Phenanthrene

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.

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.

To fight fire, use water, foam, carbon dioxide or dry chem.

Fire fighting: Self-contained breathing apparatus with a full facepiece operated in pressure-demand or other positive pressure mode. /Coal tar pitch volatiles/

Extinguishant: Foam, dry chemical, and carbon dioxide. /Coal tar pitch volatiles/

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Avoid breathing dust. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided. Methods and materials for containment and cleaning up: Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for disposal.

The particle-bound portion of polycyclic aromatic hydrocarbons (PAH) can be removed by sedimentation, flocculation, and filtration processes. The remaining ... dissolved PAH usually requires oxidation for partial removal/transformation. /Polynuclear aromatic hydrocarbons/

SMALL SPILLS AND LEAKAGE: Should a spill occur while you are handling this chemical, FIRST REMOVE ALL SOURCES OF IGNITION, then you should dampen the solid spill material with ethanol and transfer the dampened material to a suitable container. Use absorbent paper dampened with ethanol to pick up any remaining material. Seal the absorbent paper, and any of your clothes, which may be contaminated, in a vapor-tight plastic bag for eventual disposal. Solvent wash all contaminated surfaces with ethanol 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.

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; Contaminated packaging: Dispose of as unused product.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Avoid breathing dust. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided.

Precautions for safe handling: Avoid contact with skin and eyes. Avoid formation of dust and aerosols. Further processing of solid materials may result in the formation of combustible dusts. The potential for combustible dust formation should be taken into consideration before additional processing occurs. Provide appropriate exhaust ventilation at places where dust is formed.

Appropriate engineering controls: Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of workday.

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 Phenanthrene (15 total), please visit the HSDB record page.

8 Hr Time Weighted Avg (TWA): 0.2 mg/cu m. /Coal tar pitch volatiles, as benzene soluble aerosol/

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. /Coal tar pitch volatiles, as benzene soluble aerosol/

A1; Confirmed human carcinogen. /Coal tar pitch volatiles, as benzene soluble aerosol/

Biological Exposure Index (BEI): Determinant: 1-Hydroxypyrene (1-HP) in urine (with hydrolysis); Sampling Time: end of shift at end of workweek. BEI: None.; Biological monitoring should be considered for this compound based on the review; however, a specific BEI could not be determined due to insufficient data. /Polycyclic aromatic hydrocarbons/

For more Threshold Limit Values (TLV) (Complete) data for Phenanthrene (6 total), please visit the HSDB record page.

0.2 mg/m³ (benzene-soluble aerosol) [1984]

0.15 [mg/m3]

1.8 [mg/m3]

10 [mg/m3]

Phenanthrene was detected in 100% of personal air samples at a median concentration of 35 ng/cu m(1). Adipose tissue collected from Korean women during 2007/2008 contained a mean phenanthrene conentration of 12 ng/g lipid wt (93% detection frequency, range of <1.0-31 ng/g)(2). Blood plasma collected from 51 healthy females and 60 healthy males in Hong Kong during 2008 contained mean phenanthrene concentrations (ng/g lipid) of 366 (range 131-797) in females and 303 (range 116-674) in males(3).

In an analysis of 33 human placenta samples collected from non-smoking women in Beijing, China during 2005-2006, phenanthrene was detected at mean, median, minimum and maximum concentrations of 13.4, 10.4, 5.04 and 26.8 ng/g fresh weight respectively(1). In an analysis of 7 human umbilical blood samples collected from non-smoking women in Beijing, China during 2005-2006, phenanthrene was detected at mean, median, minimum and maximum concentrations of 1.88, 1.95, not detected and 8.93 ng/g fresh weight respectively(1).

The toxicity of polycyclic aromatic hydrocarbons (PAHs) was determined using mussel, sea-urchin and ascidian embryo-larval bioassays. Fluorescent light exposure enhanced phenanthrene, fluoranthene, pyrene and hydroxypyrene toxicity in comparison with dark conditions, but not naphthalene and fluorene toxicity.

The acute toxicity of metal-polynuclear aromatic hydrocarbon (PAH) mixtures (i.e., Cd, Hg, Pb, fluoranthene and phenanthrene) associated with sediments was assessed in two benthic copepods. Schizopera knabeni was exposed to sediment amended with single contaminants and mixtures. Adult S. knabeni were highly tolerant of single-contaminant exposures to phenanthrene, Cd, Hg, and Pb, as well as a mixture of Cd, Hg, and Pb. Binary experiments revealed that although phenanthrene was synergistic with Cd and Hg, the phenanthrene-Cd synergism was much stronger (2.8 x more lethal than predicted). When a mixture of Cd, Hg, and Pb was combined with phenanthrene, a synergistic response was observed, eliciting 1.5 x greater lethality than predicted. A Cd-phenanthrene synergism in S. knabeni was also observed in aqueous exposures suggesting the interaction was related to a pharmacological insult rather than a sediment-related exposure effect. An antagonism between Cd, Hg, and Pb was indicated, and this antagonism may have moderated the Cd-phenanthrene synergism in mixtures containing Cd, Hg, Pb, and phenanthrene. Experiments with Amphiascoides atopus revealed that phenanthrene and fluoranthene were each synergistic with Cd in aqueous exposures. Our studies suggest that interactive toxicity among metal-PAH mixtures may be common among benthic copepods and that strong synergistic effects observed in binary mixtures may be moderated in more diverse contaminant mixtures. However, the strength of the observed synergisms raises concerns that established sediment quality criteria may not be protective for organisms jointly exposed to PAH and metals, especially Cd-PAH mixtures.

The polycyclic aromatic hydrocarbons (PAHs) phenanthrene and retene (7-isopropyl-1-methyl phenanthrene) are lethal to rainbow trout (Oncorhynchus mykiss) larvae during chronic exposures. Phenanthrene is a low-toxicity, non-cytochrome P4501A (CYP1A)-inducing compound that accumulates in fish tissues during exposure to lethal concentrations in water. Retene is a higher toxicity CYP1A-inducing compound that is not detectable in tissue at lethal exposure concentrations. The metabolism, excretion, and toxicity of retene and phenanthrene were examined in juvenile and larval rainbow trout during coexposure to the model CYP1A inducer beta-naphthoflavone (betaNF), or to the inducer-inhibitor piperonyl butoxide to determine if modulating CYP1A activity affected PAH metabolism and toxicity. Phenanthrene metabolism, excretion rate, and toxicity increased with coexposure to betaNF. Piperonyl butoxide inhibited phenanthrene metabolism and reduced the excretion of all phenanthrene metabolites. As a consequence, embryo mortality rates increased but rates of sublethal effects did not. Coexposure of trout to retene and betaNF caused no change in retene metabolism and excretion, but retene toxicity increased, perhaps due to additivity. Piperonyl butoxide inhibited retene metabolism, decreased the excretion of some retene metabolites while increasing the excretion of others, and increased the toxicity of retene. These results support the role of CYP1A activity in PAH metabolism and excretion, and the role of the CYP1A-generated metabolites of PAHs in chronic toxicity to larval fish.

The toxicities of phenanthrene (PHE) and 9,10-phenanthrenequinone (PHQ) with or without Cu were determined using Daphnia magna. Copper was the most toxic among the three chemicals tested, followed by PHQ and then PHE, with 48-hr median effective concentrations (EC50s) of 0.96, 1.72, and 5.33 uM, respectively. Copper at 0.31 uM, or approximately the 5% effective concentration, decreased the EC50 of PHQ from 1.72 to 0.28 uM. Likewise, PHQ at 1.2 uM, or approximately the 10% effective concentration, significantly lowered the EC50 of Cu from 0.96 to 0.30 uM. This synergistic effect was not observed, however, in mixtures of Cu and PHE based on the response addition model. Assimilation of Cu was found to be similar with or without PHQ at increasing external concentrations of Cu, indicating that the increased toxicity of their mixtures is physiologically based. The ability of Cu plus PHQ to generate reactive oxygen species (ROS) was measured as well. Copper alone caused elevated ROS levels at a low concentration (0.63 uM). With PHQ present, however, this elevation in ROS occurred at an even lower Cu level (0.31 uM). Possible attenuation effects of ascorbic acid (vitamin C) on toxicity and ROS production induced by Cu, PHQ, and their mixtures were then examined. Ascorbic acid protected against Cu and Cu-plus-PHQ mixture-mediated toxicity but did not affect PHQ toxicity. Ascorbic acid also lowered ROS levels in the presence of Cu and Cu plus PHQ. ...

For more Interactions (Complete) data for Phenanthrene (17 total), please visit the HSDB record page.

LD50; Species: Neanthes arenaceodentata (Marine worm); Conditions: seawater at 22 °C in a static bioassay; Concentration: 0.6 ppm for 96 hr

EC50; Species: Enchytraeus crypticus (Earthworm) adult; direct application (natural soil, 2.3% organic matter) dosed 1 time per study; 559 umol/kg soil for 28 days; Effect: decreased progeny counts/numbers

LC50; Species: Enchytraeus crypticus (Earthworm) adult; direct application (natural soil, 2.3% organic matter) dosed 1 time per study, 2109 umol/kg soil for 28 days

LC50; Species: Eisenia fetida (earthworm) adult age >/ = 2 months, weight: 0.40 g with clitella; environmental exposure route (artificial soil) dosed 1 time per study; 293 mg/kg for 14 days

For more Ecotoxicity Values (Complete) data for Phenanthrene (30 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), Koc values of 9,180(2) to 25,300(3), indicate that phenanthrene is expected to be immobile in soil(SRC). Volatilization of phenanthrene from moist soil surfaces is expected to be an important fate process(SRC) given a Henry's Law constant of 4.23X10-5 atm-cu m/mole(4). However, adsorption to soil is expected to attenuate volatilization(SRC). Phenanthrene is not expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 1.21X10-4 mm Hg(5). Phenanthrene reached 78.9% of its theoretical BOD in 4 weeks using an activated sludge inoculum in the Japanese MITI test(6) which indicates that biodegradation may be an important environmental fate process. The half-life of phenanthrene applied to soil at 2.1 ug/g soil and incubated at 15-25 °C was 26 days(7). The half-life when applied at 25,000 ug/g soil and incubated at >25 °C was 2.5 days(7). Phenanthrene was degraded 34% in creosote contaminated soil from Hessleholm, Sweden from an initial concentration of 275 ug/g(8). Phenanthrene absorbs strongly at wavelengths >290 nm(9) and, therefore, is expected to be susceptible to direct photolysis on surfaces exposed to sunlight(SRC). The photolysis half-life of phenanthrene on spruce needle surfaces exposed to full sunlight in Munich, Germany in July 2001 was 75 hours(10).

AQUATIC FATE: Based on a classification scheme(1), Koc values of 9,180(2) to 25,300(3), indicate that phenanthrene is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected(4) based upon a Henry's Law constant of 4.23X10-5 atm-cu m/mole(5). Using this Henry's Law constant and an estimation method(4), volatilization half-lives for a model river and model lake are 1.3 and 13.7 days, respectively(SRC). However, volatilization from water surfaces is expected to be attenuated by adsorption to suspended solids and sediment in the water column. The estimated volatilization half-life from a model pond ranges from 26-70 months if adsorption is considered(6). According to a classification scheme(7), BCF values of 700 to 2,630(8,9), suggest bioconcentration in aquatic organisms is high to very high, provided the compound is not metabolized by the organism(SRC). However, phenanthrene may not bioconcentrate in aquatic organisms which contain microsomal oxidase, such as fish, as this enzyme enables the rapid metabolism of certain polycyclic aromatic hydrocarbons(10). A measured fish biotransformation half-life of 4.97 days has been reported for phenanthrene(11). Phenanthrene reached 78.9% of its theoretical BOD in 4 weeks using an activated sludge inoculum in the Japanese MITI test(12) which indicates that biodegradation may be an important environmental fate process. Phenanthrene has biodegradation half-lives in estuarine water ranging from 19 days (Georgia (US) water incubated at 27 °C) to 11,000 days (Rhode Island water incubated at 2 °C)(13). Phenanthrene has been shown to be susceptible to direct photolysis based on reported aquatic photolysis half-lives of 6.3 hrs(14) and 100 midday hrs(15). Phenanthrene is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(4).

Phenanthrene has been detected in charcoal broiled steaks at 11 ug/kg(1), barbecued ribs at 58.0 ppb, smoked mutton at 104.0 ppb and smoked mutton sausages at 17.0 ppb(2). Phenanthrene was detected but not quantified in smoked salami, smoked mortadella and heavily smoked bacon(2). Fumes collected from fried chicken contained phenanthrene at 70.3-77.55, 10.44-17.70 and 0.61-0.82 ug/g of smoke emitted using soybean oil; 39.71-59.54, 4.86-10.93, and 0.37-0.59 ug/g using sunflower oil; and 36.50-44.68, 17.56-20.26, and 0.36-0.43 ug/g using canola oil(3). Phenanthrene was detected in 97% of food samples at an average of 1.7 ug/kg(4). Liquid smoke flavorings derived from oak, cherry, beech, poplar and vine shoots all contained phenanthrene at unreported concentrations(5). Olive pomace oil from 5 sources collected 2001-2002 contained phenanthrene at 8.25-83.53 ug/kg(6). Food groups collected from supermarkets in Hong Kong during Aug-Oct 2007 (milk, meat, wine, edible oil, nuts) contained phenanthrene concentrations ranging from not detectable to 15.4 ng/g wet wt(7).

Phenanthrene concentration of 51 ppb was found in coconut oil. ... Phenanthrene concentration in charcoal broiled steaks: 21.0 ppb. /Data derived from table/

Baker's yeast concentrations of phenanthrene is as follows: French: 17.8-34.6 ppb; German: 67.0 ppb; Scottish: 1,620 ppb; Russian: 7.2 ppb. /Data derived from table/

ENVIRONMENTAL: In an analysis of 21 human milk samples collected from non-smoking women in Beijing, China during 2005-2006, phenanthrene was detected at mean, median, minimum and maximum concentrations of 3.25, 2.57, not detected and 11.8 ng/g fresh weight respectively(1). Coconut milk and Carnation evaporated milk collected from supermarkets in Hong Kong during Aug-Oct 2007 contained phenanthrene concentrations ranging from not detectable to 3.59 ng/g wet wt(2).

IDENTIFICATION AND USE: Phenanthrene is a solid polycyclic aromatic hydrocarbon (PAH). It is used for dyestuffs, explosives, synthesis of drugs, biochemical research, and manufacturing phenanthrenequinone. HUMAN EXPOSURE AND TOXICITY: Exposure to phenanthrene in PAHs may be a risk factor for hyperuricemia. A test in human lymphoblast TK6 cells with metabolic activation and 9 ug/mL phenanthrene yielded a forward mutation. ANIMAL STUDIES: Phenanthrene 150 mg/kg given to male rats produced a significant elevation of serum aspartate aminotransferase and gamma-glutamyl transpeptidase 24 hr after injection. No tumors developed in 100 mice treated with phenanthrene for 9 months. Evidence from in vivo assays indicates that phenanthrene metabolites have a relatively low tumorigenic potential. The 1,2-, 3,4- and 9,10-dihydrodiol metabolites of phenanthrene did not show tumor initiating activity in mouse skin painting assays. Genetic and cytogenetic mutagenicity tests (eg liver microsome assay, host-mediated peritoneal assay, chromosome aberrations, induction of sister-chromatid-exchanges, etc) were used to evaluate phenanthrene. The 3-methylcholanthrene-induced microsomes assay indicated that phenanthrene was inactive in the gene conversion system and yielded a weak effect only with high doses in the sister chromatid exchange system. Phenanthrene did not yield positive results in sister chromatid exchange and chromosome aberration assays in mammalian cell cultures or in cell transformation assays in several types of mammalian cells (5-40 ug/mL). Phe could induce cardiomyocyte hypertrophy in the rat and H9C2 cells. The mechanism might involve reducing miR-133a expression by DNA methylation. ECOTOXICITY STUDIES: Phenanthrene, a major component of crude oil, is one of the most abundant PAHs in aquatic ecosystems, and is readily bioavailable to marine organisms. Phenanthrene could be accumulated in fish resulting in the changes of the activities of the antioxidant enzymes and the production of ROS with the oxidative stress. Phenanthene can be maternally transferred to embryos and influence the health and sustainability of the next generation. Phenanthrene may pose a risk for mussel and sea-urchin.

The ability of PAH's to bind to blood proteins such as albumin allows them to be transported throughout the body. Many PAH's induce the expression of cytochrome P450 enzymes, especially CYP1A1, CYP1A2, and CYP1B1, by binding to the aryl hydrocarbon receptor or glycine N-methyltransferase protein. These enzymes metabolize PAH's into their toxic intermediates. The reactive metabolites of PAHs (epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations) covalently bind to DNA and other cellular macromolecules, initiating mutagenesis and carcinogenesis. (L10, L23, A27, A32)

AIR INTAKE: The average daily intake of phenanthrene is expected to be 7 ng/day/man(1), assuming atmospheric concentration of 0.01-10 ng/cu m. WATER INTAKE: Assuming a water concentration of 24-90 ng/L, avg daily uptake would be 48-180 ng of phenanthrene(1).

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 5000 lb or 2270 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).

Toxic pollutant designated pursuant to section 307(a)(1) of the Federal Water Pollution Control Act and is subject to effluent limitations. /Polynuclear aromatic hydrocarbons (including benzanthracenes, benzopyrenes, benzofluoranthene, chrysenes, dibenz-anthracenes, and indenopyrenes)/

For the maximum protection of human health from the potential carcinogenic effects of exposure to polynuclear aromatic hydrocarbons through ingestion of contaminated water and contaminated aquatic organisms, the ambient water concentration should be zero, based on the nonthreshold assumption for this chemical. However, zero level may not be attainable at the present time. Therefore, the levels which may result in incremental increase of cancer risk over the lifetime are estimated at 1X10-5, 1X10-6, and 1X10-7. The corresponding recommended criteria are 28.0 ng/L, 2.8 ng/L, and 0.28 ng/L, respectively. If these estimates are made for consumption of aquatic organisms only, excluding consumption of water, the levels are 311.0 ng/L, 31.1 ng/L, and 3.11 ng/L, respectively. /Polynuclear aromatic hydrocarbons/.

Used to make dyestuffs, explosives, phenanthrenequinone, and drugs; [Hawley]

Dyestuffs, explosives, synthesis of drugs, biochemical research, manufacturing phenanthrenequinone.

Phenanthrene forms the basis for production of 9,10-phenanthrenequinone and 2,2'-diphenic acid. It can be used to synthesize anthracene via the isomerization product of sym-octahydrophenanthrene

PAHs are released into the environment via the combustion of fossil fuels, coke oven emissions and vehicle exhausts, as well as naturally from forest fires and volcanic eruptions. PAHs from these sources may contaminate nearly water systems. They are also found in coal tar and charbroiled food. (L10)

(1978) No Data

(1982) No Data

(1986) No Data

(1978) 8.39X10+5 G

(1982) 6.49X10+4 G

(1984) 5.51X10+5 g

2023: 371,175 lb

(1978) NOT PRODUCED COMMERCIALLY IN USA

(1982) NOT PRODUCED COMMERCIALLY IN USA

Production volumes for non-confidential chemicals reported under the Inventory Update Rule. [Table#3899]

Phenanthrene is the second most abundant coal tar constituent next to naphthalene at ca. 5%. Coal tar distillation concentrates phenanthrene in the anthracene oil fraction. Once anthracene residues have been crystallized and filtered off, phenanthrene is recovered from the filtrate. Alternatively, it can be recovered from the top fraction of crude anthracene distillation by redistillation. Technically pure grades of phenanthrene are obtained by sulfuric acid refining and recrystallization from methanol. Alternatively, purification can also be accomplished by repeated rectification of the phenanthrene fraction. The accompanying substances can be separated by partial sulfonation or by partial condensation with formaldehyde and hydrogen chloride. The most persistent accompanying substance, diphenylene sulfide, can be completely removed by treating the melt with sodium and maleic anhydride.

Wood Product Manufacturing

Phenanthrene: ACTIVE

Formation from toluene, bibenzil, 9-methylfluorene or stilbene by passage through red-hot tube ... . Also from coumarone and benzene ... . Pschorr synthesis from o-nitrobenzaldehyde and phenylacetic acid ... . From diphenylethylene ... . Diene synthesis from 1-vinylnaphthalene and maleic anhydride ... . From o-phenylbenzoic acid ... . By irradiation of stilbene ... . Synthesis by double succinoylation of benzene ... .