2,4-ジニトロフェノール (約20%水湿潤品)

1.67

log Kow = 1.67

1.67 (estimated)

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

1.683 g/cu cm at 24 °C

Relative density (water = 1): 1.68

1.683 @ 24°C

Pale yellow platelets or leaflets from water

Yellowish to yellow orthorhombic crystals

less than 1 mg/mL at 67.1 °F (NTP, 1992)

2790

Soluble in ethanol, ethyl ether, benzene, methanol

Solubility at 15 °C (g/100 g solution): ethyl acetate 15.55; acetone 35.90; chloroform 5.39; pyridine 20.08; carbon tetrachloride 0.423; toluene 6.36

Soluble in aqueous alkaline solutions

In water, 5,600 mg/L at 18 °C; 43,000 mg/L at 100 °C

Sublimes (when carefully heated) (NTP, 1992)

Sublimes

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

May explosively decompose on shock, friction, or concussion.

234 to 237 °F (NTP, 1992)

115.5

114.8 °C

112 °C

114.8 °C

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

6.35 (Air = 1)

Relative vapor density (air = 1): 6.36

0.00039 [mmHg]

3.9X10-4 mm Hg at 20 °C

Danger

H300: Fatal if swallowed [Danger Acute toxicity, oral]；H311: Toxic in contact with skin [Danger Acute toxicity, dermal]；H331: Toxic if inhaled [Danger Acute toxicity, inhalation]；H372: Causes damage to organs through prolonged or repeated exposure [Danger Specific target organ toxicity, repeated exposure]；H400: Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard]

P260, P261, P262, P264, P270, P271, P273, P280, P301+P316, P302+P352, P304+P340, P316, P319, P321, P330, P361+P364, P391, P403+P233, P405, and P501 (click each P-code to see the statement)

Danger

Chemical: Phenol, 2,4-dinitro-

Hazard Traits - Hazard Trait Undefined；Authoritative List - CA TACs; CWA 303(c)；Report - if used as a fragrance or flavor ingredient

Status: Active Update: 09-03-2022 https://echa.europa.eu/registration-dossier/-/registered-dossier/10875

Phenol, 2,4-dinitro- (wetted with not less than 15% water by mass): HSNO Approval: HSR001273 Approved with controls

The New Jersey Worker and Community Right to Know Act requires public and private employers to provide information about hazardous substances at their workplaces. (N.J.S.A. 34:5A-1 et. seq.)

Combustible. May explode if subjected to heat or flame. POISONOUS GAS IS PRODUCED WHEN HEATED. Vapors are toxic. Can detonate or explode when heated under confinement. (USCG, 1999)

· 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.；· Corrosives in 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.

· Flammable/combustible material.；· May be ignited by heat, sparks or flames.；· DRIED OUT material may explode if exposed to heat, flame, friction or shock; treat as an explosive (GUIDE 112).；· Keep material wet with water or treat as an explosive (GUIDE 112).；· Runoff to sewer may create fire or explosion hazard.

Combustible. Gives off irritating or toxic fumes (or gases) in a fire. Risk of fire and explosion.

The flammability of the solution depends on the nature of the solvent. Dintrophenol is combustible though it may require some effort to ignite. /Dinitrophenol solutions/

The wet material can burn though it may require some effort to ignite. /Dinitrophenol, wetted with at least 15% water/

DUST: POISONOUS IF INHALED OR IF SKIN IS EXPOSED. SOLID: POISONOUS IF SWALLOWED. (USCG, 1999)

· TOXIC and/or CORROSIVE; inhalation, ingestion or skin contact with material may cause severe injury or death.；· Methyl bromoacetate (UN2643) is an eye irritant/lachrymator (causes flow of tears).；· Contact with molten substance may cause severe burns to skin and eyes.；· Avoid any skin contact.；· Fire may produce irritating, corrosive and/or toxic gases.；· Runoff from fire control or dilution water may be corrosive and/or toxic and cause environmental contamination.

· Some are toxic and may be fatal if inhaled, ingested or absorbed through skin. Specifically, Dinitrophenol, wetted (UN1320); Dinitrophenolates, wetted (UN1321), Sodium dinitro-o-cresolate, wetted (UN1348); and Barium azide, wetted (UN1571) are known to be toxic.；· Contact may cause burns to skin and eyes.；· Fire may produce irritating, corrosive and/or toxic gases.；· Runoff from fire control or dilution water may cause environmental contamination.

2,4-Dinitrophenol is used in the manufacture of dyes, wood preservatives, and as a pesticide. The acute (short-term) effects of 2,4-dinitrophenol in humans through oral exposure are nausea, vomiting, sweating, dizziness, headaches, and loss of weight. Chronic (long-term) oral exposure to 2,4-dinitrophenol in humans has resulted in the formation of cataracts and skin lesions, weight loss, and has caused effects on the bone marrow, central nervous system (CNS), and cardiovascular system. Limited or no information is available on the developmental, reproductive, or carcinogenic effects of 2,4-dinitrophenol in humans. EPA has not classified 2,4-dinitrophenol for carcinogenicity.

In the 1930s, it was used to treat obesity. Reported adverse effects included agranulocytosis, neuritis, and heart damage. Poisoning by ingestion causes uncoupling of oxidative phosphorylation with high fever, sweating, tachycardia, abdominal pain, anxiety, rapid breathing that may end in convulsions and death. Poisoning has also caused toxic hepatitis, renal failure, and cataract formation. [HSDB] May cause first degree burns after short exposure and second degree burns after longer contact; May cause cataracts after chronic exposure; [CHRIS] There is a case report of dinitrophenol causing cholestatic jaundice. [Zimmerman, p. 351] See Dinitrophenol.

The major hazards encountered in the use and handling of 2,4-dinitrophenol stem from its toxicologic properties. Toxic by all routes (ie, inhalation, ingestion, dermal absorption), exposure to this sweet-smelling, yellowish, crystalline substance, may occur from its use as a pesticide on wood products, and as a chemical intermediate in the production of dyes. Effects from exposure may include burns to the skin and eyes, headache, fatigue, nausea, anxiety, loss of consciousness, and death due to cardiac or pulmonary collapse. Exposure should be minimized by the use of exhaust ventilation. In addition, it is recommended that exposure be protected against by wearing butyl rubber gloves, chemical protective clothing which is specifically recommended by the shipper or producer, and, in emergency situations, a self-contained breathing apparatus. If contact does occur, immediately flush affected skin or eyes with running water for at least 15 minutes, and remove and isolate contaminated clothing at the site. 2,4-Dinitrophenol may be ignited by heat, sparks, or flames. Poisonous oxides of nitrogen are produced in a fire. Further, its vapor may explode in confined spaces, or, if the substance becomes dry, it may explode upon contact. For small fires involving 2,4-dinitrophenol, extinguish with dry chemical, CO2, Halon, water spray, or standard foam, and for large fires, use water spray, fog, or standard foam. Fight fires from a maximum distance, using an unmanned hose holder to cool containers well after the fire is out. Runoff from fire control water should be diked to prevent it from entering water sources or sewers. Stored 2,4-dinitrophenol should be kept wet with water, or treated as an explosive. Storage should be in cool, ventilated areas, away from sources of ignition, oxidizing agents, combustible materials, and heavy metals and their compounds. 2,4-Dinitrophenol which is dry, or which is wetted with not less than 15% water by weight is subject to additional restrict

1599 153

1320 113

USEPA; Health and Environmental Profiles for Dinitrophenols 39p (1988) EPA/600/X-84/153. Health and Environmental Effects Profile for 2,4-Dinitrophenol.

U.S. Dept Health & Human Services/Agency for Toxic Substances Disease Registry; Toxicological Profile for Dinitrophenols (1995) NTIS# PB/95/264339

P048; As stipulated in 40 CFR 261.33, when 2,4-dinitrophenol, as a commercial chemical product or manufacturing chemical intermediate or an off-specification commercial chemical product or a manufacturing chemical intermediate, becomes a waste, it must be managed according to federal and/or state hazardous waste regulations. Also defined as a hazardous waste is any container or inner liner used to hold this waste or any residue, contaminated soil, water, or other debris resulting from the cleanup of a spill, into water or on dry land, of this waste. Generators of small quantities of this waste may qualify for partial exclusion from hazardous waste regulations (40 CFR 261.5(e)).

Excerpt from ERG Guide 113 [Flammable Materials (Wet / Desensitized Explosive)]:；CARGO FIRE: DO NOT fight fire when fire reaches cargo! Cargo may EXPLODE! Stop all traffic and clear the area for at least 1600 meters (1 mile) in all directions and let burn. Do not move cargo or vehicle if cargo has been exposed to heat.；TIRE OR VEHICLE FIRE: Use plenty of water - FLOOD it! If water is not available, use CO2, dry chemical or dirt. If possible, and WITHOUT RISK, use unmanned master stream devices or monitor nozzles from maximum distance to prevent fire from spreading to cargo area. Pay special attention to tire fires as re-ignition may occur. Stand by, at a safe distance, with extinguisher ready for possible re-ignition. (ERG, 2024)

Use water in large amounts. In case of fire: keep drums, etc., cool by spraying with water. Combat fire from a sheltered position.

Fresh air, rest.

Remove contaminated clothes. Rinse and then wash skin with water and soap. Refer immediately for medical attention .

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

Rest. Refer immediately for medical attention.

· 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.

· 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.；Small Spill；· Flush area with large amounts of water.；Large Spill；· Wet down with water and dike for later disposal.；· KEEP "WETTED" PRODUCT WET BY SLOWLY ADDING FLOODING QUANTITIES OF WATER.

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. IMMEDIATELY call a physician and be prepared to transport the victim to a hospital even if no symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth, throat, or chest) develop. Provide proper respiratory protection to rescuers entering an unknown atmosphere. Whenever possible, Self-Contained Breathing Apparatus (SCBA) should be used; if not available, use a level of protection greater than or equal to that advised under Protective Clothing.；INGESTION: DO NOT INDUCE VOMITING. Phenols are very toxic poisons AND corrosive and irritating, so that inducing vomiting may make medical problems worse. IMMEDIATELY call a hospital or poison control center and locate activated charcoal, egg whites, or milk in case the medical advisor recommends administering one of them. If advice from a physician is not readily available and the victim is conscious and not convulsing, give the victim a glass of activated charcoal slurry in water or, if this is not available, a glass of milk, or beaten egg whites and IMMEDIATELY transport victim to a hospital. If the victim is convulsing or unconscious, do not give anything by mouth, assure that the victim's airway is open and lay the victim on his/her side with the head lower than the body. DO NOT INDUCE VOMITING. IMMEDIATELY transport the victim to a hospital. (NTP, 1992)

General First Aid:；· 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.

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

· 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.

· Wear positive pressure self-contained breathing apparatus (SCBA).；· Structural firefighters' protective clothing provides thermal protection but only limited chemical protection.

If material on fire or involved in fire: Do not extinguish fire unless flow can be stopped. Use water in flooding quantities as fog. Solid streams of water may be ineffective. Cool all affected containers with flooding quantities of water. Apply water from as far a distance as possible. Use foam, dry chemical, or carbon dioxide. /Dinitrophenol solutions/

If material on fire or involved in fire: Dangerously explosive. Do not fight fires in a cargo of explosives. Evacuate area and let burn. /Dinitrophenol, dry or wetted with less than 15% water by weight)

If material on fire or involved in fire: Dangerously explosive. Flood with water. Cool all affected containers with flooding quantities of water. Apply water from as far a distance as possible. /Dinitrophenol, wetted with at least 15% water/

Wear positive pressure self-contained breathing apparatus when fighting fires involving this material.

Evacuate persons not wearing protective equipment from area of spill or leak until clean-up is complete. Remove all ignition sources. Wet spilled material with water. Collect powdered material in the most convenient and safe manner and deposit in sealed containers. Ventilate area after clean-up is complete. It may be necessary to contain and dispose of this chemical as a hazardous waste. Keep dinitrophenol out of a confined space, such as a sewer, because of the possibility of an explosion, unless the sewer is designed to prevent the build-up of explosive concentrations. If material or contaminated runoff enters waterways, notify downstream users of potentially contaminated waters. Contact your Department of Environmental Protection of your regional office of the federal EPA for specific recommendations.

Environmental considerations: Land spill: Dig a pit, pond, lagoon, or holding area to contain liquid or solid material. /SRP: If time permits, pits, ponds, lagoons, soak holes, or holding areas should be contained with a flexible impermeable membrane liner./ Dike surface flow using soil, sand bags, foamed polyurethane, or foamed concrete. Absorb bulk liquid with fly ash or cement powder. /Dinitrophenol solutions/

Environmental considerations: Water spill: use natural barriers or oil spill control booms to limit spill travel. use surface active agent (e.g., detergent, soaps, alcohols), if approved by EPA. Inject "universal" gelling agent to solidify encircled spill and increase effectiveness of booms. If dissolved in region of 10 ppm or greater concentration, apply activated carbon at ten times the spilled amount. Use mechanical dredges or lifts to remove immobilized masses of pollutants and precipitates. /Dinitrophenol solutions/

Environmental considerations - land spill: dig a pit, pond, lagoon, holding area to contain liquid or solid material. /SRP: If time permits, pits, ponds, lagoons, soak holes, or holding areas should be sealed with an impermeable flexible membrane liner./ Cover solids with a plastic sheet to prevent dissolving in rain or fire fighting water. /Dinitrophenol, wetted with at least 15% water/

Environmental considerations - water spill: Use natural deep water pockets, excavated lagoons, or sand bag barriers to trap material at bottom. If dissolved in region of 10 ppm or greater concentration, apply activated carbon at ten times the spilled amount. Remove trapped material with suction hoses. Use mechanical dredges or lifts to remove immobilized masses of pollutants and precipitates. /Dinitrophenol, wetted with at least 15% water/

Excerpt from ERG Guide 113 [Flammable Materials (Wet / Desensitized Explosive)]:；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.；SMALL SPILL: Flush area with large amounts of water.；LARGE SPILL: Wet down with water and dike for later disposal. KEEP "WETTED" PRODUCT WET BY SLOWLY ADDING FLOODING QUANTITIES OF WATER. (ERG, 2024)

Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number P048, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.

Dinitrophenol: Incinerate (1800 °F, 2.0 sec minimum) with adequate scrubbing equipment for the removal of NOx. Dinitrophenol ... /is a/ waste chemical stream constituent which may be subjected to ultimate disposal by controlled incineration. /Dinitrophenol/

A potential candidate for rotary kiln incineration at a temperature range of 820 to 1,600 °C and residence times of seconds for liquids and gases, and hours for solids. A potential candidate for fluidized bed incineration at a temperature range of 450 to 980 °C and residence times of seconds for liquids and gases, and longer for solids.

Chemical Treatability of 2,4-Dinitrophenol; Concentration Process: Biological Treatment. Chemical Classification: Phenol; Scale of Study: Respirometer Study; Type of Wastewater Used: Synthetic Wastewater; Results of Study: Max oxygen uptake was 27.7 ppm of aeration.

For more Disposal Methods (Complete) data for 2,4-Dinitrophenol (8 total), please visit the HSDB record page.

There is no specific antidote for 2,4-DNP poisoning. Symptomatic treatment includes replacing oxygen and fluids, controlling temperature by administering sponge baths and ice packs, and using a fan to promote air flow and evaporation. In fully conscious patients, administer cold, sugar-containing liquids by mouth as tolerated. In cases of skin contact, bathe and shampoo contaminated skin and hair promptly. (L179)

2,4-DNP appears to markedly increase the rate of ethanol metabolism in rat liver slices by 100-160% and in rats in vivo by 20-30%. Because 2,4-DNP uncouples mitochondrial electron transport from oxidative phosphorylation, the oxidation of NADH to NAD+ is accelerated in the mitochondria. Reoxidation of NADH rather than the activity of alcohol dehydrogenase is the rate-limiting step in the metabolism of ethanol, and, therefore, the metabolic effect of 2,4-DNP enhances the clearance of ethanol. Because 2,4-DNP is known to augment the rate of respiration and perspiration, .2.7-8.2% of the initial dose of ethanol was also eliminated by expiration and cutaneous evaporation in the rat.

In isolated perfused rat livers, 2,4-DNP caused a depletion of the mitochondrial calcium pool, without altering the extramitochondrial calcium pool. Because 2,4-DNP uncouples oxidative phosphorylation from electron transport by dissipating the electrochemical potential, which provides the energy for the accumulation of calcium in the mitochondrial matrix, only the calcium pool in the mitochondria was affected. 2,4-DNP also caused a rapid increase in NAD, along with a decrease in NADH, a rapid decrease in protein thiol content, but only a slow decrease in nonprotein thiol (e.g., reduced glutathione [GSH]), and an increase in cytoplasmic calcium concentration in isolated rat intestinal cells. This DNP-induced protein thiol loss and/or increase of cytoplasmic calcium concentration induced cell rounding and decreased cell viability. Incubation of salicylate and 2,4-DNP with intestinal cells caused a reduction in the 2,4-DNP-induced increase in cytosolic free calcium concentration by complexation, which facilitated the release of calcium from cells. Salicylate also inhibited DNP-induced cell rounding and increased cell viability in the small intestine.

Salicylate (aspirin), which also uncouples oxidative phosphorylation in mitochondrial preparations (although at much higher concentrations than 2,4-DNP), partially inhibited a protein thiol loss induced by 2,4-DNP, but not nonprotein thiol loss by 2,4-DNP in the small intestine of rats. Although DNP inhibits the absorption of the hydrophilic drug, cefmetazole, incubation of DNP and salicylate removed this inhibitory effect in the small intestine. By preventing the DNP-induced protein thiol loss in the small intestine, salicylate appears to enhance diffusivity of cefmetazole in the small intestines. However, salicylate at very high doses can also increase respiratory rates and produce hyperthermia in humans, and possibly exaggerate these signs in persons acutely exposed to 2,4-DNP.

Pretreatment of rats with haloperidol significantly diminished the hyperpyrexia and lethality of 2,4-DNP by interfering with the uncoupling of oxidative phosphorylation by 2,4-DNP. The protection by haloperidol may have occurred by an indirect action on the mitochondrial membrane.

For more Interactions (Complete) data for 2,4-Dinitrophenol (15 total), please visit the HSDB record page.

2,4-DNP can cause cataracts following ingestion of a small dose for short or long periods. This condition could lead to blindness in both eyes. Breathing in, swallowing, or having skin contact with large amounts of DNP can lead to death.(L168)

LC50; Species: Lepomis macrochirus (bluegill); Concentration: 620 ug/L for 96 hr /Conditions of bioassay not specified in source examined/

LC50; Species: Salmo salar (Atlantic salmon); Concentration: 700 ug/L for 96 hr /Conditions of bioassay not specified in source examined/

LC50; Species: Mysidopsis bahia (Mysid shrimp); Concentration: 4850 ug/L for 96 hr /Conditions of bioassay not specified in source examined/

LC50; Species: Herring embryo; Concentration: 5,500 ug/L for 96 hr /Conditions of bioassay not specified in source examined/

For more Ecotoxicity Values (Complete) data for 2,4-Dinitrophenol (50 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), a Koc values of 13.5(2) and 16.6(3), indicate that 2,4-dinitrophenol is expected to have very high mobility in soil(SRC). The pKa of 2,4-dinitrophenol is 4.09(4), 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(5). This can be seen in the measured Koc values(SRC). 2,4-Dinitrophenol is not expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 3.9X10-4 mm Hg at 20 °C(6). A 0% of theoretical BOD using activated sludge in the Japanese MITI test(7) suggests that biodegradation is not an important environmental fate process in soil(SRC). However, the biodegradation half-life of 2,4-dinitrophenol in an acidic soil was reported as 32.1 days and the biodegradation half-life in a basic soil was reported as 4.6 days(8).

TERRESTRIAL FATE: 2,4-Dinitrophenol is a moderately weak acid that is expected to be highly labile (leachable and plant available) in high-pH soils. The adsorption and degradation behavior of 2,4-dinitrophenol in two sludge-amended, calcareous soils was determined and used to explain 2,4-dinitrophenol uptake by plants grown in the soils in the greenhouse. The 2,4-dinitrophenol adsorption was minor in both soils and was only slightly affected by sludge. The 2,4-dinitrophenol degradation was rapid in both soils and was unaffected by sludge. Thus, despite limited soil adsorption, plant uptake of 2,4-dinitrophenol was minor in all crops and plant parts owing to rapid soil 2,4-dinitrophenol degradation. Even if a municipal sludge highly contaminated with 2,4-dinitrophenol was identified (an unlikely occurrence), concerns over possible plant contamination should not limit sludge applications to calcareous soils at agronomic rates. Rapid degradation will minimize opportunities for plant uptake of 2,4-dinitrophenol from contaminated soils or leaching of 2,4-dinitrophenol to groundwater given careful water management.

AQUATIC FATE: Based on a classification scheme(1), a Koc values of 13.5(2) and 16.6(3), indicate that 2,4-dinitrophenol is not expected to adsorb to suspended solids and sediment(SRC). A pKa of 4.09(4) indicates 2,4-dinitrophenol 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(5), BCFs of <0.4-0.7 and <3.7(6), suggest the bioconcentration in aquatic organisms is low(SRC). The biodegradation half-life of 2,4-dinitrophenol was reported as 68 days and 2.8 days in aerobic and anaerobic waters, respectively(7).

AQUATIC FATE: ... The high solubility of 2,4-dinitrophenol in water (5,600 mg/L at 18 °C) and its presence in solution primarily as an anion strongly favor a partitioning tendency toward water rather than air.

For more Environmental Fate (Complete) data for 2,4-Dinitrophenol (6 total), please visit the HSDB record page.

Occupational hepatotoxin - Secondary hepatotoxins: the potential for toxic effect in the occupational setting is based on cases of poisoning by human ingestion or animal experimentation.；Nephrotoxin - The chemical is potentially toxic to the kidneys in the occupational setting.；Methemoglobinemia - The presence of increased methemoglobin in the blood; the compound is classified as secondary toxic effect；Other Poison - Uncoupler；Dermatotoxin - Skin burns.

The substance can be absorbed into the body through the skin and by ingestion.

Oral (L170); inhalation (L170) ; dermal (L170)

Acute 2,4-dinitrophenol poisoning (from ingestion) involves uncoupling of oxidative phosphorylation, which presumably reduces body's reservoirs of high-energy phosphate. This stimulates oxidative metabolism and, in turn, the heat production of the body. Oxygen consumption, body temperature, respiration and heart rate are all increased. 2,4-Dinitrophenol has been suggested to bind serum proteins such as transthyretin. In fact it was proposed as a therapeutic agent for the prevention/inhibition of amyloid diseases through stabilization of the native fold of transthyretin. (T21, A126, A127)

/BIRDS and MAMMALS/ In a study where bobwhite quail were exposed to 2,4-DNP in the diet, 1 of 6 hens in a group consuming 56.1 mg/kg/day died on the eighth and final day of exposure. Necropsy revealed a marked scarcity of subcutaneous fat, reduced visceral fat, and possibly some shrinkage of leg and breast muscles.

/BIRDS and MAMMALS/ Bobwhite quail were exposed to 2,4-dinitrophenol (DNP) in a respirometer designed to continuously monitor exchange of O2 and CO2, from which metabolic rates (MR) were estimated. After 14-16 days of acclimation to the system (temperature 22 °C, light cycle 8L:14D), hens received feed amended with 0, 625 ppm, or 1250 ppm DNP ad libitum for eight days, followed by 2-5 days of 0 ppm feed. The 625 ppm treatment produced dark period MR 31-41% higher than corresponding control values, and light period MR 23-32% higher than controls. The 1250 ppm treatment produced dark period MR 48-77% higher than control values, and light period MR 41-67% higher than control. Over the eight days of testing, the 625 ppm treatment hens expended 32% more energy than the control hens and hens consuming 1250 ppm feed expended 60% more energy than control hens and lost most of their body fat. In general, the risk of being unable to meet energy demands for survival or reproduction would probably be substantially increased by the observed elevation in MR.

/BIRDS and MAMMALS/ Ducklings fed 2,4-dinitrophenol at a concentration of 2,500 ppm developed cataracts within 24 hr ... Chickens were also susceptible. Cataract was observed in duckling only 3.5 hr after crop intubation. With no further dosing, the lesion cleared within 3 days.

/BIRDS and MAMMALS/ The effects of pharmacologically elevated metabolism on respiratory adjustments were studied in chickens. Adult female white leghorn chickens were decerebrated and allowed to recover from anesthesia. In experiment 1, birds were injected with 2.5 mg/kg 2,4-dinitrophenol. Respiratory and cardiovascular measurements were monitored continuously. After steady state conditions were reestablished, another 2.5 mg/kg 2,4-dinitrophenol injection was given and measurements were taken again. Injections and measurements continued until no further oxygen consumption increase occurred. Some birds received a single 5 mg/kg 2,4-dinitrophenol injection. Measurements were repeated every 5 minutes. In experiment 2, birds had control measurements and arterial blood samples taken at approximately 20 °C. Birds were cooled to 2 °C. After a steady respiratory response was established, measurements were taken. Successive 2,4-dinitrophenol doses caused a progressive oxygen consumption increase in the decerebrated chickens; a 7.5 to 10 mg/kg dose of 2,4-dinitrophenol elicited the maximal oxygen consumption response, approximately 275% of control values. A single 5 mg/kg 2,4-dinitrophenol injection increased oxygen consumption and the respiratory exchange ratio and increased minute ventilation. Ventilation significantly increased within 10 seconds of the start of 2,4-dinitrophenol injection. A steady state was reached approximately 10 minutes after the start of injection. Birds hyperventilated about 45 minutes after injection when the temperature reached approximately 42.3 °C. The respiratory and cardiovascular effects of the increased metabolism during cold exposure was similar to the initial elevated metabolism responses elicited by 2,4-dinitrophenol. Oxygen consumption increased to approximately 185% of control values; V1 increased in a way that oxygen extraction remained unchanged. /It was concluded/ that 2,4-dinitrophenol induced hyper metabolism in the decerebrated chi

For more Ecotoxicity Excerpts (Complete) data for 2,4-Dinitrophenol (19 total), please visit the HSDB record page.

The phytotoxic nitrophenols were analyzed in beech tree leaves (Fagus sylvatica) from two different alpine forests (Val Gerola and Val Masino) in the Lombardy Region (Northern Italy) which are in decline due to adverse effects of air pollution. Leaves from the more damaged site (Val Gerola) had higher mean total nitrophenol concentrations (313 ng/g) than the Val Masino samples (148 ng/g). 2,4-Dinitrophenol concentrations reported in beach leaves from Val Gerola and Val Masino were 8.2 and 4.1 ng/g dry weight, respectively; sampling was conducted from 1994-1995(1).

See Ingestion.

MAY BE ABSORBED! Redness. Roughness. Yellow staining of the skin. Further see Inhalation.

Yellow vision. Redness. Conjunctivitis.

Nausea. Sweating. Severe thirst. Fever. Increased heart rate. Vomiting. Shock or collapse.

Dermal contact may results in redness, roughness, yellow staining of the skin. Nausea, vomiting, palpitations, collapse, sweating occur after inhalation or ingestion. (L170)

Chemical: Phenol, 2,4-dinitro-

Hazard Traits - Hazard Trait Undefined；Authoritative List - CA TACs; CWA 303(c)；Report - if used as a fragrance or flavor ingredient

Status: Active Update: 09-03-2022 https://echa.europa.eu/registration-dossier/-/registered-dossier/10875

Phenol, 2,4-dinitro- (wetted with not less than 15% water by mass): HSNO Approval: HSR001273 Approved with controls

The New Jersey Worker and Community Right to Know Act requires public and private employers to provide information about hazardous substances at their workplaces. (N.J.S.A. 34:5A-1 et. seq.)

P048; As stipulated in 40 CFR 261.33, when 2,4-dinitrophenol, as a commercial chemical product or manufacturing chemical intermediate or an off-specification commercial chemical product or a manufacturing chemical intermediate, becomes a waste, it must be managed according to federal and/or state hazardous waste regulations. Also defined as a hazardous waste is any container or inner liner used to hold this waste or any residue, contaminated soil, water, or other debris resulting from the cleanup of a spill, into water or on dry land, of this waste. Generators of small quantities of this waste may qualify for partial exclusion from hazardous waste regulations (40 CFR 261.5(e)).

Pursuant to section 8(d) of TSCA, EPA promulgated a model Health and Safety Data Reporting Rule. The section 8(d) model rule requires manufacturers, importers, and processors of listed chemical substances and mixtures to submit to EPA copies and lists of unpublished health and safety studies. 2,4-Dinitrophenol is included on this list. Effective date 9/30/91; Sunset date: 12/19/95.

Section 8(a) of TSCA requires manufacturers of this chemical substance to report preliminary assessment information concerned with production, exposure, and use to EPA as cited in the preamble in 51 FR 41329. Effective date 9/30/91; Reporting date: 11/27/91.

As the federal pesticide law FIFRA directs, EPA is conducting a comprehensive review of older pesticides to consider their health and environmental effects and make decisions about their continued use. Under this pesticide reregistration program, EPA examines newer health and safety data for pesticide active ingredients initially registered before November 1, 1984, and determines whether the use of the pesticide does not pose unreasonable risk in accordance to newer saftey standards, such as those described in the Food Quality Protection Act of 1996. Pesticides for which EPA had not issued Registration Standards prior to the effective date of FIFRA '88 were divided into three lists based upon their potential for human exposure and other factors, with List B containing pesticides of greater concern than those on List C, and with List C containing pesticides of greater concern than those on List D. 2,4-Dinitrophenol is found on List B. Case No: 2195; Pesticide type: Insecticide, fungicide; Case Status: No products containing the pesticide are actively registered ... The case /is characterized/ as "cancelled." Under FIFRA, pesticide producers may voluntarily cancel their registered products. EPA also may cancel pesticide registrations if registrants fail to pay required fees or make/meet certain reregistration commitments, or if EPA reaches findings of unreasonable adverse effects.; Active ingredient (AI): 2,4-dinitrophenol; AI Status: The active ingredient is no longer contained in any registered pesticide products ... "cancelled."

Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. EPA is required to establish and phase in specific performance based standards for all air emission sources that emit one or more of the listed pollutants. 2,4-Dinitrophenol is included on this list.

This action promulgates standards of performance for equipment leaks of Volatile Organic Compounds (VOC) in the Synthetic Organic Chemical Manufacturing Industry (SOCMI). The intended effect of these standards is to require all newly constructed, modified, and reconstructed SOCMI process units to use the best demonstrated system of continuous emission reduction for equipment leaks of VOC, considering costs, non air quality health and environmental impact and energy requirements. 2,4-Dinitrophenol is produced, as an intermediate or a final product, by process units covered under this subpart.

Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 10 lb or 4.54 kg. The toll free number of the NRC is (800) 424-8802; The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b).

Dinitrophenol is designated as a hazardous substance under section 311(b)(2)(A) of the Federal Water Pollution Control Act and further regulated by the Clean Water Act Amendments of 1977 and 1978. These regulations apply to discharges of this substance. This designation includes any isomers and hydrates, as well as any solutions and mixtures containing this substance. /Dinitrophenol; CAS No. 51-28-5/

Toxic pollutant designated pursuant to section 307(a)(1) of the Federal Water Pollution Control Act and is subject to effluent limitations. /Nitrophenols/

For the protection of human health from the toxic properties of dinitrophenols ... ingested throughwater and contaminated aquatic organisms, the ambient water criteria /is/ determined to be 70 ug/l ... ingested through contaminated aquatic organisms alone /is/ determined to be 14.3 mg/l ... . /Dinitrophenols/

(AZ) ARIZONA 14 ug/L

(FL) FLORIDA 30 ug/L

(ME) MAINE 14 ug/L

(MN) MINNESOTA 10 ug/L

2,4-DNP was demonstrated to be an uncoupler of oxidative phosphorylation in an in vitro study. 2,4-DNP prevented phosphorylation without affecting, or with a slight stimulation of, oxidation. During the Krebs cycle, 2,4-DNP uncouples oxidative phosphorylation from electron transport by carrying protons across the inner mitochondrial membrane, thereby dissipating the pH gradient and membrane electrochemical potential and preventing the formation of adenosine triphosphate (ATP). During this uncoupling, electron transport from NADH to oxygen proceeds normally, but the energy produced, which is normally stored in high-energy phosphate bonds in ATP, is released as heat. The small amount of ATP produced directly from glycolysis is not affected. In vitro studies further demonstrated and investigated the ability of 2,4-DNP to uncouple oxidative phosphorylation. 2,4-DNP increased the rate of oxygen uptake and changed the electron microscopic appearance of rat liver mitochondria in vitro from an expanded configuration to a condensed state, with the ultrastructural change occurring in concert with the functional changes of uncoupling. All energy-dependent biochemical processes thus are likely to be affected. Many of the clinical observations of 2,4-DNP toxicity, such as elevated basal metabolic rate or oxygen consumption, elevated respiration and pulse rates, increased perspiration, increased body temperature in humans and animals are related to the uncoupling of oxidative phosphorylation. When heat production exceeds the organism's capacity to dissipate heat, fatal hyperthermia may result

The uncoupling of mitochondrial electron transport from oxidative phosphorylation with resultant decreased production of ATP by 2,4-DNP appears to be related to the cataractogenesis of 2,4-DNP. The lens epithelium is the chief source of available energy for the lens. In most animals, the energy needs are met principally by anaerobic glycolysis, and <30% by oxidative phosphorylation. In incubated bovine lenses, oxygen was not necessary for maintaining sodium levels in the presence of glucose, suggesting anaerobic respiration in the lens. Energy evolved from the breakdown of ATP by Na+/K+-activated ATPase is required for the transport of these cations across the lens epithelium to maintain proper ionic balance. Sodium is actively transported from the lens to the aqueous humor, while potassium is actively transported in the reverse direction. Interference with this active transport mechanism across the lens epithelium can result in increased sodium in the lens, disruption of the ionic balance between the lens and aqueous humor, and subsequent cataract formation. An in vitro study with rabbit lenses also demonstrated that 2,4-DNP does not cause calcium-induced cataracts by interfering with active transport of calcium from the lens, because the energy for calcium transport is derived from anaerobic glycolysis and not oxidative phosphorylation.

Transthyretin (TTR), a homotetrameric thyroxine transport protein found in the plasma and cerebrospinal fluid, circulates normally as a innocuous soluble protein. In some individuals, TTR polymerizes to form insoluble amyloid fibrils. TTR amyloid fibril formation and deposition have been associated with several diseases like familial amyloid polyneuropathy and senile systemic amyloidosis. Inhibition of the fibril formation is considered a potential strategy for the therapeutic intervention. The effect of small water-soluble, hydrophobic ligand 2,4-dinitrophenol (2,4-DNP) on TTR amyloid formation has been tested. 2,4-DNP binds to TTR both at acidic and physiological pH, as shown by the quenching of TTR intrinsic fluorescence. Interestingly, 2,4-DNP not only binds to TTR at acidic pH but also inhibits amyloid fibril formation as shown by the light scattering and Congo red-binding assay. Inhibition of fibril formation by 2,4-DNP appears to be through the stabilization of TTR tetramer upon binding to the protein, which includes active site. These findings may have implications for the development of mechanism based small molecular weight compounds as therapeutic agents for the prevention/inhibition of the amyloid diseases.

Systemic deposition of transthyretin (TTR) amyloid fibrils is always observed in familial amyloidotic polyneuropathy, senile systemic amyloidosis and familial amyloidotic cardiomyopathy patients. Destabilization of the molecule leads to a cascade of events which result in fibril formation. The destabilization of a native protein with consequent conformational changes appears to be a common link in several human amyloid diseases. Intensive research has been directed towards finding small molecules that could work as therapeutic agents for the prevention/inhibition of amyloid diseases through stabilization of the native fold of the potentially amyloidogenic protein. This work provides insight into the structural determinants of the highly stabilizing effects of 2,4-dinitrophenol on wild-type TTR. It is also shown that similar interactions are established between this molecule and two highly amyloidogenic TTR variants: TTR L55P and TTR Y78F. In the three crystal complexes, 2,4-dinitrophenol occupies the two hormone-binding sites of the TTR tetramer. As a result of 2,4-dinitrophenol binding, the two dimers in the TTR tetramer become closer, increasing the stability of the protein. The three-dimensional structures now determined allow a comprehensive description of key interactions between transthyretin and 2,4-dinitrophenol, a small compound that holds promise as a template for the design of a therapeutical drug for amyloid diseases.

For more Mechanism of Action (Complete) data for 2,4-Dinitrophenol (24 total), please visit the HSDB record page.

2,4-DNP and two of its metabolites, 2-amino-4-nitrophenol and 4-amino-2-nitrophenol, were monitored in plasma of mice at 0.5, 1, 2, 4, 6, 9, 12, 24, 48, and 96 hours following a single gavage dose of 22.5 mg/kg using a highly specific capillary GC/MS technique. /It was/ concluded that the amount of 2-amino-4-nitrophenol formed was 7.9 times the amount of 4-amino-2-nitrophenol, and that 50% of 2,4-DNP elimination involved direct conversion to these two compounds. Plasma concentrations of these two metabolites reached their highest levels within the first half hour after dosing, indicating rapid metabolism. The results demonstrate that 2-amino-4- nitrophenol is the major circulating metabolite of 2,4-DNP and that 4-amino-2-nitrophenol is also a significant circulating metabolite.

/An/ investigation of the in vitro metabolism of 2,4-DNP by rat liver homogenates found that, under optimal pH and cofactor levels, 81% of the 2,4-DNP was metabolized. 2-Amino-4-nitrophenol accounted for 75%, 4-amino-2-nitrophenol for 23%, and 2,4-diaminophenol for approx 1% of the total amine metabolites produced. Even under suboptimal conditions, 2-amino-4-nitrophenol was the predominant metabolite.

The distribution of enzyme activity was analyzed in subcellular fractions: nucleic, mitochondrial, microsomal, and cytosol. The maximum activity was found in the cytosol, which is the site of other nitroreductases, although nitroreductases can also be located in microsomes. The properties of nitroreductases have been extensively studied for the reduction of p-nitrobenzoic acid. Two separate enzyme systems are involved, one located in the cytosol, and the other in the microsomes. Both forms require the presence of reduced nicotinamide adenine dinucleotides (NADH or NADPH). The cytosolic reducing activity for 2,4-DNP required NADPH, since the activity in both the whole homogenate and in the cytosol was enhanced by adding glucose-6-phosphatase and NADP. The fact that the washed microsomal fraction contained no appreciable activity with 2,4-DNP could be due to the absence of soluble NADPH-generating enzymes, such as a glucose-6-phosphate dehydrogenase. Oxygen partially inhibited the formation of the aminonitrophenols. This inhibition is consistent with a reoxidation of cofactors FADH2 or NADPH in the presence of oxygen. Reduction of (14)C-2,4-DNP to 2-amino-4-nitrophenol and 4-amino-2-nitrophenol by rat liver homogenates was not affected by the addition of p-nitrobenzoic acid, suggesting that different nitroreductases are involved. However, p-nitrophenol, o-nitrophenol, and 2,4-dinitro-6-sec-butylphenol inhibited the reduction of 2,4-DNP. The reduction was competitively inhibited by o-nitrophenol and noncompetitively inhibited by p-nitrophenol and 2,4-dinitro-6-sec-butylphenol. These results indicate separate metabolic pathways for 2,4-DNP and p-nitrobenzoic acid. The competitive inhibition by o-nitrophenol, however, suggests that 2,4-DNP and o-nitrophenol compete for the same active site on the nitroreductase, while the noncompetitive inhibition by the other two nitro compounds suggests binding at different sites on the enzyme. Limited information indicates that 2,4-DN

In urine of /sc/ treated rabbits, dinitrophenol glucuronide, 2-aminonitrophenol & its ether sulfate were found. In vitro, but not in vivo, studies indicated presence of 4-aminonitrophenol. Latter was unstable ... .

For more Metabolism/Metabolites (Complete) data for 2,4-Dinitrophenol (8 total), please visit the HSDB record page.

2,4-DNP can readily enter the body through inhalation and ingestion. It can probably be absorbed through the skin also. Animal studies show that after 2,4-DNP enters the body, the blood can carry it to organs and tissues such as the liver, the kidneys, and the eyes. DNP does not build up in organs and tissues, but it is metabolized via reduction of the nitro groups or broken down to other chemicals. The parent compound and metabolites such as 2-amino-4-nitrophenol, 4-amino-2-nitrophenol and diaminophenol are excreted in the urine. 2,4-DNP is also excreted by mammals, partially unchanged, partially conjugated with glucuronic acid and probably as 2,4-diamenolphenol. (L168, T30)

Chemical agents that uncouple oxidation from phosphorylation in the metabolic cycle so that ATP synthesis does not occur. Included here are those IONOPHORES that disrupt electron transfer by short-circuiting the proton gradient across mitochondrial membranes.

Chemicals and substances that impart color including soluble dyes and insoluble pigments. They are used in INKS; PAINTS; and as INDICATORS AND REAGENTS.

2,4-DNP appears to be readily absorbed from the respiratory and gastrointestinal tracts. Some evidence suggests significant absorption through the skin as well. 2,4-DNP is relatively lipophilic with a pKa of 4.09 and therefore is likely to be rapidly absorbed by passive diffusion of the un-ionized form from acidic compartments like the stomach. Another factor favoring the rapid absorption of 2,4-DNP is its small molecular weight (184.1). Molecules with a molecular weight below 600 daltons can permeate cell membranes through aqueous channels regardless of their ionization state.

2,4-DNP appears to be metabolized to less toxic metabolites (primarily aminonitrophenols) that are excreted in the urine. The mechanism of excretion may be passive diffusion, in part, although there is some evidence from one in vitro study of active secretion of 2,4-DNP by the renal organic acid transport process.

It is readily absorbed from skin and through respiratory tract and GI tract.

Studies of blood aqueous barrier & differences of penetrability of 2,4-dinitrophenol into eye from blood in different species ... have shown that dinitrophenol gets into aqueous humor more readily & reaches higher concn in ducks that develop cataracts than ... rabbits that do not. Also, in immature rabbits, in which cataracts can be produced, dinitrophenol entered aqueous humor more readily than in mature rabbits which did not develop cataracts.

For more Absorption, Distribution and Excretion (Complete) data for 2,4-Dinitrophenol (10 total), please visit the HSDB record page.

2,4-Dinitrophenol is used in the manufacture of dyes and wood preservatives, as a pesticide, and as an indicator for the detection of potassium and ammonium ions. During the 1930s, 2,4-dinitrophenol was used as a diet pill, but this use was stopped in 1938.

Used as a chemical intermediate (dyes and photographic developers), biocide in metal-working fluids, wood preservative, insecticide, polymerization inhibitor (styrene production), and veterinarian medication; [HSDB]

Its use as a pesticide was cancelled. [HSDB]

Metal Machining [Category: Heat or Machine]；Applying Wood Preservatives [Category: Other]；Plastic Composites Manufacturing [Category: Industry]

For 2,4-dinitrophenol (USEPA/OPP Pesticide Code: 037509) there are 0 labels match. /SRP: Not registered for current use in the U.S., but approved pesticide uses may change periodically and so federal, state and local authorities must be consulted for currently approved uses./

The active ingredient is no longer contained in any registered pesticide products ... "cancelled."

(1972) PROBABLY GREATER THAN 4.54X10+5 G

(1975) PROBABLY GREATER THAN 4.54X10+5 G

(1977): < 1000 pounds

(1978): > 600,000 lb /From table/

For more U.S. Production (Complete) data for 2,4-Dinitrophenol (6 total), please visit the HSDB record page.

HYDROLYSIS OF 2,4-DINITRO-1-CHLOROBENZENE WITH SODIUM HYDROXIDE.

(a) By heating phenol with dilute sulfuric acid, cooling the product, and then nitrating, keeping the temperature approximately 50 °C; (b) by nitration with mixed acid with careful temperature control. /Dinitrophenol/

2,4-Dinitrochlorobenzene is hydrolyzed by heating with 6% aqueous sodium hydroxide at 95 - 100 °C for 4 hr. The product is precipitated by addition of acid, filtered off, and washed to remove acid and also a small quantity of the more soluble 2,6-isomer. The yield is 95 %.

85% with 15% water.

Osmoplastic-R wood preserving compound, solution-ready to use; 45.62% creosote oil (derived from any source), 2.0% dinitrophenol, 3.1% potassium dichromate, 44.42% sodium fluoride.

Cobra salts (Impregna salts), soluble concentrate; 20.0% arsenic trioxide, 21.5% dinitrophenol, 51.0% sodium fluoride.

Shirakiku brand mosquito coils, impregnated materials; 0.42% Allethrin (Allyl homolog of cinerin I), 78.78% Allethrin coil, 0.2% dinitrophenol, 20.6% pyrethrum powder other than pyrethrins.

For more Formulations/Preparations (Complete) data for 2,4-Dinitrophenol (6 total), please visit the HSDB record page.

Phenol, 2,4-dinitro-: ACTIVE

Commercial product is a mixture of 2,3-, 2,4- and 2,6- isomers. /Dinitrophenol/