Dichloroacetic Acid

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

H400: Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard]

P260, P264, P273, P280, P301+P330+P331, P302+P361+P354, P304+P340, P305+P354+P338, P316, P321, P363, P391, P405, and P501 (click each P-code to see the statement)

H290 (26%): May be corrosive to metals [Warning Corrosive to Metals]

H311 (54.5%): Toxic in contact with skin [Danger Acute toxicity, dermal]

H314 (100%): Causes severe skin burns and eye damage [Danger Skin corrosion/irritation]

H318 (52.2%): Causes serious eye damage [Danger Serious eye damage/eye irritation]

H351 (42.2%): Suspected of causing cancer [Warning Carcinogenicity]

H360FD (30.5%): May damage fertility; May damage the unborn child [Danger Reproductive toxicity]

H362 (23.8%): May cause harm to breast-fed children [Reproductive toxicity, effects on or via lactation]

H373 (35.1%): May causes damage to organs through prolonged or repeated exposure [Warning Specific target organ toxicity, repeated exposure]

H400 (100%): Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard]

P203, P234, P260, P262, P263, P264, P264+P265, P270, P273, P280, P301+P330+P331, P302+P352, P302+P361+P354, P304+P340, P305+P354+P338, P316, P317, P318, P319, P321, P361+P364, P363, P390, P391, P405, P406, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 538 reports by companies from 14 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.

H350: May cause cancer [Danger Carcinogenicity]

H402: Harmful to aquatic life [Hazardous to the aquatic environment, acute hazard]

H411: Toxic to aquatic life with long lasting effects [Hazardous to the aquatic environment, long-term hazard]

P203, P273, P280, P318, P391, P405, and P501 (click each P-code to see the statement)

H290: May be corrosive to metals [Warning Corrosive to Metals]

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

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

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

H351: Suspected of causing cancer [Warning Carcinogenicity]

H360: May damage fertility or the unborn child [Danger Reproductive toxicity]

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

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, P234, P260, P262, P264, P264+P265, P270, P273, P280, P301+P330+P331, P302+P352, P302+P361+P354, P304+P340, P305+P354+P338, P308+P316, P316, P317, P318, P319, P321, P361+P364, P363, P390, P405, P406, and P501 (click each P-code to see the statement)

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

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

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

P203, P234, P260, P262, P264, P264+P265, P270, P280, P301+P317, P301+P330+P331, P302+P352, P302+P361+P354, P304+P340, P305+P354+P338, P308+P316, P316, P317, P318, P319, P321, P361+P364, P363, P390, P405, P406, and P501 (click each P-code to see the statement)

P203, P260, P262, P264, P264+P265, P270, P273, P280, P301+P330+P331, P302+P352, P302+P361+P354, P304+P340, P305+P354+P338, P316, P317, P318, P321, P361+P364, P363, P391, P405, and P501 (click each P-code to see the statement)

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

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

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

Rinse mouth. Do NOT induce vomiting. Refer 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)

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.

· Removal of solidified molten material from skin requires medical assistance.

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

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)

In case of fire in the surroundings, use appropriate extinguishing media.

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

Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary.

Use dry chemical, carbon dioxide, or alcohol or foam extinguishers. ... If material or contaminated runoff enters waterways, notify downstream users of potentially contaminated waters. Notify local health and fire officials and pollution control agencies. From a secure, explosion-proof location, use water spray to cool exposed containers. If cooling streams are ineffective (venting sound increases in volume and pitch, tank discolors, or shows any signs of deforming), withdraw immediately to a secure position. ... The only respirators recommended for firefighting are self-contained breathing apparatuses that have full face-pieces and are operated in a pressure-demand or other positive-pressure mode.

If material on fire or involved in fire: Extinguish fire using agent suitable for type of surrounding fire. (Material itself does not burn or burns with difficulty.). Use water in flooding quantities as fog. Cool all affected containers with flooding quantities of water. Apply water from as far a distance as possible.

Vapors are heavier than air and will collect in low areas. Vapors in confined areas may explode when exposed to fire. Containers may explode in fire. Storage containers and parts of containers may rocket great distances, in many directions.

· 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.

· 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.

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.

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)

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.

· 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.

Personal protection: complete protective clothing including self-contained breathing apparatus. Do NOT let this chemical enter the environment. Collect leaking and spilled liquid in sealable containers as far as possible. Cautiously neutralize remainder. Then wash away with plenty of water.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Wear respiratory protection. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. 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: Soak up with inert absorbent material and dispose of as hazardous waste. Keep in suitable, closed containers for disposal.

Evacuate and restrict persons not wearing protective equipment from area of spill or leak until cleanup is complete. Remove all ignition sources. Ventilate area of spill or leak. Absorb liquids in vermiculite, dry sand, earth, peat, carbon, or a similar material and deposit in sealed containers. Keep this chemical out of a confined space, such as a sewer, because of the possibility of an explosion, unless the sewer is designed to prevent the buildup of explosive concentrations. It may be necessary to contain and dispose of this chemical as a hazardous waste. If material or contaminated runoff enters waterways, notify downstream users of potentially contaminated waters.

PRECAUTIONS FOR "CARCINOGENS": A high-efficiency particulate arrestor (HEPA) or charcoal filters can be used to minimize amt of carcinogen in exhausted air ventilated safety cabinets, lab hoods, glove boxes or animal rooms ... Filter housing that is designed so that used filters can be transferred into plastic bag without contaminating maintenance staff is avail commercially. Filters should be placed in plastic bags immediately after removal ... The plastic bag should be sealed immediately ... The sealed bag should be labelled properly ... Waste liquids ... should be placed or collected in proper containers for disposal. The lid should be secured & the bottles properly labelled. Once filled, bottles should be placed in plastic bag, so that outer surface ... is not contaminated ... The plastic bag should also be sealed & labelled. ... Broken glassware ... should be decontaminated by solvent extraction, by chemical destruction, or in specially designed incinerators. /Chemical Carcinogens/

SRP: 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 air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.

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.

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.

PRECAUTIONS FOR "CARCINOGENS": There is no universal method of disposal that has been proved satisfactory for all carcinogenic compounds & specific methods of chem destruction ... published have not been tested on all kinds of carcinogen-containing waste. ... Summary of avail methods & recommendations ... /given/ must be treated as guide only. /Chemical Carcinogens/

For more Disposal Methods (Complete) data for Dichloroacetic acid (8 total), please visit the HSDB record page.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Wear respiratory protection. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. 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.

Precautions for safe handling: Avoid contact with skin and eyes. Avoid inhalation of vapor or mist.

Appropriate engineering controls: Avoid contact with skin, eyes and clothing. Wash hands before breaks and immediately after handling the product.

Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.

For more Preventive Measures (Complete) data for Dichloroacetic acid (18 total), please visit the HSDB record page.

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)

Separated from metals, combustible substances, reducing agents, strong oxidants, strong bases and food and feedstuffs. Well closed. Ventilation along the floor.

Keep container tightly closed in a dry and well-ventilated place. Containers which are opened must be carefully resealed and kept upright to prevent leakage. Recommended storage temperature 2-8 °C. Handle and store under inert gas.

Store separately in a corrosive-resistant location. Prior to working with DCA you should be trained on its proper handling and storage. Store in tightly closed containers in a cool, well-ventilated area away from incompatible materials ... . Metal containers involving the transfer of this chemical should be grounded and bonded. Where possible, automatically pump liquid from drums or other storage containers to process containers. Drums must be equipped with self-closing valves, pressure vacuum bungs, and flame arresters. Use only non-sparking tools and equipment, especially when opening and closing containers of this chemical. Sources of ignition, such as smoking and open flames, are prohibited where this chemical is used, handled, or stored in a manner that could create a potential fire or explosion hazard. Wherever this chemical is used, handled, manufactured, or stored, use explosion-proof electrical equipment and fittings.

PRECAUTIONS FOR "CARCINOGENS": Storage site should be as close as practical to lab in which carcinogens are to be used, so that only small quantities required for ... expt need to be carried. Carcinogens should be kept in only one section of cupboard, an explosion-proof refrigerator or freezer (depending on chemicophysical properties ...) that bears appropriate label. An inventory ... should be kept, showing quantity of carcinogen & date it was acquired ... Facilities for dispensing ... should be contiguous to storage area. /Chemical Carcinogens/

· 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.

0.2 [ppm]

7.9 [mg/m3]

93 [mg/m3]

560 [mg/m3]

0.5 [ppm]

8 hr Time Weighted Avg (TWA): 0.5 ppm, skin.

Peak Exposure Recommendation: Transient increases in workers' exposure levels may exceed 3 times the value of the TLV-TWA level for no more than 15 minutes at a time, on no more than 4 occasions spaced 1 hour apart during a workday, and under no circumstances should they exceed 5 times the value of the TLV-TWA level. In addition, the 8-hour TWA is not to be exceeded for an 8-hour work period.

A3; Confirmed animal carcinogen with unknown relevance to humans.

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

0.5 ppm [2002]

1.1 mg/m

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.

In Australia and New Zealand, the drinking-water guideline for dichloroacetic acid is 100 ug/L. This guideline also notes that minimizing the concentration of all chlorination by-products is encouraged...

The WHO (1990) has established a provisional guideline of 50 ug/L for dichloroacetic acid in drinking water.

No indication can be given about the rate at which a harmful concentration of this substance in the air is reached on evaporation at 20 °C.

Corrosive. The substance is corrosive to the eyes, skin and respiratory tract. Corrosive on ingestion. Inhalation of the vapour may cause lung oedema. Exposure could cause death. Medical observation is indicated.

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

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. (ERG, 2024)

Eye/face protection: Tightly fitting safety goggles. Faceshield (8-inch minimum). Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).

Skin protection: Handle with gloves.

Body Protection: Complete suit protecting against chemicals. The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace.

Respiratory protection: Where risk assessment shows air-purifying respirators are appropriate use a full-face respirator with multipurpose combination (US) or type ABEK (EN 14387) respirator cartridges as a backup to engineering controls. If the respirator is the sole means of protection, use a full-face supplied air respirator. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).

For more Personal Protective Equipment (PPE) (Complete) data for Dichloroacetic acid (6 total), please visit the HSDB record page.

AVOID ALL CONTACT! IN ALL CASES CONSULT A DOCTOR!

Use ventilation, local exhaust or breathing protection.

Protective gloves. Protective clothing.

Dichloroacetic acid appears as a colorless crystalline solid melting at 49 °F. Corrosive to metals and tissue.

Colorless liquid with a pungent odor; [ACGIH]

COLOURLESS LIQUID WITH PUNGENT ODOUR.

A colorless crystalline solid.

Colorless liquid

Colorless crystalline solid melting at 49 °C

Pungent odor

381 °F at 760 mmHg (NTP, 1992)

194 °C @760 [mm Hg]

49.5 °F (NTP, 1992)

Liquid molar volume = 0.083010 cu m/kmol; Heat of fusion at melting point = 1.2343X10+7 J/kmol

"49.5 °F"

greater than 235 °F (NTP, 1992)

113 °C (235 °F) - closed cup

greater than or equal to 100 mg/mL at 59 °F (NTP, 1992)

Miscible with water

Miscible with ethanol, diethyl ether; soluble in acetone; slightly soluble in carbon tetrachloride

Solubility in water: miscible

1.563 at 68 °F (NTP, 1992) - Denser than water; will sink

1.5634 g/cu cm at 20 °C

Relative density (water = 1): 1.56

1.5634 @ 20°C

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

4.45 (Air = 1)

Relative vapor density (air = 1): 4.4

1 mmHg at 111 °F ; 5 mmHg at 157.6 °F (NTP, 1992)

0.17 [mmHg]

0.179 mm Hg at 25 °C (extrapolated)

Vapor pressure, Pa at 20 °C: 19

1 mmHg at 111 °F

1 [mm Hg] @44 °C

log Kow = 0.92

Henry's Law constant = 8.38X10-9 atm-cu m/mole at 25 °C

Stable under recommended storage conditions.

Hazardous decomposition products formed under fire conditions - Carbon oxides, hydrogen chloride gas.

When heated to decomposition it emits toxic fumes of /chlorides/.

Highly corrosive liquid that gives off acidic vapors.

Corrosive to metals and tissues

Odor Threshold Low: 0.04 [ppm]

Recognition odor threshold from CHEMINFO

Soluble in water.

Acids, Carboxylic

Halogenated Organic Compounds

DICHLOROACETIC ACID is probably hygroscopic. This chemical reacts with water or steam. It is incompatible with strong oxidizing agents, strong bases and strong reducing agents. (NTP, 1992)

Incompatible materials: Strong oxidizing agents, strong bases, strong reducing agents.

/Dichloroacetic acid is a/ corrosive liquid.

Will react with water or steam to produce toxic and corrosive fumes.

DCA is a medium strong acid, incompatible with nonoxidizing mineral acids, organic acids, bases, acrylates, aldehydes, alcohols, alkylene oxides, ammonia, aliphatic, amines, alkanolamines, aromatic amines, amides, glycols, isocyanates, ketones. Attacks metals generating flammable hydrogen gas. Attacks some plastics, rubber and coatings.

IDENTIFICATION AND USE: Dichloroacetic acid (DCA) is a colorless liquid. Dichloroacetic acid, particularly in the form of its esters, is an intermediate in organic synthesis, used in the production of glyoxylic acid, dialkoxy and diaroxy acids, and sulfonamides and in the preparation of iron chelates in the agricultural sector. It is also used as an analytical reagent in fiber manufacture (polyethylene terephthalate) and as a medicinal disinfectant (substitute for formalin). DCA is a cauterizing agent and is used in medical practice as dichloroacetate on calluses, hard and soft corns, xanthoma palpebrarum, seborrhoeic keratoses, in-grown nails, cysts and benign erosion of the cervix. DCA is a nonproprietary drug used for treatment of inherited mitochondrial diseases. It was discovered in 2007 that dichloroacetate sodium (the sodium salt of DCA) promotes human cancer cell death by a novel mechanism. Soon after this discovery, physicians began using it off-label for cancer treatment. Dichloroacetate inhibits pyruvate dehydrogenase kinase, an enzyme that promotes pyruvate entry into mitochondria. HUMAN STUDIES: Drowsiness is a fairly frequent side effect of DCA and has been observed in healthy volunteers, adults with type I diabetes and patients with lactic acidosis. A patient with homozygous familial hypercholesterolemia who received single doses of 50 mg/kg bw DCA daily for four months developed reversible peripheral neuropathy characterized by loss of reflexes and muscle weakness. The effect subsided several weeks after cessation of administration of DCA. Preclinical evidence suggests that dichloroacetate can reverse the "Warburg effect" and inhibit growth in cancer models. The "Warburg effect," also termed aerobic glycolysis, describes the increased reliance of cancer cells on glycolysis for ATP production, even in the presence of oxygen. Consequently, there is continued interest in inhibitors of glycolysis as cancer therapeutics. One example is dichloroacetate, a pyruvate mimetic that stimulates oxidative phosphorylation through inhibition of pyruvate dehydrogenase kinase. ANIMAL STUDIES: DCA induced severe injury when applied to eyes of rabbits. Exposure of male and female rats to DCA at target doses of 10-600 mg/kg body weight per day in the drinking water for 14 days resulted in reduced weight gain only in the group given the highest dose. Treatment also increased urinary excretion of ammonia and changed the activities of enzymes of ammoniagenesis, indicating renal compensation for an acid load. Ocular toxicity was observed in beagle dogs that were treated for 13 weeks with an approximate dose of 1100 mg/kg body weight DCA in the drinking water. No similar organ specific effect has been seen in other studies or in other species. Induction of peroxisome proliferation has been repeatedly associated with the chronic toxicity and carcinogenicity of DCA to the liver. It can induce peroxisome proliferation in the livers of both mice and rats, as indicated by increased activities of palmitoyl coenzyme A oxidase and carnitine acetyl transferase, the appearance of a peroxisome proliferation associated protein and increased volume-density of peroxisomes after exposure to DCA for 14 days. In eight studies, DCA salt administered in the drinking water to male and/or female mice increased the incidences of hepatocellular adenomas and/or carcinomas. Following oral administration of DCA in the drinking-water to male rats, an increased incidence of hepatocellular carcinomas was found at a dose that decreased body weight and an increase in the combined incidence of adenomas and carcinomas was found at a lower dose. When administered in the drinking-water, DCA promoted hepatocellular carcinomas in carcinogen-initiated male and female mice in three studies. DCA and its metabolites accumulate in rat fetuses after treatment of the dam. Maternal doses of 140-2400 mg/kg bw per day on days 6-15 of gestation altered development of the heart and major vessels and less frequently, the kidneys and the orbits of the eyes, as reported in some studies. DNA strand breaks were not induced in mammalian cells in vitro in the absence of an exogenous metabolic activation system, but contradictory results were obtained in vivo. No effect was seen in either mouse or rat hepatic cells after single or repeated dosing, and no effects were observed in epithelial cells from spleen, stomach or duodenum after a single dose. Dichloroacetic acid did not induce differential toxicity in DNA repair-deficient strains of Salmonella typhimurium but did induce prophage in Escherichia coli in one study. It was mutagenic to Salmonella typhimurium TA100 and TA98 in single studies. Most of the mutations in 400 revertants of DCA-treated Salmonella typhimurium TA100 cultures were GA AT transitions. ECOTOXICITY STUDIES: DCA is a common contaminant of aquatic ecosystems. A study to investigate potential phytotoxic effects was conducted on rooted and floating macrophytes (Myriophyllum spicatum, M. sibiricum, and Lemna gibba). The most sensitive plant endpoints were wet mass and plant length.

The dichloroacetate ion stimulates the activity of the enzyme pyruvate dehydrogenase by inhibiting the enzyme pyruvate dehydrogenase kinase. Thus, it decreases lactate production by shifting the metabolism of pyruvate from fermentation towards oxidation in the mitochondria. (Wikipedia)

Dichloroacetic acid

Reproductive

There is inadequate evidence in humans for the carcinogenicity of dichloroacetic acid. There is sufficient evidence in experimental animals for the carcinogenicity of dichloroacetic acid. Overall evaluation: Dichloroacetic acid is possibly carcinogenic to humans (Group 2B).

EPA finds there are no data on humans indicating that DCA is a carcinogen. However, there is sufficient evidence to conclude that DCA is carcinogenic in at least two species of experimental animals. A statistically significant and dose-related incidence of hepatocellular adenomas and carcinomas occur in male and female mice, and male rats. Large foci of cellular alteration (LFCA, formerly called hyperplastic nodules), which are expected to progress into hepatocellular adenomas and carcinomas, increased in rats and mice. Additional support is provided by: (1) the number of independent studies reporting consistently positive results and at roughly comparable doses, (2) site concordance for tumor formation between two species, (3) clear evidence of a dose-response relationship for tumor incidence and multiplicity, and (4) apparent development of tumors from more than one hepatic cell line and no clear data supporting a cohesive mode of action. Therefore, EPA believes that DCA is likely to be a carcinogen in humans.

A3; Confirmed animal carcinogen with unknown relevance to humans.

Group 2B: Possibly carcinogenic to humans

Volume 63: (1995) Dry Cleaning, Some Chlorinated Solvents and Other Industrial Chemicals

Volume 84: (2004) Some Drinking-water Disinfectants and Contaminants, including Arsenic

Volume 106: (2014) Trichloroethylene, Tetrachloroethylene, and Some Other Chlorinated Agents

2B, possibly carcinogenic to humans. (L135)

Multiple independent studies demonstrate that DCA has the ability to alter normal carbohydrate metabolism. Dichloroacetic acid treatment results in a significant reduction in plasma levels of glucose, pyruvate, and lactate. Another consistent finding in DCA ingestion studies is a dose-related increase in liver size, generally accompanied (or caused) by an increase in glycogen deposition in the liver. There is an extensive and consistent data base demonstrating the reproductive toxicity of DCA in males and females. Neurologic symptoms and morphologic changes in the nervous system have been reported in humans, dogs, and rats. (L2086)

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

Ingestion

Burning sensation. Sore throat. Cough. Laboured breathing. Shortness of breath. Symptoms may be delayed.

Redness. Pain. Blisters. Serious skin burns.

Redness. Pain. Severe deep burns.

Abdominal pain. Burning sensation. Shock or collapse.

Reproductive Toxin - A chemical that is toxic to the reproductive system, including defects in the progeny and injury to male or female reproductive function. Reproductive toxicity includes developmental effects. See Guidelines for Reproductive Toxicity Risk Assessment.

Dermatotoxin - Skin burns.

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

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

NTP Carcinogen - Reasonably anticipated to be a human carcinogen.

ACGIH Carcinogen - Confirmed Animal.

IRIS Current

ORAL (LD50): Acute: 2820 mg/kg [Rat]; DERMAL (LD50): Acute: 510 mg/kg [Rabbit]

LD50 Rabbit dermal 510 mg/kg

LD50 Rat oral 2.82 g/kg

In this study, groups of B6C3F1 male mice were treated with dichloroacetate (DCA), trichloroacetate (TCA), and mixtures of the compounds (Mix I, II, and III) daily by gavage, for 13 weeks. The tested doses were 7.5, 15, and 30 mg DCA/kg/day and 12.5, 25, and 50 mg TCA/kg/day. The DCA: TCA ratios in Mix I, II, and III were 7.5:12.5, 15:25, and 30:50 mg/kg/day, respectively. Peritoneal lavage cells were collected at the end of the treatment period and assayed for the biomarkers of phagocytic activation, including superoxide anion and tumor necrosis factor-alpha production, and myeloperoxidase activity. The mixtures produced nonlinear effects on the biomarkers of phagocytic activation, with Mix I and II effects were found to be additive, but Mix III effects were found to be less than additive. /Dichloroacetate/

Dichloroacetate (DCA), an inhibitor of pyruvate dehydrogenase kinase (PDK), has been recently demonstrated as a promising nontoxic antineoplastic agent that promotes apoptosis of cancer cells. In the present study, we aimed to investigate the antitumor effect of DCA combined with 5-Fluorouracil (5-FU) on colorectal cancer (CRC) cells. Four human CRC cell lines were treated with DCA or 5-FU, or a combination of DCA and 5-FU. The cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. The interaction between DCA and 5-FU was evaluated by the median effect principle. Immunocytochemistry with bromodeoxyuridine (BrdU) was carried out to determine the proliferation of CRC cells. Cell cycle and apoptosis were measured by flow cytometry, and the expression of apoptosis-related molecules was assessed by western blot. Our results demonstrated that DCA inhibited the viability of CRC cells and had synergistic antiproliferation in combination with 5-FU. Moreover, compared with 5-FU alone, the apoptosis of CRC cells treated with DCA and 5-FU was enhanced and demonstrated with the changes of Bcl-2, Bax, and caspase-3 proteins. Our results suggest that DCA has a synergistic antitumor effect with 5-FU on CRC cell lines in vitro. /Dichloroacetate/

The unique metabolic profile of cancer (aerobic glycolysis) is an attractive therapeutic target for cancer. Dichloroacetate(DCA), an inhibitor of pyruvate dehydrogenase kinase, has been shown to reverse glycolytic phenotype and induce mitochondrion-dependent apoptosis. In the present study, we investigated the effects of S6 kinase 1 (S6K1) inhibition on DCA-induced cell death and the underlying mechanisms in breast cancer cells. Cell death was evaluated by annexin V and PI staining. The synergistic effects of DCA and PF4708671 were assessed by isobologram analysis. Small interfering RNA (siRNA) was used for suppressing gene expression. The mRNA and protein levels were measured by RT-PCR and Western blot analysis, respectively. PF4708671, a selective inhibitor of S6K1, and knockdown of S6K1 with specific siRNA enhanced DCA-induced cell death. Interestingly, a combination of DCA/PF4708671 markedly reduced protein expression of a glycolytic enzyme, hexokinase 2 (HK2). Suppression of HK2 activity using specific siRNA and 2-deoxyglucose (2-DG) further enhanced cell sensitivity to DCA/PF4708671. Overexpression of Myc-tagged HK2 rescued cell death induced by DCA/PF4708671. Based on these findings, we propose that inhibition of S6K1, in combination with the glycolytic inhibitor, DCA, provides effective cancer therapy. /Dichloroacetate/

The unique metabolism of breast cancer cells provides interest in exploiting this phenomenon therapeutically. Metformin, a promising breast cancer therapeutic, targets complex I of the electron transport chain leading to an accumulation of reactive oxygen species (ROS) that eventually lead to cell death. Inhibition of complex I leads to lactate production, a metabolic byproduct already highly produced by reprogrammed cancer cells and associated with a poor prognosis. While metformin remains a promising cancer therapeutic, we sought a complementary agent to increase apoptotic promoting effects of metformin while attenuating lactate production possibly leading to greatly improved efficacy. Dichloroacetate (DCA) is a well-established drug used in the treatment of lactic acidosis which functions through inhibition of pyruvate dehydrogenase kinase (PDK) promoting mitochondrial metabolism. Our purpose was to examine the synergy and mechanisms by which these two drugs kill breast cancer cells. Cell lines were subjected to the indicated treatments and analyzed for cell death and various aspects of metabolism. Cell death and ROS production were analyzed using flow cytometry, Western blot analysis, and cell counting methods. Images of cells were taken with phase contrast microscopy or confocal microscopy. Metabolism of cells was analyzed using the Seahorse XF24 analyzer, lactate assays, and pH analysis. We show that when DCA and metformin are used in combination, synergistic induction of apoptosis of breast cancer cells occurs. Metformin-induced oxidative damage is enhanced by DCA through PDK1 inhibition which also diminishes metformin promoted lactate production. We demonstrate that DCA and metformin combine to synergistically induce caspase-dependent apoptosis involving oxidative damage with simultaneous attenuation of metformin promoted lactate production. Innovative combinations such as metformin and DCA show promise in expanding breast cancer therapies. /Dichloroacetate/

For more Interactions (Complete) data for Dichloroacetic acid (22 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 if 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/

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. Early intubation, at the first sign of upper airway obstruction, may be necessary. Positive-pressure ventilation techniques with a bag-valve-mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as 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 ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Organic acids and related compounds/

PRECAUTIONS FOR "CARCINOGENS": Whenever medical surveillance is indicated, in particular when exposure to a carcinogen has occurred, ad hoc decisions should be taken concerning ... /cytogenetic and/or other/ tests that might become useful or mandatory. /Chemical Carcinogens/

/HUMAN EXPOSURE STUDIES/ Preclinical evidence suggests dichloroacetate (DCA) can reverse the Warburg effect and inhibit growth in cancer models. This phase 1 study was undertaken to assess the safety, recommended phase 2 dose (RP2D), and pharmacokinetic (PK) profile of oral DCA in patients with advanced solid tumors. Twenty-four patients with advanced solid malignancies were enrolled using a standard 3 + 3 protocol at a starting dose of 6.25 mg/kg twice daily (BID). Treatment on 28 days cycles was continued until progression, toxicity, or consent withdrawal. PK samples were collected on days 1 and 15 of cycle 1, and day 1 of subsequent cycles. PET imaging ((18) F-FDG uptake) was investigated as a potential biomarker of response. Twenty-three evaluable patients were treated with DCA at two doses: 6.25 mg/kg and 12.5 mg/kg BID (median of 2 cycles each). No DLTs /dose limiting toxicities/ occurred in the 6.25 mg/kg BID cohort so the dose was escalated. Three of seven patients had DLTs (fatigue, vomiting, diarrhea) at 12.5 mg/kg BID. Thirteen additional patients were treated at 6.25 mg/kg BID. Most toxicities were grade 1-2 with the most common being fatigue, neuropathy and nausea. No responses were observed and eight patients had stable disease. The DCA PK profile in cancer patients was consistent with previously published data. There was high variability in PK values and neuropathy among patients. Progressive increase in DCA trough levels and a trend towards decreased (18) F-FDG uptake with length of DCA therapy was observed. The RP2D of oral DCA is 6.25 mg/kg BID. Toxicities will require careful monitoring in future trials. /Dichloroacetate/

/SIGNS AND SYMPTOMS/ The neurotoxic effects of dichloroacetic acid observed repeatedly in experimental animals have rarely been documented in clinical trails. Drowsiness is a fairly frequent side effect of dichloroacetic acid and has been observed in healthy volunteers, adults with type I diabetes and patients with lactic acidosis. A patient with homozygous familial hypercholesterolemia who received single doses of 50 mg/kg body weight dichloroacetic acid daily for four months developed reversible peripheral neuropathy characterized by loss of reflexes and muscle weakness; the effect subsided several weeks after cessation of administration of dichloroacetic acid.

EC50; Species: Xenopus laevis (African clawed frog) embryo; Conditions: freshwater, renewal, 23 °C, pH 7.0; Concentration: 3560000 ug/L for 96 hr (95% confidence interval: 2400000-4680000 ug/L); Effect: increased malformation, teratogenic measurements /formulated product/

LC50; Species: Xenopus laevis (African clawed frog) embryo; Conditions: freshwater, renewal, 23 °C, pH 7.0; Concentration: 4060000 ug/L for 96 hr (95% confidence interval: 3900000-5600000 ug/L) /Formulated product/

LC50; Species: Nitocra spinipes (Harpacticoid copepod) adult, length 0.6-0.9 mm; Conditions: saltwater, static, 21 °C, pH 7.8, salinity 7 ppt, alkalinity 75 mg/L CaCO3, dissolved oxygen >5 mg/L; Concentration: 23000 ug/L for 96 hr (95% confidence interval: 21000-25000 ug/L) /95% purity/

/AQUATIC SPECIES/ ...The kinetics and effects of dichloroacetic acid (DCA) in rainbow trout /were examined/. Branchial uptake was measured in fish confined to respirometer-metabolism chambers. Branchial uptake efficiency was <5%, suggesting passive diffusion through aqueous channels in the gill epithelium. DCA concentrations in tissues following prolonged (72, 168, or 336 hr) waterborne exposures were expressed as tissue:plasma concentration ratios. Concentration ratios for the kidney and muscle at 168 and 336 hr were consistent with the suggestion that DCA distributes primarily to tissue water. Reduced concentration ratios for the liver, particularly at 72 hr, indicated that DCA was highly metabolized by this tissue. Routes and rates of elimination were characterized by injecting chambered animals with a high (5.0 mg/kg) or low (50 ug/kg) bolus dose. DCA was rapidly cleared by naive animals resulting in elimination half-lives (t(1/2)) of less than 4 hr. Waterborne pre-treatment of fish with DCA increased the persistence of a subsequently injected dose. In high dose animals, pre-treatment caused a 4-fold decrease in whole-body clearance (CL(B)) and corresponding increases in the area under the plasma concentration-time curve (extrapolated to infinity; AUC(0-->infinity)) and t(1/2). Qualitatively similar results were obtained in low dose fish, although the magnitude of the pre-treatment effect (approximately 2.5-fold) was reduced. Renal and branchial clearance contributed little (combined, <3% of CL(B)) to the elimination of DCA. Biliary elimination of DCA was also negligible. The steady-state volume of distribution (V(SS)) did not vary among treatment groups and was consistent with results of the tissue distribution study. DCA had no apparent effects on respiratory physiology or acid-base balance; however, the concentration of blood lactate declined progressively during continuous waterborne exposures. A transient effect on blood lactate was also observed in bolus injection experiments. The results of this study suggest that clearance of DCA is due almost entirely to metabolism. The pathway responsible for this activity exhibits characteristics in common with those of mammalian glutathione S-transferase zeta (GSTzeta), including non-linear kinetics and apparent suicide inactivation by DCA. Observed effects on blood lactate are probably due to the inhibition of pyruvate dehydrogenase kinase in aerobic tissues and may require the participation of a monocarboxylase transport protein to move DCA across cell membranes.

/OTHER TERRESTRIAL SPECIES/ Dichloroacetic acid (DCA), a water disinfection by-product, has attained emphasis due to its prospect for clinical use against different diseases including cancer along with negative impact on organisms. However, these reports are based on the toxicological as well clinical data using comparatively higher concentrations of DCA without much of environmental relevance. Here, ...cellular as well as organismal effects of DCA at environmentally and mild clinically relevant concentrations (0.02-20.0 ug/mL) /are evaluated/ using an established model organism, Drosophila melanogaster. Flies were fed on food mixed with test concentrations of DCA for 12-48 hr to examine the induction of reactive oxygen species (ROS) generation, oxidative stress (OS), heat shock genes (hsps) and cell death along with organismal responses. ...Locomotor performance, ROS generation, glutathione (GSH) depletion, expression of GSH-synthesizing genes (gclc and gclm), and hsps /were also examined/ at different days (0, 10, 20, 30, 40, 50) of the age in flies after prolonged DCA exposure. ...Mild OS and induction of antioxidant defense system in 20.0 ug/mL DCA-exposed organism after 24 hr. After prolonged exposure to DCA, exposed organism exhibited improved survival, elevated expression of hsp27, gclc, and gclm concomitant with lower ROS generation and GSH depletion and improved locomotor performance. Conversely, hsp27 knockdown flies exhibited reversal of the above end points. The study provides evidence for the attenuation of cellular and functional decline in aged Drosophila after prolonged DCA exposure and the effect of hsp27 modulation which further incites studies towards the therapeutic application of DCA.

/FIELD STUDIES/ Dichloroacetic acid (DCA), a haloacetic acid, is a common contaminant of aquatic ecosystems. A study to investigate potential phytotoxic effects on rooted and floating macrophytes (Myriophyllum spicatum, M. sibiricum, and Lemna gibba) was conducted. Replicate 12,000 L outdoor microcosms (n = 3) were treated with 3, 10, 30, and 100 mg/L of DCA that had been neutralized to the sodium salt, plus controls. Plants were sampled regularly over 21 days and assessed for a variety of endpoints including plant growth, root growth, number of nodes, wet and dry mass, chlorophyll-a, chlorophyll-b, carotenoids, and citrate levels. EC10, EC25, and EC50 values were calculated for each endpoint that exhibited a concentration-response. Overall, M. sibiricum was slightly more sensitive than M. spicatum to DCA exposure. The most sensitive plant endpoints were wet mass and plant length. Pigments showed no response with exposure to DCA. The probability of current concentrations of DCA in Canadian lake water and Swiss river waters exceeding thresholds of toxicity derived from single species effect measure distributions (EC10s) is << 0.01%... Currently, environmental levels of DCA do not pose a risk to these plants.

1.10e+01

4.60e+01

1.50e+00

6.0E+01(G)

3.10e-04

1.20e-02

5.00e-02

4.00e-03

Volatile

7.60e+02

4.60e+03

1.50e+02

6.0E+01 (G)

The substance is harmful to aquatic organisms.

Dichloroacetic acid's production and use as a chemical intermediate, in pharmaceuticals and administration as a medicine may result in its release to the environment through various waste streams. Its formation as a chemical byproduct of chlorination and chloramination of drinking water may result in its direct release to the environment. If released to air, a vapor pressure of 0.179 mm Hg at 25 °C indicates dichloroacetic acid will exist solely as a vapor in the atmosphere. Vapor-phase dichloroacetic 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. Dichloroacetic acid does not contain chromophores that absorb at wavelengths >290 nm and, therefore, is not expected to be susceptible to direct photolysis by sunlight. If released to soil, dichloroacetic acid is expected to have very high mobility based upon an estimated Koc of 2. The pKa of dichloroacetic acid is 1.26, indicating that this compound will exist almost entirely in the 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 is not expected because the compound exists as an anion and anions do not volatilize. Dichloroacetic acid has a vapor pressure of 0.179 mm Hg and exists as a liquid under environmental conditions; therefore, dichloroacetic acid may volatilize from dry soil. Utilizing the Japanese MITI test, 97% of the Theoretical BOD was reached in 2 weeks indicating that biodegradation is an important environmental fate process in soil. If released into water, dichloroacetic acid is not expected to adsorb to suspended solids and sediment based upon the estimated Koc. Biodegradation of 14 and 8% for river water and seawater, respectively, after 3 days incubation suggests that biodegradation may be an important fate process in water. The pKa indicates dichloroacetic acid will exist almost entirely in the anion form at pH values of 5 to 9 and, therefore, volatilization from water surfaces is not expected to be an important fate process. 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 dichloroacetic acid may occur through inhalation and dermal contact with this compound at workplaces where it is produced or used. Monitoring data indicate that the general population may be exposed to dichloroacetic acid via ingestion of and dermal contact with chlorinated or chloraminated water. The general public may also be exposed to dichloroacetic acid by direct medical treatment. (SRC)

Dichloroacetic acid's production and use as a chemical intermediate, in pharmaceuticals and administration as a medicine(1) may result in its release to the environment through various waste streams(SRC). Its formation as a chemical byproduct of chlorination and chloramination of water(2,3) may result in its direct release to the environment(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 2(SRC), determined from a structure estimation method(2), indicates that dichloroacetic acid is expected to have very high mobility in soil(SRC). A pKa of 1.26(3), indicating that this compound will exist almost entirely in the anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4). Dichloroacetic acid has a vapor pressure of 0.179 mm Hg(5) and exists as a liquid under environmental conditions: therefore, dichloroacetic acid may volatilize from dry soil(SRC). Utilizing the Japanese MITI test, 97% of the Theoretical BOD was reached in 2 weeks(6) indicating that biodegradation is an important environmental fate process in soil(SRC).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 2(SRC), determined from a structure estimation method(2), indicates that dichloroacetic acid is not expected to adsorb to suspended solids and sediment(SRC). A pKa of 1.26(3) indicates dichloroacetic acid will exist almost entirely in the anion form at pH values of 5 to 9 and, therefore, volatilization from water surfaces is not expected to be an important fate process(SRC). According to a classification scheme(4), an estimated BCF of 3(SRC), from its log Kow of 0.92(5) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Biodegradation of 14 and 8% for river water and seawater, respectively, after 3 days incubation(6) suggests that biodegradation may be an important fate process in water(SRC).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), dichloroacetic acid, which has a vapor pressure of 0.179 mm Hg at 25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase dichloroacetic 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 rate constant of 7.3X10-13 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Dichloroacetic acid does not contain chromophores that absorb at wavelengths >290 nm(4) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC).

AEROBIC: The biodegradability of dichloroacetic acid, at 10 ppm, was measured in both river water and seawater using the cultivation method; 14 and 8% degradation was reported for river water and seawater, respectively, after 3 days incubation(1). Based on these results, this compound was determined to be difficult to degrade(1). 0, 27, and 68% of the theoretical BOD in a BOD test was reached in 2, 5, and 10 days, respectively, following inoculation with sewage(2). Dichloroacetic acid was not biodegraded during a 5 day BOD test using a sewage inoculum(3). Dichloroacetic acid at 20 mg/L was >95% degraded in a 20 day BOD test; in a second screening test, this compound was 83% degraded after 30 days(4). Dichloroacetic acid, present at 100 mg/L, reached 97% of its theoretical BOD in 2 weeks using an activated sludge inoculum at 30 mg/L in the Japanese MITI test(5). Pure culture experiments show that aerobic degradation occurs via dehalogenation(6).

The rate constant for the vapor-phase reaction of dichloroacetic acid with photochemically-produced hydroxyl radicals has been estimated as 7.3X10-13 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 22 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Dichloroacetic acid is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(2). Dichloroacetic acid does not contain chromophores that absorb at wavelengths >290 nm(2) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC). Aqueous solutions of ferric ions and dichloroacetic acid were photolyzed by light with wavelengths greater than 300 nm; dichloroacetic acid was photolyzed at a rate of 2X10-7 Einsteins/sec-mL(3).

An estimated BCF of 3.2 was calculated for dichloroacetic acid(SRC), using a log Kow of 0.92(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).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of dichloroacetic acid can be estimated to be 2(SRC). According to a classification scheme(2), this estimated Koc value suggests that dichloroacetic acid is expected to have very high mobility in soil. The pKa of dichloroacetic acid is 1.26(3), indicating that this compound will exist almost entirely in the anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4).

A pKa of 1.26(1) indicates dichloroacetic acid will exist almost entirely in the anion form at pH values of 5 to 9 and, therefore, volatilization from water surfaces is not expected to be an important fate process(SRC). Dichloroacetic acid has a vapor pressure of 0.179 mm Hg(2) and exists as a liquid under environmental conditions: therefore, dichloroacetic acid may volatilize from dry soil(SRC).

DRINKING WATER: Water sampled from 6 full-scale treatment drinking water plants from 1983 to 1984 contained dichloroacetic acid at concentrations ranging from 8 to 79 ug/L(1). During a survey of drinking waters at water treatment plants treating lowland river water in England, dichloroacetic acid was detected at unreported concentrations(2). Water samples collected from 35 drinking water treatment facilities during 1988 contained dichloroacetic acid at concentrations ranging from 5.0 to 7.3 ug/L(3). Tap water from Japan contained dichloroacetic acid at concentrations of 2.8 to 10.9 ug/L during 1987 to 1988(4). 20 Drinking water samples collected in The Netherlands contained dichloroacetic acid ranging from <0.1 ug/L (below detection) to 3.0 ug/L; dichloroacetic acid was found only in drinking water prepared from surface waters and not from water prepared from groundwater sources(5). Tap water collected near 2 Massachusetts water treatment plants immediately following treatment contained dichloroacetic acid at concentrations ranging from 63.1 to 133 ug/L(6).

DRINKING WATER: Dichloroacetic acid was measured as a disinfection by-product at two water treatment plants(1). After chlorine treatment, concentrations of dichloroacetic acid ranged from 9.4 to 23 ug/L; after both ozone and chlorine treatment, concentrations of dichloroacetic acid ranged from 4.7 to 21 ug/L(1). Drinking water samples collected from Cincinnati, OH (in 1978 and 1980), Miami, FL (in 1976), Philadelphia, PA (in 1976), Ottumwa, IA (in 1976), and Seattle, WA (in 1976) contained dichloroacetic acid at unreported concentrations(2). Dichloroacetic acid levels in finished drinking water samples from the Philadelphia, PA Suburban Water Co., Houston, TX, Metropolitan Water District of Southern California and Corpus Christi, TX were 2.15, 12.7, 7.02 and 5.45 ug/L, respectively(3).

DRINKING WATER: Water collected from fifty-three Canadian drinking water treatment facilities in winter of 1993 contained dichloroacetic acid(1). When bromide concentrations were very low (<0.01 mg/L), the water contained 20.6 ug/L dichloroacetic acid; when bromide was low (0.06 mg/L), the water contained 3.8 ug/L dichloroacetic acid; when bromide was moderate (0.5 mg/L), the water contained 0.3 ug/L dichloroacetic acid(1). A mean concentration of 1.07 ug/L dichloroacetic acid was measured in post-treatment surface water from disinfection utilities in Belgium, France, Germany, Spain, The Netherlands, and Italy; post-treatment groundwater from disinfection utilities contained a mean 0.83 ug/L dichloroacetic acid(2).

DRINKING WATER: Swiss drinking water monitored between 1996 and 1997 contained <6-217 ng/L dichloroacetic acid(1). Dichloroacetic acid was measured in water samples taken from Barcelona's water treatment plant between November 1997 and March 1998; the compound was detected in prechlorinated water (2.8-16 ug/L), sand-filtered water (2.8-14 ug/L), ozonated water (3.4-10 ug/L), granulated activated carbon-filtered water (not detected-2.7 ug/L), and postchlorinated water (not detected-2.0 ug/L)(2). Dichloroacetic acid was detected at 31 of 35 Finnish waterworks between January and October 1994 with concentrations between 3 and 42 ug/L; levels at all other facilities were below quantitation limits(3).

For more Environmental Water Concentrations (Complete) data for Dichloroacetic acid (6 total), please visit the HSDB record page.

Dichloroacetic acid was detected in the spent chlorination liquor from the bleaching of sulphite pulp at concentrations ranging from 0.2 to 0.5 g/ton pulp(1). Kraft pulp mill bleach plant effluents contained dichloroacetic acid from 12-20 g/ton pulp(2). Dichloroacetic acid was measured in the flue gases from the municipal incinerator at Boras, Sweden at concentrations from 1.3 to 5.7 ug/cu m(3). Effluent from a Pomona, CA advanced waste treatment plant contained dichloroacetic acid at unreported concentrations(4). The mean concentration in wastewater effluents entering the Tama River, Japan was reported as 0.81 ug/L(5).

Dichloroacetic acid was detected in the Tres Rios Wetlands, which receive tertiary-treated sewage effluent from the 91st Ave Wastewater Treatment Plant southwest of Phoenix, AZ, at concentrations of 2.3-27 ug/L(1). Dichloroacetic acid was detected in communal wastewater (<0.01-1.41 ug/L) and industrial wastewater (0.4-34.8 ug/L) collected in Switzerland from 1996 to 1997(2).

SOIL: Mean concentration ranges of 3.5-49, <2.3-36.5, 4-140 and <2.3-640 ng/g dry wt were reported in preciptation samples from Canada, Malawi, UK and Chile, respectively, sampled in 1999. Concentrations in archived soils from UK were 315, 3, 9 and 12 ng/g dry weight in soil samples from 1865, 1881, 1944 and 1956, resepctively(1).

URBAN/SUBURBAN: Vapor-phase and particulate-phase dichloroacetic acid was detected in air collected from semi-rural Guelph, Ontario and from urban Toronto, Ontario from January to December, 2000(1).

Pine needles taken from trees surrounding a pulp and paper mill in western Finland contained 0-3.80 ng/g fresh weight dichloroacetic acid, while pine needles taken from areas surrounding a metal reclamation plant in southern Finland contained 0.65-2.55 ng/g fresh weight dichloroacetic acid(1). Mean concentrations of <2, <2, 2, 2 and 12 ng/g wet weight were reported in conifer needle samples from Chilo, Banff Natl Park, Canada, Gulephy Ontario, Canada, Malwai and Lancaster UK, respectively, sampled 1999-2000(2).

SRP: 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 air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.

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.

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.

PRECAUTIONS FOR "CARCINOGENS": There is no universal method of disposal that has been proved satisfactory for all carcinogenic compounds & specific methods of chem destruction ... published have not been tested on all kinds of carcinogen-containing waste. ... Summary of avail methods & recommendations ... /given/ must be treated as guide only. /Chemical Carcinogens/

For more Disposal Methods (Complete) data for Dichloroacetic acid (8 total), please visit the HSDB record page.

/GUIDE 153 SUBSTANCES - TOXIC and/or CORROSIVE (Combustible)/ Fire or Explosion: Combustible material: may burn but does not ignite readily. When heated, vapors may form explosive mixtures with air: indoors, outdoors and sewers explosion hazards. Those substances designated with a (P) may polymerize explosively when heated or involved in a fire. Contact with metals may evolve flammable hydrogen gas. Containers may explode when heated. Runoff may pollute waterways. Substance may be transported in a molten form.

/GUIDE 153 SUBSTANCES - TOXIC and/or CORROSIVE (Combustible)/ Health: TOXIC; inhalation, ingestion or skin contact with material may cause severe injury or death. Contact with molten substance may cause severe burns to skin and eyes. Avoid any skin contact. Effects of contact or inhalation may be delayed. Fire may produce irritating, corrosive and/or toxic gases. Runoff from fire control or dilution water may be corrosive and/or toxic and cause pollution.

/GUIDE 153 SUBSTANCES - TOXIC and/or CORROSIVE (Combustible)/ 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 in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids. Keep unauthorized personnel away. Stay upwind, uphill and/or upstream. Ventilate enclosed areas.

/GUIDE 153 SUBSTANCES - TOXIC and/or CORROSIVE (Combustible)/ 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.

For more DOT Emergency Guidelines (Complete) data for Dichloroacetic acid (8 total), please visit the HSDB record page.

UN 1764; Dichloroacetic acid

IMO 8; Dichloroacetic acid

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. Dichloroacetic acid is included on the dangerous goods list.

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. Dichloroacetic acid is included on the dangerous goods list.

Corrosive

Unbreakable packaging. Put breakable packaging into closed unbreakable container. Do not transport with food and feedstuffs.

Symbol: C, N; R: 35-50; S: (1/2)-26-45-61

UN Hazard Class: 8; UN Pack Group: II