C (261 °F) (Closed cup)

127 °C c.c.

greater than or equal to 100 mg/mL at 70.7 °F (NTP, 1992)

In water, 4.61X10+5 mg/L at 25 °C

Soluble in chloroform, ether; very soluble in pyridine, aqueous alkalis

Very soluble in alcohol, ethyl ether, acetate

461.0 mg/mL

Solubility in water, g/100ml at 20 °C: 43

1.344 at 68 °F (USCG, 1999) - Denser than water; will sink

Density: 1.371

Relative density (water = 1): 1.3

1.344 @ 20°C

3.79 (NTP, 1992) - Heavier than air; will sink (Relative to Air)

3.79 (Air = 1)

Relative vapor density (air = 1): 3.8

5 mmHg at 219 °F ; 10 mmHg at 244.9 °F (NTP, 1992)

0.03 [mmHg]

VP: 10 mm Hg at 118.3 °C

3X10-2 mm Hg at 20 °C (extrapolated)

Section 10. Stability and Reactivity

Turns brown on exposure to air and light, especially when moist. Water soluble. Aqueous solutions soon turn brown on exposure to air and light.

Phenols and Cresols

POISONOUS GASES MAY BE PRODUCED WHEN HEATED. CATECHOL may form toxic fumes at high temperatures. (USCG, 1999). This compound can react with acid chlorides, acid anhydrides, bases and oxidizing agents. It reacts violently on contact with concentrated nitric acid. It acts as a reducing agent (NTP, 1992).

Can react vigorously with oxidizing materials

Strong oxidizers, nitric acid.

The phenol is hypergolic with concentrated nitric acid, with a 1 ms ignition delay. /Nitric acid/

Incompatible with strong acids or bases, acid chlorides, anhydrides. Exothermic reactions with oxidants.

Incompatible materials: Oxidizing agents.

Strong oxidizers, nitric acid

Section 11. Toxicological Information

The CIR Expert Panel concludes that Pyrocatechol is unsafe for use in leave-on products, and that the available data are insufficient to support the safety of Pyrocatechol as used in hair dyes.

The ingredient is unsafe for use in cosmetics

Ingredients for which the data are insufficient and their use in cosmetics is not supported

IDENTIFICATION AND USE: Catechol is a tablet or colorless crystal, prism or aqueous solution, which discolors to brown on exposure to air and light. It has a faint characteristic odor. It is used as antioxidant in the rubber, chemical, photographic, dye, fat, and oil industries. It was formerly used as an antiseptic. Catechol was found unsafe for use in cosmetics. HUMAN EXPOSURE AND TOXICITY: Catechol contact with the skin has been known to cause an eczematous dermatitis. It is highly irritating upon direct contact; severe eye and deep skin burns result. Well absorbed by skin. Systemic toxicity similar to that of phenol however, catechol may be more likely to cause convulsions and hypertension. At high doses, renal and liver injury may occur. Absorption through the skin, in a few instances, has resulted in symptoms of illness resembling closely those induced by phenol, except for certain central effects (convulsions) that were more marked. Death apparently is initiated by respiratory failure. Catechol was found to be a more harmful toxin than phenol in human blood cells in vitro, since it provokes statistically significant changes in the function of erythrocytes even at low doses. Both compounds induced methemoglobin formation, glutathione depletion and conversion of oxyhemoglobin to methemoglobin, which is associated with superoxide anion production and lead to formation of ferryl hemoglobin, hydrogen peroxide or hydroxyl radicals. It is known that oxidation of catechol leads to formation of semiquinone radicals. Catechol induced DNA damage in human peripheral blood lymphocytes, and in proliferating human T-lymphocytes. Catechol is confirmed animal carcinogen with unknown relevance to humans. ANIMAL STUDIES: Instillation of 100 mg of catechol into the eyes of rabbits caused a moderate conjunctivitis with exudate and corneal opacity that progressed to a severe conjunctivitis, iritis, and widely diffuse corneal opacity at 72 hours. Fourteen days after instillation, the corneas were vascularized, had infiltration of granulation tissue, and were protruding (keratoconus). Hyperemia of the stomach and intestines was reported after lethal oral doses in rats. Repeated absorption of sublethal doses by animals has induced methemoglobinemia, leucopenia and anemia. Death is apparently initiated by respiratory failure. Catechol clearly induced increases in DNA synthesis in rat forestomach epithelium independent of sex. In the glandular stomach, catechol treatment for 4 weeks increased crypt height due to elevation of DNA synthesis and caused submucosal growth of pyloric mucosal cells. Administration of catechol (1.5% in the diet) for 20 weeks induced mild to moderate hyperplasia in the forestomach. Rats fed catechol in the diet at concentrations of 0 or 1.5% for four weeks followed by 0.8% for 47 weeks either with no other exposure or one week after exposure to N-methyl- N'-nitro-N-nitrosoguanidine increased the incidence of forestomach papillomas, glandular stomach adenocarcinomas, squamous-cell carcinomas of the forestomach, and adenocarcinomas in the pyloric region of the glandular stomach in rats. Regenerative cell proliferation due to toxicity plays an important role in catechol-induced glandular stomach carcinogenesis. Catechol also exhibited developmental toxicity in rats. Litter size and weights were reduced at the maternally toxic doses. Malformations involving limbs, tail and urogenital systems were reported at all doses. Catechol was negative in the Ames assay, but induced sister chromatid exchanges in Chinese hamster ovary V79 cells. In in vivo mouse micronucleus assays, in which the conjugation enzymes responsible for detoxication were present, both positive and negative results were reported. ECOTOXICITY STUDIES: Catechol-treated sea bass showed disorders in the metabolic toxicity indicators such as hypoglycemia, low blood urea nitrogen level and decrease of alkaline phosphatase activity.

Evaluation: No epidemiological data relevant to the carcinogenicity of catechol were available. There is sufficient evidence in experimental animals for the carcinogenicity of catechol. OVERALL EVALUATION: Catechol is possibly carcinogenic to humans (Group 2B).

A3; Confirmed animal carcinogen with unknown relevance to humans.

Catechol

Group 2B: Possibly carcinogenic to humans

Volume 15: (1977) Some Fumigants, the Herbicides 2,4-D and 2,4,5-T, Chlorinated Dibenzodioxins and Miscellaneous Industrial Chemicals

Volume Sup 7: Overall Evaluations of Carcinogenicity: An Updating of IARC Monographs Volumes 1 to 42, 1987; 440 pages; ISBN 92-832-1411-0 (out of print)

Volume 71: (1999) Re-evaluation of Some Organic Chemicals, Hydrazine and Hydrogen Peroxide (Part 1, Part 2, Part 3)

2B, possibly carcinogenic to humans. (L135)

The substance can be absorbed into the body by inhalation of its aerosol, through the skin and by ingestion.

inhalation, skin absorption, ingestion, skin and/or eye contact

Cough. Sore throat. Burning sensation behind the breastbone. Laboured breathing. Convulsions.

MAY BE ABSORBED! Redness. Convulsions.

Redness. Pain. Severe burns.

Abdominal pain. Vomiting. Diarrhoea. Convulsions. Respiratory arrest.

irritation eyes, skin, respiratory system; skin sensitization, dermatitis; lacrimation (discharge of tears), burns eyes; convulsions, increased blood pressure, kidney injury

Eyes, skin, respiratory system, central nervous system, kidneys

Neurotoxin - Other CNS neurotoxin

Methemoglobinemia - The presence of increased methemoglobin in the blood; the compound is classified as secondary toxic effect

Dermatotoxin - Skin burns.

Skin Sensitizer - An agent that can induce an allergic reaction in the skin.

IARC Carcinogen - Class 3: Chemicals are not classifiable by the International Agency for Research on Cancer.

ACGIH Carcinogen - Confirmed Animal.

LD50 Rat oral 300 mg/kg

LD50 Mouse oral 260 mg/kg

LD50 Mouse ip 190 mg/kg

LD50 Rabbit dermal 800 mg/kg

For more Non-Human Toxicity Values (Complete) data for CATECHOL (8 total), please visit the HSDB record page.

Catechol (25, 50, 75 or 100 mg/kg bw, single ip administration) decreased the incorporation of (59)Fe to erythrocytes in a dose-dependent fashion in female Swiss mice, when administered with phenol (50 mg/kg bw, single ip administration).

Intake of antioxidants from the diet has been recognized to have beneficial health effects, but the potential benefit of taking antioxidants such as beta-carotene as supplements is controversial. The aim of the present study was to evaluate the potential protective effects of a physiologically relevant concentration (2 uM) of beta-carotene on the DNA damaging effects of catechol in mouse lymphoma L5178Y cells. Two different exposure protocols were used: simultaneous exposure to beta-carotene and catechol for 3 hr; and exposure to catechol for 3 hr after 18 hr pre-treatment with the vitamin. DNA damage was evaluated using the comet assay (employing one procedure for general damage, and another procedure, which also included oxidative DNA damage). Independent of exposure protocol and procedure for comet assay, beta-carotene did not increase the basal level of DNA damage. However, at the highest concentration of catechol (1 mM), beta-carotene was found to clearly increase the level of catechol-induced DNA damage, especially in the pre-treated cells. Interestingly, an opposite effect was observed at lower concentrations of catechol, but the beta-carotene related reduction of catechol-induced genotoxicity was significant (P < 0.05) only for the procedure including oxidative damage induced by 0.5 mM catechol. Taken together our results indicate that beta-carotene can both reduce and enhance the DNA damaging effects of a genotoxic agent such as catechol. This indicates that it is the level of catechol-induced DNA damage that seems to determine whether beta-carotene should be regarded as a beneficial or detrimental agent when it comes to its use as a dietary supplement.

Continuous oral treatment of rats with 0.8% catechol for 51 weeks after a single intragastric dose of 150 mg/kg of N-methyl-N'-nitro-N-nitrosoguanidine strongly enhanced both forestomach and glandular stomach carcinogenesis. In addition, and more importantly, catechol alone induced adenocarcinoma and adenomatous hyperplasia in the pyloric region of the glandular stomach.

Catechol and N-methyl-N'-nitro-N-nitrosoguanidine are gastric carcinogens in rats. Catechol, sodium chloride and bile salts have enhancing effects on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in rats. The effects of these compounds on proliferation of pyloric mucosa cells in male F344 rats were examined immunohistochemically using bromodeoxyuridine and anti-bromodeoxyuridine monoclonal antibody. Rats were given N-methyl-N'-nitro-N-nitrosoguanidine (83 ug/ml in their drinking water), catechol (0.8% in their diet), sodium taurocholate (0.3% in their diet), sodium taurodeoxycholate (0.3% in their diet), or sodium chloride (10% in their diet or by intragastric administration of 1 ml of saturated solution once a week) for 4 weeks. All these treatments markedly enhanced cell proliferation of the pyloric epithelium.

For more Interactions (Complete) data for CATECHOL (15 total), please visit the HSDB record page.

Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand-valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR as necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Phenols and related compounds/

Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist respirations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Administer activated charcoal ... . Do not use emetics ... . Cover skin burns with dry, sterile dressings after decontamination ... . Maintain body temperature. /Phenols and related compounds/

Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Monitor cardiac rhythm and treat arrhythmias if necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's(LR) if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Consider vasopressors if patient is hypotensive with a normal fluid volume. Watch for signs of fluid overload ... . Administer 1% solution methylene blue if patient is sympotomatic with severe hypoxia, cyanosis, and cardiac compromise not responding to oxygen ... . Treat seizures with diazepam (Valium) or lorazepam (Ativan) ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Phenols and related compounds/

Emergency and supportive measures. 1. Maintain an open airway and assist ventilation if necessary. 2. Treat coma, seizures, hypotension, and arrhythmias if they occur. 3. If corrosive injury to the GI tract is suspected, consult a gastroenterologist for possible endoscopy. /Phenols and related compounds/

Section 12. Ecological Information

EC50; Species: Pimephales promelas (Fathead minnow); Conditions: flow through bioassay with measured concentrations, 25.6 °C, dissolved oxygen 6.4 mg/L, hardness 46.0 mg/L calcium carbonate, alkalinity 40.2 mg/L calcium carbonate, and pH 7.7; Concentration: 9.00 mg/L for 96 hr (confidence limit: 8.47-9.65 mg/L); Effect: loss of equilibrium

LC50; Species: Pimephales promelas (Fathead minnow); Conditions: flow through bioassay with measured concentrations, 25.6 °C, dissolved oxygen 6.4 mg/L, hardness 46.0 mg/L calcium carbonate, alkalinity 40.2 mg/L calcium carbonate, and pH 7.7; Concentration: 9.22 mg/L for 96 hr (confidence limit: 8.62-9.87 mg/L)

LC50; Species: Crangon septemspinosa (Bay shrimp); Conditions: renewal; Concentration: >44 mg/L for 96 hr

EC50; Species: Elodea canadensis (Broad waterweed); Conditions: renewal; Concentration: 0.00025 mol/L for < or =9 days; Effect: decreased population growth

For more Ecotoxicity Values (Complete) data for CATECHOL (8 total), please visit the HSDB record page.

/AQUATIC SPECIES/ Sea bass (Dicentrarchus labrax) were injected intraperitoneally once (single dose) or three times (fractionated dose) with phenol or OH-phenols (hydroquinone, resorcinol, and pyrocatechol). On the basis of the lethal doses, OH-phenols were more toxic than phenol, and pyrocatechol was the most powerful compound. Hematological, metabolic and antioxidant blood parameters were measured 3 days after the end of the treatment. Metabolic variations as specific effects on erythrocytes were revealed and differences between single and fractionated doses were observed. OH-phenols-treated fish showed disorders in the metabolic toxicity indicators as hypoglycemia, low blood urea nitrogen level (BUN) and decrease of alkaline phosphatase activity (ALP).

/PLANTS/ ... The acute toxicity of 15 compounds with low molecular weight (<350 Da), catechol, four benzoic acids, three phenylacetic acids, three phenylethanols, and four cinnamic acids, already isolated from the reverse osmosis in the fractionation of OMW /olive mill wastes/, was assessed on ... the seeds of two dicotyledonous species Cucumis sativus and Lepidium sativum, and on one monocotyledon Sorghum bicolor. Results of phytotoxicity showed that the most toxic compounds were catechol (EC50s ranging from 0.40 mmol/L for S. bicolor to 1.09 for C. sativus) and hydroxytyrosol, (EC50s ranging from 0.47 mmol/L for S. bicolor to 1.55 for C. sativus) ... These results suggested that the risk of OMW disposal may be more elevated for the water compartment than for the soil.

The substance is toxic to aquatic organisms.

Catechol's production and use in the synthesis of pharmaceutical and agricultural products as well as in the rubber, chemical, photographic, dye, and oil industries may result in its release to the environment through various waste streams. Catechol is found in many plants including tobacco, onions, some fruits and herbs. If released to air, a vapor pressure of 3.66X10-3 mm Hg at 25 °C indicates catechol will exist solely as a vapor in the atmosphere. Vapor-phase catechol will be degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals; the half-life for this reaction in air is estimated to be 2.8 hours. Reaction of catechol with nitrate radicals during nighttime may be an important removal process based on a rate constant of 3.8X10-12 cu cm/molecule sec for the reaction of phenol with nitrate radicals; this corresponds to a half-life of 15 minutes at an atmospheric concentration of 2X10+8 nitrate radicals per cu cm. Catechol in its nonionized form will not be subject to direct photolysis since this form does not absorb light above 300 nm in methanol solution. If released to soil, catechol is expected to have high mobility based upon a Koc of 118. Volatilization from moist soil surfaces is not expected to be an important fate process based upon an estimated Henry's Law constant of 1.2X10-9 atm-cu m/mole. Catechol is not expected to volatilize from dry soil surfaces based upon its vapor pressure. The percent biodegradation after 6 months in various loam soils ranged from 24 to 50%, indicating that biodegradation may be a moderate environmental fate process in soil. If released into water, catechol is not expected to adsorb to suspended solids and sediment based upon the Koc. Utilizing the Japanese MITI test, 83% of the Theoretical BOD was reached in 2 weeks indicating that biodegradation is an important environmental fate process in water. Volatilization from water surfaces is not expected to be an important fate process based upon this compound's estimated Henry's Law constant. An estimated BCF of 3 suggests the potential for bioconcentration in aquatic organisms is low. Hydrolysis is not expected to be an important environmental fate process since this compound lacks functional groups that hydrolyze under environmental conditions. Occupational exposure to catechol may occur through inhalation and dermal contact with this compound at workplaces where catechol is produced or used. Monitoring data indicate that the general population may be exposed to catechol via ingestion of food, inhalation of wood, fuel and cigarette smokes, and dermal contact with consumer products containing catechol. (SRC)

Catechol is a component of lignin(1). It is found in Douglas fir (Pseudotsuga menziesii) heartwood(2). Catechol is found in many plants including tobacco, onions, some fruits and herbs(3). It also a component in coal(4).

Catechol's production and use in the synthesis of food, pharmaceutical and agricultural products(1) as well as in the rubber, chemical, photographic, dye, cosmetic, and oil industries(2) may result in its release to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), a Koc value of 118(2), indicates that catechol is expected to have high mobility in soil(SRC). Volatilization of catechol from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 1.2X10-9 atm-cu m/mole(SRC), based upon its vapor pressure, 3.66X10-3 mm Hg(3), and water solubility, 4.61X10+5 mg/L(4). Catechol is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(3). The percent biodegradation after 6 months in various loam soils ranged from 24 to 50%(5), indicating that biodegradation is a moderate environmental fate process in soil(SRC).

AQUATIC FATE: Based on a classification scheme(1), a Koc value of 118(2), indicates that catechol is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 1.20X10-9 atm-cu m/mole(SRC), derived from its vapor pressure, 3.66X10-3 mm Hg(4), and water solubility, 4.61X10+5 mg/L(5). According to a classification scheme(6), an estimated BCF of 3(SRC), from its log Kow of 0.88(7) and a regression-derived equation(8), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Utilizing the Japanese MITI test, 83% of the Theoretical BOD was reached in 2 weeks(9) indicating that biodegradation is an important environmental fate process in water(SRC).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), catechol, which has a vapor pressure of 3.66X10-3 mm Hg at 25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase catechol is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 2.8 hrs(SRC), calculated from its rate constant of 1.04X10-10 cu cm/molecule-sec at 25 °C(3). Catechol in its nonionized form will not be subject to direct photolysis since this form does not absorb light above 300 nm in methanol solution(4). Reaction of catechol with nitrate radicals during nighttime may be an important removal process based on a rate constant of 3.8X10-12 cu cm/molecule sec for the reaction of phenol with nitrate radicals(2) which corresponds to a half-life of 15 minutes at an atmospheric concentration of 2X10+8 nitrate radicals per cu cm(SRC). The ionized form of catechol may photolyze based on an absorption maximum at 313 nm in basic aqueous solution(6) and at 289 nm in basic methanol solution(4). Therefore, catechol may be susceptible to direct photolysis by sunlight(SRC).

AEROBIC: Catechol is moderately to readily biodegraded in soils based on a residence time of 1 day for 500 mg of catechol in chernozem soil on hard carbonaceous woody loam (pH 7.1-7.5, 19 °C)(1). The percent biodegradation (measured as percentage of recovered 14CO2 activity) after 6 months at 23 °C in Steinbeck loam (pH 5.0), Fallbrook sandy loam (pH 5.5), Greenfield sandy loam (pH 7.0), and Sorrento loam (pH 7.4) were 24, 50, 28, and 26%, respectively(2). The soil bacteria Agrobacterium radiobacter was shown to biodegrade catechol(3).

AEROBIC: Catechol, present at 100 mg/L, reached 83% of its theoretical BOD in two weeks using an activated sludge inoculam at 30 mg/L in the Japanese MITI test(1). When present at 50 mg/L, catechol reached 80% of its theoretical BOD in two weeks using an activated sludge inoculam at 30 mg/L in the Japanese MITI test(2). 100% theoretical BOD was reported using activated sludge incubated 96 hrs at 16-20 °C(3). A chemical oxygen demand rate of 55.5 mg COD/g-hr was obtained, corresponding to 96% degradation in 5 days at 20 °C using acclimated activated sludge and a catechol concentration of 200 mg/L(4). Using non-acclimated activated sludge, a rate of 1.31X10-5/hr was reported corresponding to a half-life of 0.22 days(5). Catechol, at a concentration of 2 ppm, was degraded by sewage seed using the Closed Bottle test resulting in 89% theoretical BOD following a 30 day incubation(2); 62% mineralization as evolved CO2 in 28 days (including a 14-day lag period) at 25 °C was reported using the Sturm-CO2 evolution test(2). Using the OECD Coupled-Units test, 98% DOC removal was observed following 7 days acclimation of 2500 mg/L synthetic sewage under continuous feed operation and 12 ppm carbon catechol concentration(2).

ANAEROBIC: Anaerobic biodegradation of 39% (as CH4 produced) reported after 42 days (including 31 day lag period) using digester sludge; respiking this medium at 4 days gave 99% biodegradation after 21 days (including a 14-day lag period)(1). Anaerobic biodegradation of catechol using digester sludge reported to be 67% (as CH4/CO2 produced) in 13 days following a 21-day lag period(3) and 98% biodegradation (as CH4 produced) in 28 days (incl a 21-day lag period)(3).

The rate constant for the vapor-phase reaction of catechol with photochemically-produced hydroxyl radicals is 1.04X10-10 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(2). This corresponds to an atmospheric half-life of about 2.8 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(2). Catechol is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(3). Since the pKa for the initial ionization of catechol is 9.45(4), it will exist in a partially dissociated state in water and moist soils and, therefore, its transport and reactivity may be affected by pH(SRC). Catechol in its nonionized form will not be subject to direct photolysis since this form does not absorb light above 300 nm in methanol solution(5,6). The ionized form of catechol may photolyze based on an absorption maximum at 313 nm in basic aqueous solution(7) and at 289 nm in basic methanol solution(5). Direct photolysis of catechol is negligible under UVB irradiation(6).

As a class, phenols react relatively rapidly in sunlit natural water via reaction with photochemically produced hydroxyl radicals and peroxy radicals(1); typical half-lives for hydroxyl and peroxyl radical reactions are on the order of 100 and 19.2 hrs of sunlight, respectively(1). Reaction of catechol with nitrate radicals during nighttime may be an important removal process based on a rate constant of 3.8X10-12 cu cm/molecule sec for the reaction of phenol with nitrate radicals(2) which corresponds to a half-life of 15 minutes at an atmospheric concentration of 2X10+8 nitrate radicals per cu cm(SRC). The catechol nitrate transformation rate is higher at lower pH, and the pH trend suggests the influence of the acid-base equilibrium of photo HNO2/NO(-2)(3).

An estimated BCF of 3 was calculated for catechol(SRC), using a log Kow of 0.88(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

The Koc of catechol in Brookston clay loam has been reported to be 118(1). According to a classification scheme(2), this Koc value suggests that catechol is expected to have high mobility in soil.

The Henry's Law constant for catechol is estimated as 1.2X10-9 atm-cu m/mole(SRC) derived from its vapor pressure, 3.66X10-3 mm Hg(1), and water solubility, 4.61X10+5 mg/L(2). This Henry's Law constant indicates that catechol is expected to be essentially nonvolatile from water and moist soil surfaces(3). Catechol is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(1).

DRINKING WATER: Catechol was identified, not quantified, in drinking water from unspecified sources(1).

Catechol concentrations in coal conversion wastewaters were reported as follows: Lurgi gasification plant, Westfield, Scotland, 190-555 ppm; bench-scale hydrocarbonization coal liquification operation, 1700 ppm; identified, not quantified, in wastewaters from the Synthane coal gasification process, the Solvent Refined Coal plant in Ft. Lewis, WA; identified, not quantified in the Char Oil Energy Development liquification project, Princeton, NJ(1); condensate from slagging-bed gasifier at Univ of North Dakota Energy Research Center, Grand Forks, ND, 1980-81, samples from 4 condensate waters, 100% pos, 2-990 ppm, 473 ppm average(2). Catechol was identified, not quantified in drainage water from bituminous shale and effluent from coal-tar chemical production(3).

Catechol was present at 142, 467, and 384 mg/kg dry wood burned in open, half-closed, and closed airflow emissions using woodheaters commonly used in central Australia. Higher burn rates (open fair flow) producing much less particle mass per kg wood burned than the low burn rates (closed airflow). Wood used was White gum (Eucalyptus viminalis)(1).

Catechol was detected at concentrations ranging from 15-65 ng/cu m in air samples from unspecified locations(1). Catechol was one of the 4th largest contaminants present in the Gulf of Mexico in 1989(2).

Catechol occurrence in plants(1).[Table#3179]

Catechol is a component of cigarette smoke(1,2).

Catechol has been detected in the gas phase of burning pine, oak and eucalyptus with mean concentrations of 312, 142 and 215 mg/kg wood burned, respectively; wood was obtained from a large firewood distributor in the residential suburbs in Los Angeles, CA(1). Catechol was detected in burning wood emissions from red maple (Acer rubrum), northern red oak (Quercus rubra), paper birch (Betula papyrifera), eastern white pine (Pinus strobus), hemlock (Tsuga canadensis) and balsam fir (Abies balsemea) in concentrations of 0.799, 5.434, 1.110, 1.512, 0.952 and 7.114 mg/g organic carbon emitted, respectively; species are found in the United States(2). Catechol was detected in yellow poplar (Liriodendron tulipifera), white ash (Fraxinus americana), sweetgum (Liquidambar styraciflua), mockernut hickory (Carya tomentosa), loblolly pine (Pinus taeda) and slash pine (Pinus elliottii) at concentrations of 4.127, 1.741, 1,383, 9.865, 2.600 and 1.711 mg/g organic carbon emitted, respectively; species are native to the southern United States(3).

Catechol was present at 142, 467 and 384 mg/kg dry wood burned in open, half-closed and closed airflow emissions, erspectively, using woodheaters commonly used in central Australia. Higher burn rates (open fair flow) producing much less particle mass per kg wood burned than the low burn rates (closed airflow). Wood used was White gum (Eucalyptus viminalis)(1).

According to the 2006 TSCA Inventory Update Reporting data, the number of persons reasonably likely to be exposed in the industrial manufacturing, processing, and use of catechol is 1000 or greater; the data may be greatly underestimated(1).

NIOSH (NOES Survey 1981-1983) has statistically estimated that 13,516 workers (7,799 of these were female) were potentially exposed to catechol in the US(1). Occupational exposure to catechol may occur through inhalation and dermal contact with this compound at workplaces where catechol is produced or used. Monitoring data indicate that the general population may be exposed to catechol via ingestion of food, inhalation of wood, fuel and cigarette smokes, and dermal contact with consumer products containing catechol(SRC).

Section 13. Disposal Considerations

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal and plant life; and conformance with environmental and public health regulations.

Incineration: It should be combined with paper or other flammable material. An alternate procedure is to dissolve the solid in a flammable solvent and spray the solutions into the fire chamber.

Waste treatment methods. Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber. Contaminated packaging: Dispose of as unused product.

SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.

Section 14. Transport Information

Do not transport with food and feedstuffs.

Symbol: Xn; R: 21/22-36/38; S: (2)-22-26-37

UN Hazard Class: 6.1; UN Pack Group: III

Source: PubChem CID 289 (NIH/NLM, public domain). Retrieved from PubChem, a public-domain chemistry database maintained by the U.S. National Library of Medicine. Last updated: 2026-08-02 09:11:55.
Disclaimer: This information is compiled for reference only and does not replace the manufacturer's official Safety Data Sheet. Always consult the supplier's SDS before handling any chemical.