1,2-Naphthoquinone

158.15300

158.15

208-360-2

804K62F61Q

9831

2811

DTXSID2060171

Golden yellow needles|Red needles from ether

2914690090

34.14000

1.4652

Dark brown powder

1.450 g/cm³ @ Temp: 25 °C

7-145 °C (decomp)

117.4ºC

1.617

In water, 181 mg/L at 25 deg C (est)

9.9X10-5 mm Hg at 25 deg C (est)

Odorless

Henry's Law constant = 4.2X10-9 atm-cu m/mole at 25 °C (est)

1,2-Naphthoquinone is involatile /(non-volatile)/ in steam, and is a relatively weak oxidizing agent.|Hydroxyl radical reaction rate constant = 1.30X10-11 cu cm/molecule-sec at 25 °C (est)

The neat chemical may be sensitive to prolonged exposure to air and light. Insoluble in water.

Ketones

Ketones, such as 1,2-NAPHTHOQUINONE, are reactive with many acids and bases liberating heat and flammable gases (e.g., H2). The amount of heat may be sufficient to start a fire in the unreacted portion of the ketone. Ketones react with reducing agents such as hydrides, alkali metals, and nitrides to produce flammable gas (H2) and heat. Ketones are incompatible with isocyanates, aldehydes, cyanides, peroxides, and anhydrides. They react violently with aldehydes, HNO3, HNO3 + H2O2, and HClO4.

NONH for all modes of transport

3

R22; R36/37/38

S26-S36

QL7000000

Xn; Xi; C; F

P261-P305 + P351 + P338

H302-H315-H319-H335

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

Flash point data for this chemical are not available. It is probably combustible. (NTP, 1992)

|Warning|H302 (95.24%): Harmful if swallowed [Warning Acute toxicity, oral]|P261, P264, P270, P271, P280, P301+P312, P302+P352, P304+P340, P305+P351+P338, P312, P321, P330, P332+P313, P337+P313, P362, P403+P233, P405, and P501|Aggregated GHS information provided by 45 companies from 6 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Fires involving this material can be controlled with a dry chemical, carbon dioxide or Halon extinguisher. (NTP, 1992)

Excerpt from ERG Guide 154 [Substances - Toxic and/or Corrosive (Non-Combustible)]: 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. SPILL: Increase, in the downwind direction, as necessary, the isolation distance shown above. FIRE: If tank, rail car or tank truck 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, 2016)

SMALL SPILLS AND LEAKAGE: If a spill of this chemical occurs, FIRST REMOVE ALL SOURCES OF IGNITION, then you should dampen the solid spill material with acetone and transfer the dampened material to a suitable container. Use absorbent paper dampened with acetone to pick up any remaining material. Seal your contaminated clothing and the absorbent paper in a vapor-tight plastic bag for eventual disposal. Solvent wash all contaminated surfaces with acetone followed by washing with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned. STORAGE PRECAUTIONS: You should protect this chemical from exposure to light. Keep the container tightly closed under an inert atmosphere, and store under refrigerated temperatures. (NTP, 1992)

RECOMMENDED RESPIRATOR: Where the neat test chemical is weighed and diluted, wear a NIOSH-approved half face respirator equipped with an organic vapor/acid gas cartridge (specific for organic vapors, HCl, acid gas and SO2) with a dust/mist filter. (NTP, 1992)

...The toxicity of 1-naphthol and the naphthoquinones was potentiated by dicoumarol, an inhibitor of DT-diaphorase (NADPH:quinone oxidoreductase). This enhanced toxicity was accompanied by a greater amount of surface blebbing, an increased depletion of intracellular GSH, particularly in the case of 1-naphthol and 1,4-naphthoquinone, and a decreased metabolism of 1-naphthol to its conjugates with variable effects on the amount of covalently bound products formed.

1,2-Naphthoquinone's production and use as a chemical reagent and intermediate(1) may result in its release to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 20(SRC), determined from a structure estimation method(2), indicates that 1,2-naphthoquinone is expected to have very high mobility in soil(SRC). Volatilization of 1,2-naphthoquinone from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 4.2X10-9 atm-cu m/mole(SRC), using a fragment constant estimation method(3). 1,2-Naphthoquinone is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 9.9X10-5 mm Hg(SRC), determined from a fragment constant method(4). Biodegradation data were not available(SRC, 2006).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 20(SRC), determined from a structure estimation method(2), indicates that 1,2-naphthoquinone is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 4.2X10-9 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 8.4(SRC), from an estimated log Kow of 2.11(6) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Biodegradation data were not available(SRC, 2006).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), 1,2-naphthoquinone, which has an estimated vapor pressure of 9.9X10-5 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase 1,2-naphthoquinone 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 about 30 hours(SRC), calculated from its rate constant of 1.3X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Vapor-phase 1,2-naphthoquinone is also degraded in the atmosphere by reaction with ozone; the half-life for this reaction in air is estimated to be about 13 hours(SRC), calculated from its rate constant of 2.1X10-17 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). 1,2-Naphthoquinone absorbs at wavelengths between 290 and 480 nm(4) and therefore may be susceptible to direct photolysis by sunlight(SRC). Particulate-phase 1,2-naphthoquinone may be removed from the air by wet or dry deposition(SRC).

The rate constant for the vapor-phase reaction of 1,2-naphthoquinone with photochemically-produced hydroxyl radicals has been estimated as 1.30X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 30 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). The rate constant for the vapor-phase reaction of 1,2-naphthoquinone with ozone has been estimated as 2.10X10-17 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(1). This corresponds to an atmospheric half-life of about 13 hours at an atmospheric concentration of 7X10+11 ozone molecules per cu cm(2). 1,2-Naphthoquinone is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(3). 1,2-Naphthoquinone absorbs at wavelengths between 290 and 480 nm(4) and therefore may be susceptible to direct photolysis by sunlight(SRC).

An estimated BCF of 8.4 was calculated for 1,2-naphthoquinone(SRC), using an estimated log Kow of 2.11(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 1,2-naphthoquinone can be estimated to be 20(SRC). According to a classification scheme(2), this estimated Koc value suggests that 1,2-naphthoquinone is expected to have very high mobility in soil.

The Henry's Law constant for 1,2-naphthoquinone is estimated as 4.2X10-9 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that 1,2-naphthoquinone is expected to be essentially nonvolatile from water surfaces(2).

Occupational exposure to 1,2-naphthoquinone may occur through inhalation and dermal contact with this compound at workplaces where 1,2-naphthoquinone is produced or used. (SRC)

Exptl Therapy: 1-Naphthol was selectively toxic to human colorectal tumors compared to corresponding normal colonic tissue removed at surgery and maintained in short-term organ culture. Nineteen of 24 tumors studied showed a differential response. Three human colonic adenocarcinoma xenografts, in a short-term organ culture system, displayed the same response to 1-naphthol as primary tumors removed at surgery. 1-Naphthol, 1,2-, and 1,4-naphthoquinone were also toxic to two human colonic adenocarcinoma cell lines, LoVo, and COLO 206. The selective toxicity of 1-naphthol was mediated in part through an accumulation of 1-naphthol in the tumor tissue due to an impaired conjugation by the tumor. The higher concentrations of 1-naphthol may then exert their toxicity either directly or by formation of naphthoquinones. Some indirect evidence was obtained for the possible involvement of 1,2- or 1,4-naphthoquinone in the cytotoxicity of 1-naphthol. These studies suggest that further studies are warranted of the possible use of 1-naphthol or related compounds as antitumor agents.

1,2-Naphthoquinone is metabolized to 1,2-dihydroxynaphthalene in pigs. /From Table/|1-Naphthol was metabolized by tyrosinase, polyphenol oxidase, primarily to 1,2-naphthoquinone and to small amounts of 1,4-naphthoquinone as well as to covalently bound products. The inhibition of covalent binding by ethylenediamine, which reacts specifically with 1,2-naphthoquinone but not 1,4-naphthoquinone, suggested that most of the covalent binding was due to 1,2-naphthoquinone or a metabolite of similar structure.|In rat liver microsomal preparations, 1-naphthol is metabolized by the cytochrome p450 mixed function oxidase to 1,4-naphthoquinone and covalently bound species. The major binding species are derived from 1,4-naphthoquinone but not 1,2-naphthoquinone. 1-Naphthol is also metabolized by tyrosinase (monophenol monooxygenase; polyphenol oxidase) primarily to 1,2-naphthoquinone and covalently bound products; most of the covalent binding was derived from a 1,2-naphthoquinone derivative.|The hepatic microsomal metabolism of 1-naphthol, 1,2- and 1,4-naphthoquinone has been shown to generate active oxygen species by using electron spin resonance spin-trapping techniques. 1-Naphthol, in the presence of NADPH, and 1,2- and 1,4-naphthoquinone, with either NADH or NADPH, caused a stimulation in both the rate of microsomal oxygen consumption and the formation of superoxide spin adduct, 5,5-dimethyl-2-hydroxyperoxypyrrolidino-1-oxyl (DMPO-OOH). Superoxide dismutase, but not catalase, prevented the formation of this spin adduct, further supporting the suggestion that the superoxide free radical was the major oxy-radical formed during the microsomal metabolism of 1-naphthol and the naphthoquinones. These results are compatible with the suggestion that 1-naphthol may exert its toxicity to isolated hepatocytes and other cellular systems by metabolism to naphthoquinones followed by their redox cycling with concomittant generation of active oxygen species, in particular superoxide free radicals.|...The toxicity of 1-naphthol may be mediated by the formation of 1,2-naphthoquinone and/or 1,4-naphthoquinone, which may then be metabolized by 1-electron reduction to naphthoquinone radicals. These, in turn, may covalently bind to important cellular macromolecules or enter a redox cycle with molecular oxygen thereby generating active oxygen species. Both of these processes appear to play a role in producing the cytotoxic effects of 1-naphthol.

The mechanisms of toxicity of 1-naphthol and two of its metabolites 1,2-, and 1,4-naphthoquinone, to freshly isolated rat hepatocytes was studied. 1-Naphthol and both naphthoquinones exhibited a dose-dependent toxicity to hepatocytes. (14)C-1-Naphthol was metabolized by hepatocytes predominantly to its glucuronate and sulfate conjugates, but small amounts of covalently bound products were also formed. Blebbing on the surface of the hepatocytes was observed following exposure to 1-naphthol and the naphthoquinones, together with a dose-dependent decr in intracellular GSH, which preceded the onset of cytotoxicity. The toxicity of 1-naphthol and the naphthoquinones was potentiated by dicoumarol, an inhibitor of DT-diaphorase (NADPH:quinone oxidoreductase). This enhanced toxicity was accompanied by a greater amount of surface blebbing, an increased depletion of intracellular GSH, particularly in the case of 1-naphthol and 1,4-naphthoquinone, and a decreased metabolism of 1-naphthol to its conjugates with variable effects on the amount of covalently bound products formed. Apparently, the toxicity of 1-naphthol may be mediated by the formation of 1,2-naphthoquinone and/or 1,4-naphthoquinone, which may then be metabolized by 1-electron reduction to naphthoquinone radicals. These, in turn, may covalently bind to important cellular macromolecules or enter a redox cycle with molecular oxygen thereby generating active oxygen species. Both of these processes appear to play a role in producing the cytotoxic effects of 1-naphthol.|Quinones are alpha-beta-unsaturated ketones & react with sulfhydryl groups. ... Critical biochem lesion ... /involves/ -SH groups of enzymes such as amylase & carboxylase which are inhibited by quinones. Overall mechanism may involve binding of enzyme to quinone nucleus by substitution or addition at the double bond, an oxidative reaction with -SH group, and change in redox potential. /Quinones/

ACUTE/CHRONIC HAZARDS: This compound is an irritant. When heated to decomposition it emits acrid smoke and fumes. (NTP, 1992)

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. If symptoms such as redness or irritation develop, IMMEDIATELY call a physician and be prepared to transport the victim to a hospital for treatment. 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. 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. Be prepared to transport the victim to a hospital if advised by a physician. 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. IMMEDIATELY transport the victim to a hospital. (NTP, 1992)

Basic treatment: Establish a patent airway. Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . For contamination, flush eyes immediately with water. Irrigate each eye continuously with normal saline 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. Administer activated charcoal ... . /Ketones and related compounds/|Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious or in respiratory arrest. Positive pressure ventilation techniques with a bag valve mask device may be beneficial. Monitor cardiac rhythm and treat arrhythmias if necessary ... . Start an IV with D5W /SRP: "To keep open", minimal flow rate/. Use lactated Ringer's if signs of hypovolemia are present. Watch for signs of fluid overload. Consider drug therapy for pulmonary edema ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Ketones and related compounds/|Basic treatment: Establish a patent airway. Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations 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 ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with normal saline during transport ... . Administer activated charcoal ... . Do not use emetics. Cover skin burns with dry, sterile dressings after decontamination ... . Maintain body temperature. /Phenols and related compounds/|Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious or in respiratory arrest. Positive pressure ventilation techniques with a bag valve mask device may be beneficial. Monitor cardiac rhythm and treat arrhythmias if necessary ... . Start an IV with D5W /SRP: "To keep open", minimal flow rate/. Use lactated Ringer's if signs of hypovolemia are present. Watch for signs of fluid overload. Consider drug therapy for pulmonary edema ... . For hypotension with signs of hypovolemia, administer fluid cautiously. Consider vasopressors for hypotension with a normal fluid volume. Watch for signs of fluid overload ... Administer 1% solution methylene blue if patient is symptomatic with severe hypoxia, cyanosis, and cardiac compromise not responding to oxygen. ... .Treat seizures with diazepam (Valium). ... Use proparacaine hydrochloride to assist eye irrigation ... . /Phenols and related compounds/

/SIGNS AND SYMPTOMS/ 1,2-naphthoquinone appears to be the metabolite in naphthalene poisoning that reacts with ocular tissues and is responsible for production of cataract and damage to the retina.|/SIGNS AND SYMPTOMS/ Chronic neurotoxic effects include vision disturbances. /From Table; Quinones/|/BIOMONITORING/ ...The utility of adducts formed by the reaction of the naphthalene metabolites naphthalene-1,2-oxide, 1,2-naphthoquinone (1,2-NPQ), and 1,4-naphthoquinone (1,4-NPQ) with serum albumin (Alb) as biomarkers of exposure to polycyclic aromatic hydrocarbons /was investigated/. Cysteinyl serum Alb adducts of 1,2- and 1,4-NPQ (1,2-NPQ-Alb and 1,4-NPQ-Alb, respectively) but not of naphthalene-1,2-oxide were detected in 28 coke oven workers and 22 controls from the steel industry of northern China. The median level of 1,2-NPQ-Alb in coke oven workers (76.6 pmol/g) was significantly higher than that observed in controls (44.9 pmol/g; P=0.0027). However, the median level of 1,4-NPQ-Alb in exposed subjects was not significantly different from that of controls (48.6 versus 44.2 pmol/g; P=0.296). Levels of 1,2-NPQ-Alb were significantly correlated with exposure category (controls, side and bottom workers, and top-of-oven workers) as well as with previously measured levels of urinary naphthalene, 1- and 2-naphthol, and 1-pyrenol in these subjects. Multiple linear regression analysis revealed that 35% of the variation in 1,2-NPQ-Alb could be explained by the work category and age. A negative relationship between 1,2-NPQ-Alb and age was observed, suggesting that cytochrome P450 c metabolism diminished with age at approximately 3%/year of life.

1,2-naphthoquinone

1,2-Naphthalenedione: INACTIVE

Method: EPA-OSW 8091; Procedure: gas chromatography with electron capture detection or nitrogen-phosphorus detection; Analyte: 1,2-naphthoquinone; Matrix: water, soil, and waste matrices; Detection Limit: not provided.