aceticacid

H226: Flammable liquid and vapor [Warning Flammable liquids]

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

P210, P233, P240, P241, P242, P243, P260, P264, P280, P301+P330+P331, P302+P361+P354, P303+P361+P353, P304+P340, P305+P354+P338, P316, P321, P363, P370+P378, P403+P235, P405, and P501 (click each P-code to see the statement)

This chemical does not meet GHS hazard criteria for < 0.1% (3 of 5076) of reports.

H226 (99.7%): Flammable liquid and vapor [Warning Flammable liquids]

H314 (> 99.9%): Causes severe skin burns and eye damage [Danger Skin corrosion/irritation]

H318 (14.7%): Causes serious eye damage [Danger Serious eye damage/eye irritation]

P210, P233, P240, P241, P242, P243, P260, P264, P264+P265, P280, P301+P330+P331, P302+P361+P354, P303+P361+P353, P304+P340, P305+P354+P338, P316, P317, P321, P363, P370+P378, P403+P235, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 5076 reports by companies from 68 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Reported as not meeting GHS hazard criteria per 3 of 5076 reports by companies.

There are 67 notifications provided by 5073 of 5076 reports by companies with hazard statement code(s).

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.

H312: Harmful in contact with skin [Warning Acute toxicity, dermal]

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

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

P210, P233, P240, P241, P242, P243, P260, P264, P264+P265, P270, P280, P301+P330+P331, P302+P352, P302+P361+P354, P303+P361+P353, P304+P340, P305+P354+P338, P308+P316, P316, P317, P321, P362+P364, P363, P370+P378, P403+P235, P405, and P501 (click each P-code to see the statement)

H303: May be harmful if swallowed [Warning Acute toxicity, oral]

H334: May cause allergy or asthma symptoms or breathing difficulties if inhaled [Danger Sensitization, respiratory]

H371: May cause damage to organs [Warning Specific target organ toxicity, single exposure]

P210, P233, P240, P241, P242, P243, P260, P264, P264+P265, P270, P271, P280, P284, P301+P317, P301+P330+P331, P302+P352, P302+P361+P354, P303+P361+P353, P304+P340, P305+P354+P338, P308+P316, P316, P317, P321, P342+P316, P362+P364, P363, P370+P378, P403, P403+P235, P405, and P501 (click each P-code to see the statement)

Fresh air, rest. Half-upright position. Refer immediately for medical attention.

Remove contaminated clothes. Rinse and then wash skin with water and soap. Rinse skin with plenty of water or shower for at least 15 minutes. Refer immediately for medical attention.

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

Rinse mouth. Do NOT induce vomiting. If within a few minutes after ingestion, one small glass of water may be given 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. Corrosive chemicals will destroy the membranes of the mouth, throat, and esophagus and, in addition, have a high risk of being aspirated into the victim's lungs during vomiting which increases the medical problems. If the victim is conscious and not convulsing, give 1 or 2 glasses of water to dilute the chemical and IMMEDIATELY call a hospital or poison control center. IMMEDIATELY transport the victim to a hospital. If the victim is convulsing or unconscious, do not give anything by mouth, ensure 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. Transport the victim IMMEDIATELY to a hospital. (NTP, 1992)

Excerpt from ERG Guide 153 [Substances - Toxic and/or Corrosive (Combustible)]:

Refer to the "General First Aid" section. Specific First Aid: For corrosives, in case of contact, immediately flush skin or eyes with running water for at least 30 minutes. Additional flushing may be required. Removal of solidified molten material from skin requires medical assistance. (ERG, 2024)

Excerpt from ERG Guide 132 [Flammable Liquids - Corrosive]:

Refer to the "General First Aid" section. Specific First Aid: For corrosives, in case of contact, immediately flush skin or eyes with running water for at least 30 minutes. Additional flushing may be required. In case of burns, immediately cool affected skin for as long as possible with cold water. Do not remove clothing if adhering to skin. (ERG, 2024)

General First Aid:

· Call 911 or emergency medical service.

· Ensure that medical personnel are aware of the material(s) involved, take precautions to protect themselves and avoid contamination.

· Move victim to fresh air if it can be done safely.

· Administer oxygen if breathing is difficult.

· If victim is not breathing:

-- DO NOT perform mouth-to-mouth resuscitation; the victim may have ingested or inhaled the substance.

-- If equipped and pulse detected, wash face and mouth, then give artificial respiration using a proper respiratory medical device (bag-valve mask, pocket mask equipped with a one-way valve or other device).

-- If no pulse detected or no respiratory medical device available, provide continuous compressions. Conduct a pulse check every two minutes or monitor for any signs of spontaneous respirations.

· Remove and isolate contaminated clothing and shoes.

· For minor skin contact, avoid spreading material on unaffected skin.

· In case of contact with substance, remove immediately by flushing skin or eyes with running water for at least 20 minutes.

· For severe burns, immediate medical attention is required.

· Effects of exposure (inhalation, ingestion, or skin contact) to substance may be delayed.

· Keep victim calm and warm.

· Keep victim under observation.

· For further assistance, contact your local Poison Control Center.

· Note: Basic Life Support (BLS) and Advanced Life Support (ALS) should be done by trained professionals.

Specific First Aid:

· For corrosives, in case of contact, immediately flush skin or eyes with running water for at least 30 minutes. Additional flushing may be required.

· In case of burns, immediately cool affected skin for as long as possible with cold water. Do not remove clothing if adhering to skin.

In Canada, an Emergency Response Assistance Plan (ERAP) may be required for this product. Please consult the shipping paper and/or the "ERAP" section.

(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 flush immediately - If this chemical contacts the skin, immediately flush the contaminated skin with water. If this chemical penetrates the clothing, immediately remove the clothing and flush the skin with water. Get medical attention promptly.

Breathing: Respiratory support

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

Excerpt from ERG Guide 132 [Flammable Liquids - Corrosive]:

Some of these materials may react violently with water.

SMALL FIRE: Dry chemical, CO2, water spray or alcohol-resistant foam.

LARGE FIRE: Water spray, fog or alcohol-resistant foam. If it can be done safely, move undamaged containers away from the area around the fire. Dike runoff from fire control for later disposal. Do not get water inside containers.

FIRE INVOLVING TANKS, RAIL TANK CARS OR HIGHWAY TANKS: Fight fire from maximum distance or use unmanned master stream devices or monitor nozzles. Cool containers with flooding quantities of water until well after fire is out. Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank. ALWAYS stay away from tanks in direct contact with flames. For massive fire, use unmanned master stream devices or monitor nozzles; if this is impossible, withdraw from area and let fire burn. (ERG, 2024)

Excerpt from ERG Guide 153 [Substances - Toxic and/or Corrosive (Combustible)]:

SMALL FIRE: Dry chemical, CO2 or water spray.

LARGE FIRE: Dry chemical, CO2, alcohol-resistant foam or water spray. If it can be done safely, move undamaged containers away from the area around the fire. Dike runoff from fire control for later disposal.

FIRE INVOLVING TANKS, RAIL TANK CARS OR HIGHWAY TANKS: Fight fire from maximum distance or use unmanned master stream devices or monitor nozzles. Do not get water inside containers. Cool containers with flooding quantities of water until well after fire is out. Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank. ALWAYS stay away from tanks in direct contact with flames. (ERG, 2024)

Use powder, alcohol-resistant foam, water spray, carbon dioxide. In case of fire: keep drums, etc., cool by spraying with water.

Use water spray, dry chemical, "alcohol resistant" foam, or carbon dioxide. Use water to keep fire-exposed containers cool.

/When fighting fire/ use self-contained breathing apparatus with a full facepiece operated in pressure-demand or other positive pressure mode.

Advice for firefighters: wear self contained breathing apparatus for fire fighting. ...

Combustion may produce irritants and toxic gases.

· CALL 911. Then call emergency response telephone number on shipping paper. If shipping paper not available or no answer, refer to appropriate telephone number listed on the inside back cover.

· Keep unauthorized personnel away.

· Stay upwind, uphill and/or upstream.

· Ventilate closed spaces before entering, but only if properly trained and equipped.

· ELIMINATE all ignition sources (no smoking, flares, sparks or flames) from immediate area.

· All equipment used when handling the product must be grounded.

· Do not touch or walk through spilled material.

· Stop leak if you can do it without risk.

· Prevent entry into waterways, sewers, basements or confined areas.

· A vapor-suppressing foam may be used to reduce vapors.

· Absorb with earth, sand or other non-combustible material.

· For hydrazine, absorb with DRY sand or inert absorbent (vermiculite or absorbent pads).

· Use clean, non-sparking tools to collect absorbed material.

Large Spill

· Dike far ahead of liquid spill for later disposal.

· Water spray may reduce vapor, but may not prevent ignition in closed spaces.

Excerpt from ERG Guide 132 [Flammable Liquids - Corrosive]:

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

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)

Excerpt from ERG Guide 153 [Substances - Toxic and/or Corrosive (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.

Immediate precautionary measure

· Isolate spill or leak area for at least 50 meters (150 feet) in all directions.

· For highlighted materials: see Table 1 - Initial Isolation and Protective Action Distances.

· For non-highlighted materials: increase the immediate precautionary measure distance, in the downwind direction, as necessary.

· 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.

Remove all ignition sources. Personal protection: chemical protection suit including self-contained breathing apparatus. Do NOT let this chemical enter the environment. Collect leaking liquid in sealable containers. Cautiously neutralize spilled liquid with sodium carbonate only under the responsibility of an expert.

Collect leaking liquid in sealable containers. Cautiously neutralize spilled liquid with sodium carbonate only under the responsibility of an expert. Wash away remainder with plenty of water (extra personal protection: chemical protection suit including self-contained breathing apparatus).

Remove all ignition sources, ventilate area of spill or leak. If in liquid form, for small quantities, absorb on paper towels ... large quantities can be collected & atomized in suitable combustion chamber, or diluted ... neutralized & flushed into a sewer. If in the solid form, collect in the most safe & convenient manner for reclamation or allow to melt & collect as above.

Methods and materials for containment and cleaning up: soak up with inert absorbent material (e.g. sand, silica gel, acid binder, universal binder, sawdust). Contain spillage, soak up with non-combustible absorbent material, (e.g. sand, earth, diatomaceous earth, vermiculite) and transfer to a container for disposal according to local/national regulations.

Environmental precautions: prevent further leakage or spillage if safe to do so. Do not let product enter drains.

For more Cleanup Methods (Complete) data for ACETIC ACID (7 total), please visit the HSDB record page.

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.

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.

Burn in a chemical incinerator equipped with an afterburner and scrubber but exert extra care in igniting as this material is highly flammable. Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Contaminated packaging: dispose of as unused product.

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: 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.

Precautions for safe handling: avoid inhalation of vapor or mist. Keep away from sources of ignition - No smoking. Take measures to prevent the build up of electrostatic charge.

Special precautions: Liquid acetic acid will attack some forms of plastics, rubber, and coatings.

Excerpt from ERG Guide 132 [Flammable Liquids - Corrosive]:

ELIMINATE all ignition sources (no smoking, flares, sparks or flames) from immediate area. All equipment used when handling the product must be grounded. Do not touch or walk through spilled material. Stop leak if you can do it without risk. Prevent entry into waterways, sewers, basements or confined areas. A vapor-suppressing foam may be used to reduce vapors. Absorb with earth, sand or other non-combustible material. For hydrazine, absorb with DRY sand or inert absorbent (vermiculite or absorbent pads). Use clean, non-sparking tools to collect absorbed material.

LARGE SPILL: Dike far ahead of liquid spill for later disposal. Water spray may reduce vapor, but may not prevent ignition in closed spaces. (ERG, 2024)

Excerpt from ERG Guide 153 [Substances - Toxic and/or Corrosive (Combustible)]:

ELIMINATE all ignition sources (no smoking, flares, sparks or flames) from immediate area. Do not touch damaged containers or spilled material unless wearing appropriate protective clothing. Stop leak if you can do it without risk. Prevent entry into waterways, sewers, basements or confined areas. Absorb or cover with dry earth, sand or other non-combustible material and transfer to containers. DO NOT GET WATER INSIDE CONTAINERS. (ERG, 2024)

Fireproof. Separated from food and feedstuffs, strong oxidants, strong acids and strong bases. Store only in original container. Well closed. Keep in a well-ventilated room. Store in an area without drain or sewer access.

Store in a dry, well-ventilated place. Separate from oxidizing materials and alkaline substances.

Fireproof. Separate from food and feedstuffs. Keep in a well-ventilated room.

... Quantities greater than 1 liter should be stored in tightly sealed metal containers in areas separate from oxidizers.

· Wear positive pressure self-contained breathing apparatus (SCBA).

· Wear chemical protective clothing that is specifically recommended by the manufacturer when there is NO RISK OF FIRE.

· Structural firefighters' protective clothing provides thermal protection but only limited chemical protection.

163.0 [ppm]

10.0 [ppm]

5.0 [ppm]

35 [ppm]

250 [ppm]

10 ppm (25 mg/m³)

15 ppm (37 mg/m³)

TWA 10 ppm (25 mg/m3) ST 15 ppm (37 mg/m3)

TWA 10 ppm (25 mg/m3)

50 ppm (NIOSH, 2024)

50 ppm [From NPG: Acetic acid] (NIOSH, 2024)

50.0 [ppm]

Excerpts from Documentation for IDLHs: Human data: Marked irritation of the eyes, nose, and upper respiratory tract which could not be tolerated for more than 3 minutes was noted at 816 to 1,226 ppm [von Oettingen 1960]. It has been reported that 50 ppm or more is intolerable to most persons due to intense lacrimation and irritation of the eyes, nose, and throat [AIHA]. It has also been stated that repeated exposures to high concentrations may produce respiratory tract irritation with pharyngeal edema and chronic bronchitis [AIHA 1972].

See: 64197

15.0 [ppm]

8 hr Time Weighted Avg (TWA): 10 ppm; 15 min Short Term Exposure Limit (STEL): 15 ppm.

10 ppm as TWA; 15 ppm as STEL

· Some of these materials may react violently with water.

Small Fire

· Dry chemical, CO2, water spray or alcohol-resistant foam.

Large Fire

· Water spray, fog or alcohol-resistant foam.

· If it can be done safely, move undamaged containers away from the area around the fire.

· Dike runoff from fire control for later disposal.

· Do not get water inside containers.

Fire Involving Tanks, Rail Tank Cars or Highway Tanks

· Fight fire from maximum distance or use unmanned master stream devices or monitor nozzles.

· Cool containers with flooding quantities of water until well after fire is out.

· Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank.

· ALWAYS stay away from tanks in direct contact with flames.

· For massive fire, use unmanned master stream devices or monitor nozzles; if this is impossible, withdraw from area and let fire burn.

ERPG-1: 5 ppm - one hour exposure limit: 1 = mild transient health effects or objectionable odor [AIHA]

ERPG-2: 35 ppm - one hour exposure limit: 2 = impaired ability to take protective action [AIHA]

ERPG-3: 250 ppm - one hour exposure limit: 3 = life threatening health effects [AIHA]

Emergency Response Planning Guidlines (ERPGs) for acetic acid:[Table#36]

A harmful contamination of the air can be reached rather quickly on evaporation of this substance at 20 °C.

The substance is corrosive to the eyes, skin and respiratory tract. Corrosive on ingestion. Inhalation may cause lung oedema, but only after initial corrosive effects on eyes and/or airways have become manifest.

Acetic acid, glacial appears as a clear colorless liquid with a strong odor of vinegar. Flash point 104 °F. Density 8.8 lb / gal. Corrosive to metals and tissue. Used to make other chemicals, as a food additive, and in petroleum production.

Acetic acid, solution, more than 10% but not more than 80% acid appears as a colorless aqueous solution. Smells like vinegar. Corrosive to metals and tissue.

Acetic acid, solution, more than 80% acid is a clear colorless aqueous solution with a pungent odor.

Liquid; Other Solid; Liquid; CBI

Clear, colourless liquid having a pungent, characteristic odour

Colorless liquid or crystals with a sour, vinegar-like odor; Note: Pure compound is a solid below 62 degrees F. Often used in an aqueous solution; [NIOSH]

COLOURLESS LIQUID WITH PUNGENT ODOUR.

clear, colourless liquid/pungent odour

Colorless liquid or crystals with a sour, vinegar-like odor.

Colorless liquid or crystals with a sour, vinegar-like odor. [Note: Pure compound is a solid below 62 °F. Often used in an aqueous solution.]

Clear, colorless liquid

Colorless liquid or crystals (Note: Pure compound is a solid below 62 degrees F). Often used in an aqueous solution).

Sour, vinegar-like odor

Burning taste

244 °F at 760 mmHg (NTP, 1992)

117.9 °C

117.9 °C @760 [mm Hg]

61.9 °F (NTP, 1992)

16.635 °C

16.64 °C

104 °F (NTP, 1992)

103 °F (NFPA, 2010)

The Guide from the Emergency Response Guidebook is for "acetic acid, glacial." 39 °C

103 °F (39 °C) Closed cup

112 °F (open cup); 104 °F (closed cup)

39 °C c.c.

greater than or equal to 100 mg/mL at 73 °F (NTP, 1992)

Miscible with water

Miscible with ethanol, ethyl ether, acetone, benzene; soluble in carbon tetrachloride, carbon disulfide

Miscible with glycerol; insoluble in carbon disulfide

1000.0 mg/mL

Solubility in water: miscible

miscible with water, alcohol, and glycerrin

(in ethanol)

Miscible

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

1.0446 g/cu cm at 25 °C

Density: 1.266 at 16.60 °C (solid); 1.053 at 16.67 °C (liquid); contracts slightly on freezing

Relative density (water = 1): 1.05

1.049 @ 20°C

Flammable. Water soluble. Dissolution generates some heat.

Dilution with water releases some heat.

An aqueous solution. Dilution can generate heat.

Acids, Carboxylic

Water and Aqueous Solutions

CSL00067

Acetic anhydride + ACETIC ACID + NITRIC ACID

Potentially explosive

Explosive

User-Reported

CSL00202

1,3,5-Benzenetriol, 2,4,6-trinitro-, potassium salt + Water + Acetic Acid + Potassium nitrite + Potassium hydroxide + Ethanol

"The potassium salt of 2,4,6-trinitroso-1,3,5-benzenetriol, prepared in our laboratory precisely according to the literature procedure of R. Benedikt (Chem. Ber. 1878, 11, 1374), unexpectedly exploded. 1,3,5-Benzenetriol (1 g, 7.9 mmol) dissolved in 30 mL of H2O and 3 mL of glacial acetic acid was cooled at 6-9 °C and 3 equivalents of potassium nitrite (2 g, 23.7 mmol) in 2 mL water was added. The reaction mixture immediately became brownish and was stirred an additional 30 minutes. Potassium hydroxide (1.4 g, 23.7 mmol) was added, followed by 10 mL of ethanol. The precipitate of dark green crystals was filtered off to give the potassium salt (48%), which was stored in a covered flask on the bench. An hour and a half later, it exploded spontaneously, damaging some glass containers. According to the original report, 2,4,6-trinitroso-1,3,5-benzenetriol decomposes on heating at 130 °C." (reprint of full text)

Response by Neal Langerman" "Nitroso compounds are well documented as energetic and frequently spontaneously decompose (“Bretherick’s Handbook of Reactive Chemical Hazards,” P. G. Urben, editor, 7th Ed., Academic Press, 2007, and “Explosives,” Rudolf Meyer, Josef Köhler, Axel Homburg, 6th Ed., Wiley-VCH, 2007). The compound being synthesized by Katritzky is very similar to the known explosive compound 2,4,6-trinitrobenzene-1,3-diol and the unstable compound 2,4,6-trinitrobenzene-1,3,5-triol (see Bretherick’s). The metal salts of the latter are explosive. Given this literature information, it is reasonable to expect the trinitroso compound to be unstable and explosive. Under these circumstances, synthetic chemistry should be conducted with appropriate controls to prevent an explosion and to limit the size of an energetic event, should one occur." (reprint of full text). Literature citation: Langerman, Neal. esponse to an unexpected explosion. Chem. Eng. News 2008, 86 (40), 5. DOI: 10.1021/cen-v086n040.p004. (Letters: chemical safety)

10.1021/cen-v086n040.p004

Literature Reference

10/20/2022

CSL00208

3-Iodoxybenzoic Acid + Acetic acid + Sodium hypochlorite; Bleach

"We wish to warn the chemical community of a serious shock sensitivity hazard associated with 3-iodoxybenzoic acid [64297-65-0], a reagent popularized by Derek Barton and coworkers [J. Chem. Soc., Perkin Trans. I, 8, 1947 (1982)] for preparing enones from ketones in the presence of catalytic diphenyl diselenide. We recently prepared this reagent on a 200-g scale following the generic one-step procedure for iodoxybenzene given in the above reference using acetic acid and commercial bleach. After collecting the solid product in a Buchner fritted glass funnel, rinsing, and air drying, the compound was being transferred with a spoon into a bottle for storage when it suddenly exploded. The funnel was destroyed, and glass fragments were propelled with such force to break several glass items in the vicinity. Fortunately, the operator received only minor cuts and skin/eye irritation as a result of wearing proper gloves, lab coat, and safety glasses, and was fine after prompt treatment. While this compound was known to deflagrate at its melting point, 225°C [J. Labelled Compd. Radiopharm., 19, 1161 (1982)], its shock sensitivity has not been reported. Our incident prompts us to warn that 3-iodoxybenzoic acid, prepared according to the Barton reference above, presents a severe shock hazard, and utmost care is required for its handling. We cannot state with certainty whether the explosion was due to the compound itself or was perhaps initiated by residual bleach or other impurities." (reprint of full text)

Large (>100g)

10.1021/cen-v080n026.p002

10/22/2022

Mixing acetic acid in equal molar portions with any of the following substances in a closed container caused the temperature and pressure to increase: 2-Aminoethanol, chlorosulfonic acid, ethylene diamine, ethyleneimine [NFPA 1991]. Acetic acid or acetic anhydride can explode with nitric acid if not kept cold. Potassium hydroxide residue in a catalyst pot reacted violently when acetic acid was added [MCA Case History 920. 1963]. During the production of terephthalic acid, n-xylene is oxidized in the presence of acetic acid. During these processes, detonating mixtures may be produced. Addition of a small amount of water may largely eliminate the risk of explosion [NFPA 491M.1991.p. 7]. Acetaldehyde was put in drums previously pickled with acetic acid. The acid caused the acetaldehyde to polymerize and the drums got hot and vented [MCA Case History 1764. 1971]. A mixture of ammonium nitrate and acetic acid ignites when warmed, especially if concentrated [Von Schwartz 1918. p. 322 ]. Several laboratory explosions have been reported using acetic acid and phosphorus trichloride to form acetyl chloride. Poor heat control probably caused the formation of phosphine [J. Am. Chem. Soc. 60:488. 1938]. Acetic acid forms explosive mixtures with p-xylene and air (Shraer, B.I. 1970. Khim. Prom. 46(10):747-750.).

ACETIC ACID reacts exothermically with chemical bases. Subject to oxidation (with heating) by strong oxidizing agents. Dissolution in water moderates the chemical reactivity of acetic acid, A 5% solution of acetic acid is ordinary vinegar. Acetic acid forms explosive mixtures with p-xylene and air (Shraer, B.I. 1970. Khim. Prom. 46(10):747-750.).

Mixing ACETIC ACID in equal molar portions with any of the following substances in a closed container caused the temperature and pressure to increase: 2-Aminoethanol, chlorosulfonic acid, ethylene diamine, ethyleneimine [NFPA 1991]. Acetic acid or acetic anhydride can explode with nitric acid if not kept cold. Potassium hydroxide residue in a catalyst pot reacted violently when acetic acid was added [MCA Case History 920. 1963]. During the production of terephthalic acid, n-xylene is oxidized in the presence of acetic acid. During these processes, detonating mixtures may be produced. Addition of a small amount of water may largely eliminate the risk of explosion [NFPA 491M.1991.p. 7]. Acetaldehyde was put in drums previously pickled with acetic acid. The acid caused the acetaldehyde to polymerize and the drums got hot and vented [MCA Case History 1764. 1971]. A mixture of ammonium nitrate and acetic acid ignites when warmed, especially if concentrated [Von Schwartz 1918. p. 322 ]. Several laboratory explosions have been reported using acetic acid and phosphorus trichloride to form acetyl chloride. Poor heat control probably caused the formation of phosphine [J. Am. Chem. Soc. 60:488. 1938]. Acetic acid forms explosive mixtures with p-xylene and air (Shraer, B.I. 1970. Khim. Prom. 46(10):747-750.).

Incompatibilities: carbonates, hydroxides, many oxides, and phosphates.

Cooling is necessary to prevent possible explosion from contact of potassium permanganate (or the calcium or sodium salts) with acetic acid

Liquid acetic acid will attack some forms of plastics, rubber, and coatings.

An explosion occurred during initial heating up of a large volume of glacial acetic acid being treated with chromium trioxide. This was attributed to violent interaction of solid chromium trioxide and liquid acetic acid on a hot, exposed steam coil, and subsequent initiation of an explosive mixture of acetic acid vapor and air. The risk has been obviated by using a solution of dichromate in sulfuric acid as oxidant, in place of chromium trioxide. The sulfuric acid is essential, as the solid dichromate moist with acetic acid, obtained by evaporating an acetic acid solution to near-dryness, will explode.

For more Hazardous Reactivities and Incompatibilities (Complete) data for ACETIC ACID (22 total), please visit the HSDB record page.

Strong oxidizers (especially chromic acid, sodium peroxide & nitric acid), strong caustics [Note: Corrosive to metals.]

Safe in the present practices of use and concentration. Ingredient, concentration, and use information are available in documents discoverable at https://cir-reports.cir-safety.org

IDENTIFICATION AND USE: Acetic acid is a colorless liquid or solid, having a pungent characteristic odor, and when diluted in water an acidic taste. Glacial acetic acid is a 99% active chemical. It is used as an acidifier, flavoring agent, for the prevention of rope in baking, and as a solvent. Acetic acid is used as a laboratory reagent in chemical and biochemical analysis, in field testing of lead fumes, vinyl chloride determination, uric acid in urine, aniline vapors, and separation of gases. In addition, acetic acid is used in pesticide formulations as a herbicide to controls weeds on fruits, vegetables, ornamentals and turf. It is also a component of the hydraulic fracturing fluids preventing precipitation of metal oxides (iron control). Registered for use in the U.S., but approved pesticide uses may change periodically, so federal, state and local authorities must be consulted for currently approved uses. Three to 5% acetic acid is commonly used in the field of gynecology for colposcopic examinations of the cervix. It gives an 'acetowhite' effect that may assist clinicians in identifying neoplastic areas. HUMAN EXPOSURE AND TOXICITY: Acetic acid is absorbed from the gastrointestinal tract and through the lungs and almost completely oxidized by tissues. The metabolic pathways are reasonably well known and involve the formation of ketone bodies. As little as 1.0 mL of glacial acetic acid has resulted in perforation of the esophagus. During acetic acid dialysis, patients showed a frequent onset of sudden hypotension and arrhythmia with concomitant symptoms of the so-called disequilibrium syndrome. Extreme eye and nasal irritation has occurred at concentrations in excess of 25 ppm and conjunctivitis from concentrations below 10 ppm has been reported. Glacial acetic acid has caused permanent corneal opacification. Ingestion of 200 mL of an 80% solution of acetic acid caused repeated shock due to myocardial infarction and massive intestinal bleeding led to an organic brain psychosyndrome. The patient survived the intoxication by use of hemodialysis and intensive care therapy. An excess of prostate cancer was observed among former chemical plant workers, some of whom had been exposed to both acetic acid and acetic anhydride. ANIMAL STUDIES: Toxic effects of acetic acid are due to irritant properties as well as its effect on the central nervous system and kidneys. Large oral doses cause CNS depression and death in rats and mice. Inhalation of 16,000 ppm killed 1 of 6 exposed rats. Groups of 3-6 rats were given acetic acid in drinking water for periods from 9-15 weeks. Fluid uptake was the same in all treatment groups, at the high dose group there was a progressive reduction in body weight gain, loss of appetite and fall in food consumption. Four groups of two young pigs were fed daily diets for successive 30 day periods for a total of 150 days. There were differences in growth rate, weight gain, early morning urinary ammonia and terminal blood pH between controls and test groups. Acetic acid had no effects on implantation or on maternal or fetal survival in rats, mice or rabbits dosed via gavage during gestation days 6-19 at doses up to 1600 mg/kg/day. The number of abnormalities seen in either soft or skeletal tissues of the test groups did not differ from the number occurring in the controls. Acetic acid has shown no evidence of mutagenic activity with or without metabolic activation using several strains of Salmonella typhimurium. Acetic acid did not show clastogenicity on cultured Chinese hamster ovary K1 cells at neutral pH, but it was clastogenic at pH 5.2 to 6.0 with or without metabolic activation. ECOTOXICITY STUDIES: Acetic acid was harmful to aquatic life. High concentrations produced pH levels toxic to oxidizing bacteria, inhibiting oxygen demand. It was lethal to Mosquito fish: at 320 ppm and higher all fish were dead at 24 hours.

Acetic acid is toxic due to its corrosive nature. In addition to causing skin burns and irritation to the mucous membranes, ingestion can result in severe damage to the digestive system and a potentially lethal change in the acidity of the blood. (L1885)

No indication of carcinogenicity to humans (not listed by IARC).

Concentrated acetic acid is corrosive and can cause skin burns, permanent eye damage, and irritation to the mucous membranes. Ingestion can cause severe damage to the digestive system and a potentially lethal change in the acidity of the blood. (L1885)

Serious local effects by all routes of exposure.

inhalation, skin and/or eye contact

Oral (L1886) ; ihalation (L1886) ; ingestion (L1886)

Sore throat. Cough. Burning sensation. Headache. Dizziness. Shortness of breath. Laboured breathing.

Pain. Redness. Skin burns. Blisters.

Redness. Pain. Severe burns. Loss of vision.

Sore throat. Burning sensation. Abdominal pain. Vomiting. Shock or collapse.

irritation eyes, skin, nose, throat; eye, skin burns; skin sensitization; dental erosion; black skin, hyperkeratosis; conjunctivitis, lacrimation (discharge of tears); pharyngeal edema, chronic bronchitis

Acetic acid is corrosive and can cause skin burns and irritation to the mucous membranes. These burns or blisters may not appear until hours after exposure. (L1885)

Eyes, skin, respiratory system, teeth

Dermatotoxin - Skin burns.

Lacrimator (Lachrymator) - A substance that irritates the eyes and induces the flow of tears.

Asthma - Reversible bronchoconstriction (narrowing of bronchioles) initiated by the inhalation of irritating or allergenic agents.

Toxic Pneumonitis - Inflammation of the lungs induced by inhalation of metal fumes or toxic gases and vapors.

LC50 (mice) = 5,620 ppm/1 hr

LD50: 3.53 g/kg (Oral, Rat) (T66)

LD50: 525 mg/kg (Intravenous, Mouse) (T14)

LD50: 1060 mg/kg (Dermal, Rabbit) (T14)

LC50: 5620 ppm over 1 hour (Inhalation, Mouse) (A717)

LD50 Rat oral 3.53 g/kg

LD50 Mouse iv 525 mg/kg

LD50 Rabbit dermal 1060 mg/kg

LD50 Mouse oral 4960 mg/kg

For more Non-Human Toxicity Values (Complete) data for ACETIC ACID (9 total), please visit the HSDB record page.

In cases of skin or eye exposure, the area should be flushed with water and burns covered with dry, sterile dressings after decontamination. If ingested, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution. Watch for signs of respiratory insufficiency and assist respiration if necessary. (A569)

Pain increases the rate, frequency, or intensity of some behaviors (eg, withdrawal responses) and suppresses other behaviors (eg, feeding). /The study is/ developing assays to test analgesic drug candidates using measurements of pain-suppressed rather than pain-elicited behaviors. Such assays may model important aspects of clinical pain and provide a means for distinguishing true analgesics from drugs that produce motor impairment. The present study compared effects of the mu opioid analgesic morphine and the nonanalgesic neuroleptic haloperidol on intraperitoneal acetic acid-induced writhing (a pain-elicited behavior) and suppression of feeding behavior (a pain-suppressed behavior). In feeding studies, C57BL/6J mice were given access to a dish containing 8 mL Ensure (trade mark) liquid food (0-100% in water) during daily sessions (7.5-120 min). Levels of consumption were dependent on both Ensure concentration and session duration. Intraperitoneal injection of acetic acid (0.10-0.56%) produced a time- and concentration-dependent decrease in Ensure consumption. Morphine (1 mg/kg) prevented both acid-induced writhing and acid-induced suppression of feeding, whereas the dopamine antagonist haloperidol inhibited writhing without preventing acid-induced suppression of feeding. The effects of morphine were time-dependent, selective for acid-suppressed feeding, and naltrexone-reversible. These results suggest that assays of pain-suppressed behaviors may complement assays of pain-elicited behaviors in preclinical studies of candidate analgesics...

Amylin is a member of calcitonin or calcitonin gene-related peptide (CGRP) family. Immunohistochemical study revealed a dense network of amylin-immunoreactive (irAMY) cell processes in the superficial dorsal horn of the mice. Numerous dorsal root ganglion (DRG) and trigeminal ganglion cells expressed moderate to strong irAMY. Reverse transcriptase-polymerase chain reaction (RT-PCR) revealed amylin receptor mRNA in the mouse spinal cord, brain stem, cortex, hypothalamus and hippocampus. The nociceptive or antinociceptive effects of amylin were evaluated in the acetic acid-induced writhing test. Amylin (0.1, 0.5 and 1 mg/kg, intraperitoneally (i.p.) or 1-10 microg, intrathecally (i.t.)) reduced the number of writhes in a dose-dependent manner. Pretreatment of the mice with the amylin receptor antagonist salmon calcitonin (8-32), either by i.p. or i.t., antagonized the effect of amylin on acetic acid-induced writhing test. Locomotor activity was not significantly modified by amylin injected either i.p. (0.01-1 mg/kg) or i.t. (1-10 microg). Measurement of c-fos mRNA by RT-PCR or proteins by Western blot showed that the levels were upregulated in the spinal cord of mice injected with acetic acid and the increase was attenuated by pretreatment with amylin (10 microg, i.t.). Collectively, /these/ result demonstrates that irAMY is expressed in DRG neurons with their cell processes projecting to the superficial layers of the dorsal horn, and that the peptide by interacting with amylin receptors in the spinal cord may be antinociceptive.

INTRODUCTION: Increased free-radical production, decreased antioxidant capacity, and excessive inflammation are well-known features in the pathogenesis of inflammatory bowel disease. Melatonin is a powerful antioxidant and a scavenger of hydroxyl radicals. Melatonin has also been shown to have anti-inflammatory activities in tissues. /This/ study objective is to investigate the effects of melatonin on tissue inflammatory activities using an ulcerative colitis (UC) model induced by acetic acid (AA) in rats. METHODS: Wistar rats (n = 32) were divided into four groups. AA-induced colitis was performed in two of the groups, while the other two groups were injected with saline intrarectally. One of the AA-induced colitis groups and one of the control groups were administered 100 mg/kg/day melatonin intraperitoneally, and the pair groups were given saline. After 4 days, colonic changes were evaluated biochemically by measuring proinflammatory cytokines [tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6], myeloperoxidase (MPO), malondialdehyde (MDA), glutathione (GSH), and superoxide dismutase (SOD) levels in tissue homogenates and by histopathological examination. RESULTS: AA caused colonic mucosal injury, whereas melatonin suppressed these changes in the AA-induced colitis group (P < 0.001). AA administration resulted in increased TNF-alpha, IL-1beta, IL-6, MPO, and MDA levels, and decreased GSH and SOD levels, whereas melatonin administration reversed these effects (all P < 0.001). CONCLUSIONS: The present study proposes that melatonin has a dual action as an effective anti-inflammatory and an antioxidant, and may be a hopeful therapeutic agent for UC.

In the present study, the effect of chronic oral administration of curcumin in the presence or absence of morphine and noloxone was investigated on the visceral nociception induced by acetic acid in rats. Intraperitoneal injection of acetic acid (1 mL, 2%) produced contractions in the abdominal musculature (writhes). The latency time to the beginning of the first writhe was measured and the total number of writhes in the 1 hr after acetic acid injection was counted. The latency time to the beginning of the first writhe was significantly (p < 0.05) increased and the number of writhes was significantly (p < 0.05) decreased by curcumin (20 and 40 mg/kg body weight). The same results were obtained after subcutaneous injection of morphine (1 mg/kg b.wt.). Naloxone at the dose of 1 mg/kg body weight had no effect on pain intensity. Curcumin significantly (p < 0.05) enhanced the effect of morphine on the visceral pain responses, however did not reverse the effect of naloxone. Present data suggest that in the acetic acid-induced visceral nociception of rats, curcumin may produce an antinociceptive effect and the endogenous analgesic opioid system is involved in the curcumin-induced antinociception.

Nine out bred white male rats weighing approximately 100 g were used in /this/ study. Rats were given either N-nitrosarcosin ethyl ester (NSEE) alone, NSEE with the acetic acid solution, or the acetic acid solution alone. doses (0.5 mL of 3% water solution of acetic acid (about 60 mg/kg bw/treatment) were given by intubation into the esophagus 3 times per week. Animals were killed by ether inhalation after 8 months of experiments and autopsied. As expected, rats treated with the carcinogen NSEE had high incidences of pre-neoplastic lesions of the esophagus and forestomach, as well as benign tumors, carcinomas and squamous cell cancer. Prolonged administration of acetic acid in combination with NSEE resulted in an increase in the number of benign and malignant tumors and carcinomas in the esophagus. Prolonged administration of acetic acid alone did not induce tumors. All nine of these rats, however, did experience hyperplasia in the esophagus and forestomach.

Garlic contains many sulfhydryl compounds that act as antioxidants. However, the role of nitric oxide (NO) in inflammation is controversial. The aim of the present study is to investigate the possible protective effect of garlic against acetic acid-induced ulcerative colitis in rats, as well as the probable modulatory effect of L-arginine (NO precursor) on garlic activity. Intra-rectal inoculation of rats with 4% acetic acid for 3 consecutive days caused a significant increase in the colon weight and marked decrease in the colon length. In addition, acetic acid induced a significant increase in serum levels of nitrate as well as colonic tissue content of malondialdehyde (MDA). Moreover, colonic tissue contents of glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) were markedly reduced. On the other hand, pre-treatment of rats with garlic (0.25 g/kgbwt, orally) for 4 consecutive weeks and 3 days during induction of colitis significantly reduced the increase in the colon weight induced by acetic acid and ameliorated alterations in oxidant and antioxidant parameters. Interestingly, oral co-administration of garlic (0.25 g/kgbwt) and L-arginine (625 mg/kgbwt) for the same period of garlic administration mitigated the changes in both colon weight and length induced by acetic acid and increased garlic effect on colon tissue contents of MDA and GSH. In conclusion, L-arginine can augment the protective effect of garlic against ulcerative colitis; an effect that might be mainly attributed to its NO donating property resulting in enhancement of garlic antioxidant effect...

The "cholinergic anti-inflammatory pathway" provides neurological modulation of cytokine synthesis to limit the magnitude of the immune response. This study aimed to evaluate the impact of the cholinergic anti-inflammatory pathway on the extent of tissue integrity, oxidant-antioxidant status and neutrophil infiltration to the inflamed organ in a rat model of acetic acid-induced colitis. Colitis was induced by intrarectal administration of 5% acetic acid (1mL) to Sprague-Dawley rats (200-250g; n=7-8 per group). Control group received an equal volume of saline intrarectally. The rats were treated with either nicotine (1mg/kg/day) or huperzine A (0.1mg/kg/day) intraperitoneally for 3 days. After decapitation, the distal colon was scored macroscopically and microscopically. Tissue samples were used for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels, and myeloperoxidase (MPO) activity. Formation of reactive oxygen species was monitored by using chemiluminescence (CL). Nuclear factor (NF)-kappaB expression was evaluated in colonic samples via immunohistochemical analysis. Trunk blood was collected for the assessment of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-10, resistin and visfatin levels. Both nicotine and huperzine A reduced the extent of colonic lesions, increased colonic MDA level, high MPO activity and NF-kappaB expression in the colitis group. Elevation of serum IL-1beta level due to colitis was also attenuated by both treatments. Additionally, huperzine A was effective to reverse colitis-induced high lucigenin-enhanced CL values and serum TNF-alpha levels. Colitis group revealed decreased serum visfatin levels compared to control group which was completely reversed by nicotine. In conclusion, modulation of the cholinergic system either by nicotine or ACh esterase inhibition improved acetic acid-induced colonic inflammation as confirmed by macroscopic and microscopic examination and biochemical assays.

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. /Organic acids 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 necessary. 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 ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool. Activated charcoal is not effective ... . Do not attempt to neutralize because of exothermic reaction. Cover skin burns with dry, sterile dressings after decontamination ... . /Organic acids and related compounds/

For more Antidote and Emergency Treatment (Complete) data for ACETIC ACID (6 total), please visit the HSDB record page.

Employees should be screened for history of ... /chronic respiratory, skin and, eye diseases/ ... which might place the employee at an increased risk from acetic acid exposure.

/HUMAN EXPOSURE STUDIES/ Six patients with frequent episodes of symptomatic hypotension during acetate dialysis were treated with bicarbonate dialysis. ... During acetate dialysis, the patients showed a frequent onset of sudden hypotension and arrhythmia with concomitant symptoms of the so-called disequilibrium syndrome. None of these symptoms were seen during bicarbonate dialysis. /Acetate/

/HUMAN EXPOSURE STUDIES/ Acetic acid is used in plastics, chemical and pharmaceutical industries. ...The aim of this study was to evaluate acute irritation during controlled exposure to vapors of acetic acid. Six female and six male healthy volunteers were exposed to 0 ppm (control exposure), 5 and 10 ppm acetic acid vapor for 2 hr at rest in a balanced order. Subjective ratings of nasal irritation and smell increased significantly with exposure level. Except for smell, all average ratings at 10 ppm were at the lower end of the 0-100mm visual analogue scale, and did not exceed the verbal expression "somewhat" (26 mm). No effects on pulmonary function, nasal swelling, nasal airway resistance or plasma inflammatory markers (C-reactive protein, and interleukin-6), measured before and after exposure, were seen. There was a non-significant tendency to increased blinking frequency, as measured continuously during exposure, after exposure to 10 ppm acetic acid. In conclusion, our study suggests a mild irritative effect at 10 ppm acetic acid.

EC50; Species: Chlorococcales (Green Algae Order); Conditions: freshwater, static; Concentration: 156000 ug/L for 24 hr; Effect: physiology, assimilation efficiency /formulation/

LC50; Species: Crangon septemspinosa (Bay Shrimp, Sand Shrimp) weight 0.003 g; Conditions: saltwater, renewal, 15 °C, pH 3.64-8.07; Concentration: 116000 ug/L for 14 days (95% confidence interval: 85900-157000 ug/L) /99.7% purity/

LC50; Species: Crangon septemspinosa (Bay Shrimp, Sand Shrimp) weight 0.003 g; Conditions: saltwater, static, 15 °C, pH 2.26-7.96; Concentration: 158000 ug/L for 96 hr (95% confidence interval: 50000-500000 ug/L) /99.7% purity/

EC50; Species: Daphnia magna (Water flea); Conditions: static bioassay, neutralized to pH 8.0 and 20 °C; Concentration: 6,000 mg/L for 24 hr; Effect: immobilization

For more Ecotoxicity Values (Complete) data for ACETIC ACID (25 total), please visit the HSDB record page.

/AQUATIC SPECIES/ Acetic acid is harmful to aquatic life. High concentrations will produce pH levels toxic to oxidizing bacteria, inhibiting oxygen demand.

/AQUATIC SPECIES/ Ten Mosquito fish were exposed to test concentrations for a period of 96 hours. The concentrations used for the first experiment were 10, 18, 32, 56 and 100 ppm. When deaths did not occur at these concentrations within 96 hours the same series was run between 100 and 1,000 ppm. The temperature, turbidity, and pH of the experimental water were measured after the test substance was added and daily throughout the experiment. Survivor observations were made at 24, 48, 72 and 96 hours. Test water was maintained at pH 6.9 -8.7 and 16-25 °C. Fish transferred to concentrations between 100 and 1,000 ppm swam frantically and at 100 and 180 ppm returned to normal in 24 hours. At 320 ppm and higher all fish were dead at 24 hours.

The substance is harmful to aquatic organisms.

Acetic acid's production and use in the in the manufacture of various acetates and other chemicals, food preservation, textile dyeing, and as a pharmaceutical aid may result in its release to the environment through various waste streams. Its use in hydrofracking operations will result in its direct release to the environment. Atmospheric emissions occur from combustion of biomass, plastics and refuse and in exhaust from gasoline and diesel engines. Acetic acid is a natural product of fermentation and widely used in the form of common vinegar. Acetic acid occurs in ocean water, oilfield brines, rain, and at trace concentrations in many plant and animal liquids. Formation of acetic acid can occur via the reaction of olefins with ozone in the atmosphere. Decomposition of solid biological wastes produces acetic acid which is readily metabolized by living organisms; acetic acid occurs as a normal metabolite in both plants and animals. If released to air, a vapor pressure of 15.7 mm Hg at 25 °C indicates acetic acid will exist solely as a vapor in the ambient atmosphere. The pure compound is a solid below 68 °F. Vapor-phase acetic acid 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 22 days. Particulate-phase acetic acid will be removed from the atmosphere by wet and dry deposition. Acetic acid does not absorb light with wavelengths >290 nm, and is not expected to be susceptible to direct photolysis by sunlight. Acetic acid occurs in rainwater, cloud water and fog and can be removed from the atmosphere by wet deposition. If released to soil, acetic acid is expected to have very high mobility based upon a Koc value of 1.0. The pKa of acetic acid is 4.76, indicating that this compound will exist partially in anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts. Volatilization from moist soil surfaces is not expected to be an important fate process based upon a Henry's Law constant of 1.43X10-7 atm-cu m/mole. Acetic acid is expected to volatilize from dry soil surfaces based upon its vapor pressure. Using a modified Organization of Economic Cooperation and Development (OECD) protocol, 75% degradation was reported in 14 days using garden soil as an inoculum, indicating that biodegradation is an important environmental fate process in soil. A variety of biological screening studies have determined that acetic acid biodegrades readily under anaerobic conditions. If released into water, acetic acid is not expected to adsorb to suspended solids and sediment based upon the Koc value. Utilizing the Japanese MIT test, a 74% of theoretical BOD in 2 weeks using activated sludge indicates 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 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 acetic acid may occur through inhalation and dermal contact with this compound at workplaces where acetic acid is produced or used. Acetic acid occurs ubiquitously and is a normal metabolite in animals; therefore, the general population is continually exposed to the compound. Monitoring data indicate that the general population may be exposed to acetic acid via inhalation of ambient air, ingestion of food, and dermal contact with consumer products containing acetic acid. (SRC)

Acetic acid was reported as a reaction product from the biodegradation of petroleum compounds in groundwater(1). Formation of acetic acid can occur via the reaction of olefins with ozone in the atmosphere(2). Decomposition of solid biological wastes produces acetic acid which is readily metabolized by living organisms(3); acetic acid occurs as a normal metabolite in both plants and animals(3). It occurs in various vegetation(4). Acetic acid was one of the compounds identified in the volatile emission samples from various plant species sampled in the US(5).

Acetic acid is found in ocean water, oilfield brines, rain, and at trace concentrations in many plant and animal liquids. It is central to all biological energy pathways. Fermentation of fruit and vegetable juices yields 2-12% acetic acid solutions, usually called vinegar. Any sugar-containing sap or juice can be transformed to dilute acetic acid by bacterial or fungal processes(1). Acetic acid has been detected in various plants including gum tragacanth, cacao, flax, linseed, purging croton, grapes, grapevine, merrill flowers, ginseng, licorice, parsley, cilantro, coriandor, myrtle, blueberry and pineapple(2).

Acetic acid's production and use in the manufacture of various acetates, acetyl compounds, cellulose acetate, acetate rayon, plastics and rubber in tanning; as laundry sour; printing calico and dyeing silk; as acidulant and preservative in foods; solvent for gums, resins, volatile oils and many other substances, wide use in commercial organic syntheses, aqueous and non-aqueous acid-base titrations, trace metal analysis, and as a pharmaceutic aid (acidifier)(1) may result in its release to the environment through various waste streams(SRC). Its use in hydrofracking operations(2) will result in its direct release to the environment(SRC). Atmospheric emissions occur from combustion of biomass, plastics and refuse and in exhaust from gasoline and diesel engines(3-6).

TERRESTRIAL FATE: Based on a classification scheme(1), an experimentally derived Koc value of 1.0(2,3), indicates that acetic acid is expected to have very high mobility in soil(SRC). No detectable sorption was measured for acetic acid using the OECD Guideline 106 method in three different soils(4). The pKa of acetic acid is 4.76(5), indicating that this compound will exist predominantly in anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(6). Volatilization of acetic acid from moist soil surfaces is not expected to be an important fate process(SRC) given a Henry's Law constant of 1.43X10-7 atm-cu m/mole(7). Acetic acid is expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 15.7 mm Hg at 25 °C(8). Using a modified Organization of Economic Cooperation and Development (OECD) protocol, 75% degradation was reported in 14 days using garden soil as an inoculum(9), indicating that biodegradation is an important environmental fate process in soil(SRC).

AQUATIC FATE: Based on a classification scheme(1), a Koc value of 1.0(2,3), indicates that acetic acid is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(4) based upon a Henry's Law constant of 1.43X10-7 atm-cu m/mole(5). The pKa of acetic acid is 4.76(6), indicating that this compound will exist predominantly in anion form at an environmental pH range of 5-9. According to a classification scheme(7), an estimated BCF of 3(SRC), from its log Kow of -0.71(8) and a regression-derived equation(9), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Hydrolysis is not expected to be an important environmental fate process(SRC) since this compound lacks functional groups that hydrolyze under environmental conditions(4). Utilizing the Japanese MITI test, a 74% of theoretical BOD in 2 weeks using activated sludge(10) indicates that biodegradation is an important environmenal fate process in water(SRC).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), acetic acid, which has a vapor pressure of 15.7 mm Hg at 25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. The pure compound is a solid below 68 °F(3). Particulate-phase acetic acid will be removed from the atmosphere by wet and dry deposition. Vapor-phase acetic acid 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 22 days(SRC), calculated from its measured rate constant of 7.4X10-13 cu cm/molecule-sec at 25 °C(4). Particulate-phase acetic acid will be removed from the atmosphere by wet and dry deposition. Acetic acid does not absorb light with wavelengths >290 nm(5) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC). Acetic acid occurs in rainwater, cloud water and fog(6-8) and can be removed from the atmosphere by wet deposition(SRC).

Biological oxygen demand after 10 days at 20 °C is: 82% biological oxidation in fresh water and 88% biological oxidation in sea water

AEROBIC: In a closed bottle test, acetic acid (2 ppm) achieved 51-99% of its theoretical Biochemical Oxygen Demand (BOD) after 5-30 days(1). In a 30-day Warburg respirometer test, acetic acid achieved 60% of its theoretical BOD using acclimated sewage seed(2). Acetic acid was found to degrade >90% after 3 days in a Zahn-Wellens test using an activated sludge inoculum(3). In a 5-day French Association for Standardization (AFNOR) T 90/103 test, acetic acid achieved 36% of its theoretical BOD using microbes from 3 polluted surface waters(4). Acetic acid reached an average 5-day theoretical BOD of 57.7% using standard dilution BOD water(5). In water-die away tests, acetic acid was found to degrade 12.3% per hr in estuarine water, 1.0% per hr in Belgian coastal water, and 0.06% per hr in open seawater(6). In five days, the BOD consumed was 76% and 66% of theoretical using a sewage inoculum and freshwater and synthetic seawater, respectively(7). Using batch aeration in sewage, acetic acid degraded 99.5% in 24 hr(8). In a Warburg respirometer test, 40% of its theoretical BOD was achieved for acetic acid after 24 hours using activated sludge inoculum(9). Acetic acid, present at 100 mg/L, reached 74% of its theoretical BOD in 2 weeks using an activated sludge inoculum at 30 mg/L in the Japanese MITI test(10). A laboratory soil degradation half-life of 2 days was measured in two soils collected from north-eastern Poland(11).

AEROBIC: In a 5-day Warburg respirometer test using sewage inoculum, acetic acid lost 77% of its theoretical BOD(1). Nearly complete loss of BOD for acetic acid was observed after 6 hr aeration with settled, acclimated domestic sewage inocula(2). Acetic acid (4 ppm) reached 81.3 and 77.6% of its theoretical BOD after 5 days using a standard dilution method and a sea water dilution method, respectively(3). In a 10-day electrolytic respirometer test, acetic acid reached 87% of its theoretical BOD(4). Using a modified Organization of Economic Cooperation and Development (OECD) protocol, 75 and >90% degradation of acetic acid was observed after 14 days using garden soil and sediment from the Rhine River as inoculum, respectively(5).

ANAEROBIC: In a biofilm column study, 95% removal of acetic acid under aerobic conditions, and 99% removal under methanogenic conditions was observed(1).

The rate constant for the vapor-phase reaction of acetic acid with photochemically-produced hydroxyl radicals has been measured as 7.40X10-13 cu cm/molecule-sec at 25 °C(1). This corresponds to an atmospheric half-life of about 22 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(2). Acetic acid is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(3). Acetic acid does not absorb light with wavelengths >290 nm(4) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC).

An estimated BCF of 3 was calculated in fish for acetic acid(SRC), using a log Kow of -0.17(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).

Acetic acid shows no potential for biological accumulation or food chain contamination.

A log Koc of 0.00 (Koc = 1), which was derived from experimental measurements, has been reported for acetic acid(1,2). According to a classification scheme(3), this Koc value suggests that acetic acid is expected to have very high mobility in soil. No detectable sorption was measured for acetic acid using the OECD Guideline 106 method employing an acidic forest soil, pH 2.8, an agricultural soil, pH 6.7, and a lake sediment, pH 7.1(4). Adsorption of acetic acid to 3 nearshore marine sediments collected from three different locations resulted in Kd values of 0.65 (Koc = 228), 0.085 (Koc = 6.5) and 0.046 (Koc = 27) using clastic mud (3.5% organic carbon, pH 7.0), muddy sand (1.3% organic carbon, pH 7.7), and carbonate sand (0.17% organic carbon, pH 8.1), respectively(5). The pKa of acetic acid is 4.76(6), indicating that this compound will exist partially in anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(7).

In 24 hr aqueous adsorption studies using montmorillonite and kaolinite clay adsorbents, 2.4-30.4% of added acetic acid was observed to be in the adsorbed phase(1). In adsorption studies using the adsorbent hydroxyapatite (a mineral which occurs in the environment as a result of the diagenesis of skeletal apatite), only 5% of added acetic acid (in aqueous solution, pH 8.0) became adsorbed to the hydroxyapatite(2). Acetic acid has been noted to leach from biological disposal areas(3).

The Henry's Law constant for acetic acid has been experimentally determined to be 1.43X10-7 atm-cu m/mole at 25 °C(1). This Henry's Law constant indicates that acetic acid is expected to be essentially nonvolatile from water surfaces(2). Acetic acid's Henry's Law constant indicates that volatilization from moist soil surfaces is not expected to be an important fate process(SRC). Acetic acid is expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 15.7 mm Hg at 25 °C(3).

GROUNDWATER: Acetic acid was qualitatively detected in groundwater from a landfill well in Norman, OK in 1972(1). Acetic acid levels of 0.66-4.60 ppm were identified in groundwater below a closed wood treatment facility in Pensacola, FL in 1984(2). Acetic acid was qualitatively identified in groundwater associated with an Australian quarry where dumping of organic wastes had occurred(3). Acetic acid was measured in the groundwater downgradient of the Bemidji oil spill in 1990 at concentrations from 1.47 to 12.5 uM(4). Acetic acid was reported in groundwater at a concentration of 43 ug/L in a shallow coastal plain aquifer near Atlantic City, NJ in 1990(5). Acetic acid at concentrations from 3.52 to 67.1 mg/L was measured in groundwater from the Pensacola, FL aquifer which had been contaminated with wood-preserving chemicals(6).

SURFACE WATER: Acetic acid was detected at concentrations of 12-198 ppb in the Scheldt estuary in Belgium during 1977-8(1). Acetic acid concentrations of 75-300 ppb were found at various depths of Lake Kizaki in Japan(2). Acetic acid concentrations of 13-72, 6-12, and 25 ppb were detected in Ohio, Little Miami, and Tannes Rivers, respectively(3). Concentrations of acetic acid generally below 0.1 ppb were monitored in the Lee River in Great Britain(4).

SEAWATER: Acetic acid was detected at concentrations of 2.4-144 ppb near the Belgian coast and 12-240 ppb near Calais on the English Channel during 1977-8 monitoring(1).

RAIN/SNOW: Rainwater collected in Wilmington, NC between 1987 and 1990 contained acetic acid at concentrations of 1.3 to 8.4 uM; concentrations were highly correlated with hydrogen ion, nitrate, and non-sea-salt sulfate(1). Higher concentrations were reported for local thunderstorms and were lowest in maritime storm rain(1). Rainwater collected by event during January to March 1985 at Brookhaven National Laboratory, NY, contained acetic acid at concentrations from 0.1 to 0.4 ppm; snow contained acetic acid at concentrations from trace quantities to 0.3 ppm(2). Rainwater and snow collected at different locations, both urban and nonurban, in southern California from 1982 to 1984 contained acetic acid at 0.37 to 13.45 uM(3). Acetic acid was measured in cloud water obtained at a forested ridge top in central Virginia, September 1990, at 2.8 to 7.4 uM(4). Fogwater obtained from Corvallis, OR in 1989 contained acetic acid at concentrations from 8.3 to 233.1 uM(5). Acetic acid was measured in both dew and fog from Altos de Pipe, Venezuala at concentrations from 4.9-15.2uM and 4.3-12.7 uM, respectively(6). Rainwater collected in Wilmington, NC between Jan 2008 and March 2009 contained volume weighted acetic concentrations of 2.6 uM(7).

Acetic acid was qualitatively detected in wastewater effluents from publicly owned treatment works (POTW) in Decatur and Bensenville, IL(1). Acetic acid concentrations of 125 ppm were identified in wastewaters from a coal gasification facility in North Dakota(2). Wastewater from a shale oil process in Australia contained 140 ppm acetic acid(3). Acetic acid was detected in leachate from a sanitary landfill in Barcelona, Spain(4). Acetic acid has reportedly been detected in wastewater effluents from chemical, resin, and paper manufacturing plants, from various landfill leachates, and from sewage treatment facilities(5,10). Acetic acid is released to water during manufacture of dimethyl terephthalate and acetaldehyde, and to air during the production of acrylic acid and acrylic ester(6). Acetic acid was emitted at a mean concentration of 0.22 mg/sq m/hr from particle board with attached carpet using a test chamber method(7). Using a large-scale environmental chamber, acetic acid was identified in the emission from a carpet with a PVC backing(8). Acetic acid was identified in the emissions from rubberized jute cushions at unreported concentrations(9). Acetic acid was identified as one of the predominate compounds emitted by a plywood specimen; the emission rate at 72 hours was 340 ug/m-hr(11). Acetic acid concentrations in gasoline and diesel exhausts from 5 different automobiles ranged from 9.57-61.5 ppb/vol in the particulate phase and from 16.3-262 ppb/vol in the gaseous phase(12). Acetic acid was found in the volatile organic compound emissions from various furniture coatings(13). Emission of acetic acid during extrusion of polyethylene resins was measured as <0.17 lbs/million lbs for blown film and blow molding and ranged from <0.17 to 2.0 lbs/million lbs for extrusion coating (higher value for extrusion at higher melt temperature)(14). Gasoline engine exhaust from a 1982 Toyota Corolla contained 31.81 ppb acetic acid(15).

Acetic acid was emitted from burning polyethylene as an oxidative degradation product(1). Acetic acid was found in oil-shale gas-condensate retort water and in process retort water at 3.4 mg/L and 1188 mg/L, respectively(2). Acetic acid was identified in the stack emission during waste incineration(3). Acetic acid concentrations were measured in smoke condensates of Ponderosa pine wood (4.4 g/kg smoldering; 0.34 g/kg flaming), needles (7.6 g/kg smoldering), bark (5.4 g/kg smoldering; 3.3 g/kg self-substained smoldering), litter (2.4 g/kg smoldering; 1.3 g/kg self-substained smoldering), duff (0.85 g/kg smoldering; 0.66 g/kg self-substained smoldering), and humus (0.19 g/kg smoldering)(4). Acetic acid was measured in active compost blower exhaust at 2574 ug/cu-m from a wastewater treatment sludge/wood chip compost pile(5). Acetic acid (concentrations not reported) was a component of volatile organics collected from garden waste exudate, and in laboratory studies in the head space of waste material(6).

SEDIMENT: Acetic acid concentrations of 17.3-48.5 mmol/kg wet mud were detected in bottom sediments of Lake Biwa in Japan; however, no acetic acid was found in the interstitial water(1). Concentrations of 0.133-1.836 mg/g (dry wt) were detected in sediments from Loch Eil in Scotland. Water removed from sediments contained levels of 0.244-0.251 mg/mL(2).

URBAN/SUBURBAN: Mean atmospheric concentrations in Los Angeles, CA between July and Sept 1984 were 0.262-3.90 ppb(1). Levels of 1-6 ppb were reported for ambient air in Tucson, AZ(1). Acetic acid concentrations (ppb) from a source-dominated coastal site and a smog-receptor inland site ranged from 1.9-3.5 (summer) and 4.5-9.4 (fall), and 2.5-5.1 (summer), respectively(2). Air samples collected from the Pomona College campus, Claremont, CA in September 1985, contained acetic acid at concentrations from 2.5 to 9.5 ppb(3). Acetic acid was reported in air samples collected from Palm Springs and Perris, CA giving seasonal averages ranging from 0.4-2.3 ppb and 0.6 to 2.2 ppb, respectively(4). Air samples collected from the Citrus College, Glendora, CA, a California South Coast Air Basin smog receptor site, contained acetic acid with 4- and 8-hour averaged concentrations from 2 to 16 ppb(5).

URBAN/SUBURBAN: Concentrations of acetic acid over central Germany ranged from 0.72 to 1.24 ppb volume for marine influence and continental anticyclone weather, respectively(1). Acetic acid concentrations, obtained from a semiurban site (Schenectady, NY) over a 2-day period in 1991, ranged from 0.60 to 3.4 ppb volume (2). Concentrations of acetic acid in air collected in Uniontown, PA (during summer 1990) and Boston, MA (during summer 1991) ranged from 0-44.6 ppb volume (average = 9.3 ppb volume) to 1.8-14.8 ppb volume (average = 5.4 ppb volume ), respectively(3). Air samples collected from Fukaya, Takasaki, and Karuizawa, Japan in 1986, contained average acetic acid concentrations of 4.71, 3.96, and 3.48 ppb, respectively, due to long-range transport of smog from the coastal region near Tokyo(4).

URBAN/SUBURBAN: Acetic acid was measured at a concentration of 0.43 ug/cu m in airborne aerosols in the urban area of Sao Paulo during July 1996(1). Concentrations of acetic acid ranged from 1.21 to 56.6 ppb volume in air during winter atmospheric measurements at two urban sites in Sao Paulo, Brazil in August 1999(2). Average urban concentrations of acetic acid measured during a severe Los Angeles area photochemical smog episode on September 8-9, 1993 were 16.1 ug/cu m, compared to an acetic acid concentration of 1.76 ug/cu m measured at a remote site(3). Atomspheric concentrations of acetic acid in urban particles collected during 1998-1999 in Kobe City town area, Japan ranged from not detected to 1.06 ng/cu m(4). The average acetic acid concentration in air in the city of Albuquerque were 6.7, 1.3, and 0.5 ppb during summer 1993, winter 1994, and winter 1995, respectively(5). Acetic acid concentrations ranged from not detected (approx. 0.0005 ppb volume) to 0.15 and from 0.053 to 1.28 ppb volume in the particulate and gaseous phase, respectively, in the Los Angeles atmosphere in October 1994(6).

INDOOR AIR: Acetic acid concentrations of 40-224 ug/cu m were detected in indoor air of homes in Italy(1). Indoor air samples from 26 of 26 houses with Sick Building Syndrome contained acetic acid at a medium relative abundance when compared with other compounds present in that sample(6); acetic acid concentrations were not given for indoor air from normal houses(2). Acetic acid was measured in indoor air samples from 4 residences in the winter of 1993 (14 samples indoors, mean = 15.5 ppb, maximum = 19.9 ppb; 8 samples outdoors, mean = 1.8 ppb, maximum = 3.2 ppb) and in 9 residences in the summer of 1993 (26 samples indoors, mean = 17.8 ppb, maximum = 33.1 ppb; 17 samples outdoors, mean = 2.0 ppb, maximum = 6.2 ppb) in Boston, MA(3). Ten (7 indoor, 3 outdoor) of 16 samples (12 indoor, 4 outdoor) from 4 buildings contained acetic acid(4). Simultaneous indoor and outdoor measurements of organic acids were performed at 6 residential house in suburban New Jersey during June-August 1992; concentrations of acetic acid were 23.97 ppb indoors(5). Acetic acid concentrations range from 4 to 11 ppb, with a geometric mean of 6 ppb of in the cabin of 2 types of commercial aircraft(6). Acetic acid was one of the predominant airborne compound found in both manufactured and site-built homes; concentrations ranged from 24.9-275 ppb in 4 manufacture homes and from 36.0-91.8 ppb in 7 site-built homes(7).

For more Atmospheric Concentrations (Complete) data for ACETIC ACID (6 total), please visit the HSDB record page.

Acetic acid was identified as the major volatile constituent of commercial brown sugars(1); concentrations ranging from 31-827 ppm were detected in 26 brown sugars collected worldwide(1). The source of the acetic acid was found to be bacterial action in recycled sweet waters containing low levels of sucrose(1). Acetic acid was qualitatively detected as a volatile component of fried bacon, smoked pork, baked potatoes, soy sauce, roasted filbert nuts and frankfurters(2-6). Mean acetic acid concentrations of 39.6-116.6 were detected in several honeydew honey extracts(7).

Acetic acid was measured as a volatile compound in popped popcorn at a concentration of 4000 ug/kg(1), and in the extract of edible Korean chamchwi(2), cured pork(3), and volatiles from boiled short-necked clams, clams, and corbicula(4) at unreported concentrations. Volatile compounds from Bisbee Delicious apples included acetic acid present at concentrations from 25.6 to 3505.0 picoliter/kg-hr depending on the date of harvest(5). Acetic acid was reported in 7 different wines, ciders, and dessert wines and brandies from Germany at concentrations from 80 to 363 mg/L(6).

Twenty-two acids in ground roast coffees and instant coffees were determined by GLC (gas liquid chromatography) of their silyl derivatives (after preseparation by gel electrophoresis or isotachophoresis). The contribution to the total acidity (which was estimated by titration to pH 8 after cation exchange of the coffee solutions) was calculated for each individual acid. The acids contribute 67% (roast coffee) and 72% (instant coffee) to the total acidity. Citric acid (12.2% in roast coffee/10.7% in instant coffee), acetic acid (11.2%/8.8%) and the high MW acids (8%/9%) contribute to the total acidity.

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.

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.

Burn in a chemical incinerator equipped with an afterburner and scrubber but exert extra care in igniting as this material is highly flammable. Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Contaminated packaging: dispose of as unused product.

/GUIDE 132 FLAMMABLE LIQUIDS - CORROSIVE/ Fire or Explosion: Flammable/combustible material. May be ignited by heat, sparks or flames. Vapors may form explosive mixtures with air. Vapors may travel to source of ignition and flash back. Most vapors are heavier than air. They will spread along ground and collect in low or confined areas (sewers, basements, tanks). Vapor explosion hazard indoors, outdoors or in sewers. Those substances designated with a (P) may polymerize explosively when heated or involved in a fire. Runoff to sewer may create fire or explosion hazard. Containers may explode when heated. Many liquids are lighter than water. /Acetic acid, solution, more than 80% acid; Acetic acid, glacial; ID: 2789/

/GUIDE 132 FLAMMABLE LIQUIDS - CORROSIVE/ Health: May cause toxic effects if inhaled or ingested/swallowed. Contact with substance may cause severe burns to skin and eyes. Fire will produce irritating, corrosive and/or toxic gases. Vapors may cause dizziness or suffocation. Runoff from fire control or dilution water may cause pollution. /Acetic acid, solution, more than 80% acid; Acetic acid, glacial; ID: 2789/

/GUIDE 132 FLAMMABLE LIQUIDS - CORROSIVE/ Public Safety: CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number listed on the inside back cover. As an immediate precautionary measure, isolate spill or leak area for at least 50 meters (150 feet) in all directions. Keep unauthorized personnel away. Stay upwind. Keep out of low areas. Ventilate closed spaces before entering. /Acetic acid, solution, more than 80% acid; Acetic acid, glacial; ID: 2789/

/GUIDE 132 FLAMMABLE LIQUIDS - CORROSIVE/ Protective Clothing: Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection. Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible. /Acetic acid, solution, more than 80% acid; Acetic acid, glacial; ID: 2789/

For more DOT Emergency Guidelines (Complete) data for ACETIC ACID (16 total), please visit the HSDB record page.

2790 153(10-80% acid)

2789 132(>80% acid)

UN 2789; Acetic acid, glacial or acetic acid solution, with more than 80% acid, by mass

UN 2790; Acetic acid solution, not less than 50% but not more than 80% acid, by mass; Acetic acid solution, with more than 10% and less than 50% acid, by mass

IMO 8.0; Acetic acid, glacial or acetic acid solution, more than 80% acid, by mass; Acetic acid solution not less than 50% but not more than 80% acid, by mass; Acetic acid solution more than 10% and less than 50% acid, by mass

49 314 01; Acetic acid, aqueous solution

49 313 03; Acetic acid, glacial

No person may /transport,/ offer or accept a hazardous material for transportation in commerce unless that person is registered in conformance ... and the hazardous material is properly classed, described, packaged, marked, labeled, and in condition for shipment as required or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./

The International Air Transport Association (IATA) Dangerous Goods Regulations are published by the IATA Dangerous Goods Board pursuant to IATA Resolutions 618 and 619 and constitute a manual of industry carrier regulations to be followed by all IATA Member airlines when transporting hazardous materials.

The International Maritime Dangerous Goods Code lays down basic principles for transporting hazardous chemicals. Detailed recommendations for individual substances and a number of recommendations for good practice are included in the classes dealing with such substances. A general index of technical names has also been compiled. This index should always be consulted when attempting to locate the appropriate procedures to be used when shipping any substance or article.

Corrosive Flammable Liquid

Corrosive

Do not transport with food and feedstuffs.

Symbol: C; R: 10-35; S: (1/2)-23-26-45; Note: B

UN Hazard Class: 8; UN Subsidiary Risks: 3; UN Pack Group: II