Fluoranthene

Other Classes -> Polycyclic Aromatic Hydrocarbons

Polycyclic aromatic hydrocarbon

1.252 at 32 °F (NTP, 1992) - Denser than water; will sink

1.252 at 0 °C/4 °C

1.252 @ 0°C

Colored needles

Pale yellow needles or plates from alcohol

Pale yellow crystals

Pale yellow needles or plates

less than 1 mg/mL at 64 °F (NTP, 1992)

Virtually insoluble (0.20-0.26 mg/L) in water

Soluble in ethanol, ether, benzene, chloroform and carbon disulfide

Solubility in seawater at 22 °C: 0.1 + or - 0.06 ppm, 0.120 mg/L at 24 °C (99% purity)

/Fluoranthene/ has a high molecular weight and its relative non-polarity makes this cmpd very insoluble in water.

For more Solubility (Complete) data for FLUORANTHENE (6 total), please visit the HSDB record page.

482 °F at 60 mmHg (NTP, 1992)

384 °C

384 °C @760 [mm Hg]

Hazardous decomposition products formed under fire conditions. - Carbon oxides.

When heated to decomp, it emits acrid smoke and irritating fumes.

This chemical does not meet GHS hazard criteria for 0.5% (1 of 193) of reports.

Warning

H302 (97.9%): Harmful if swallowed [Warning Acute toxicity, oral]

P264, P270, P273, P301+P317, P330, P391, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 193 reports by companies from 9 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Warning

Chemical: Fluoranthene

Hazard Traits - Bioaccumulation; Environmental Persistence; Hematotoxicity; Hepatotoxicity and Digestive System Toxicity; Nephrotoxicity and Other Toxicity to the Urinary System

Fluoranthene is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of Fluoranthene are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)

Restricted substance: Fluoranthene

Substance: Fluoranthene

Fluoranthene: Does not have an individual approval but may be used under an appropriate group standard

Minimal Risk Level (oral intermediate) = 0.4 mg/kg/day (Hepatic); [ATSDR] May cause irritation; [MSDSonline] See POLYCYCLIC AROMATIC HYDROCARBONS.

The major hazards encountered in the use and handling of fluoranthene stem from its toxicologic properties. Toxic by all routes (ie, inhalation, ingestion, dermal contact), exposure to this pale yellow, crystalline substance may occur from its presence in coal tar products used in coatings for pipes and storage tanks, in roofing materials, and asphalt. Effects from exposure (based on analogy to phenol) may include contact burns to the skin and eyes, nausea, tachycardia, cardiac arrhythmias, liver injury, pulmonary edema, and respiratory arrest. In addition, NIOSH recommends that fluoranthene be regulated as an occupational carcinogen. In activities and situations where over-exposure via coal tar products may occur, wear a self-contained breathing apparatus, amd personal protective clothing to prevent skin contact. All such equipment and clothing should be removed in change rooms at the end of the workday, and maintained in a clean condition. Alsom workers should wash thoroughly at the end of the workday. While fluoranthene's fire hazard is only slight when exposed to heat and flame, it may be decomposed by heat, emitting acrid smoke and fumes. Spills of hot coal tar products may be covered with sand. Fluoranthene is a good candidate for disposal by rotary kiln or fluidized bed forms of incineration. Before implementing land disposal of fluoranthene, consult with environmental regulatory agencies for guidance.

NIOSH; Criteria Document: Coal Tar Products (1977) DHEW Pub NIOSH 78-107

USEPA; Ambient Water Quality Criteria Doc: Fluoranthene (1980)

USEPA; Ambient Water Quality Criteria Doc: Polynuclear Aromatic Hydrocarbons (1980)

U.S. Dept Health & Human Services/Agency for Toxic Substances Disease Registry; Toxicological Profile for Polycyclic Aromatic Hydrocarbons (Update) (1995) NTIS# PB/95/264370

U120; As stipulated in 40 CFR 261.33, when fluoranthene, 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 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).

Vigorous reactions, sometimes amounting to explosions, can result from the contact between aromatic hydrocarbons, such as FLUORANTHENE, and strong oxidizing agents. They can react exothermically with bases and with diazo compounds. Substitution at the benzene nucleus occurs by halogenation (acid catalyst), nitration, sulfonation, and the Friedel-Crafts reaction.

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.

Storage conditions shall be controlled to prevent overheating and pressure buildup in containers of coal tar products. Transfer and storage systems shall be designed and operated to prevent blockage by condensed coal tar products. /Coal tar products/

Keep container tightly closed in a dry and well-ventilated place.

Adsorption by activated carbon.

Spills and leaks of coal tar products must be cleaned up immediately, and employees engaged in cleanup must wear adequate personal protective garments and approved respiratory protective devices. Spills of hot coal tar, coal tar pitch ... may be covered with sand or other suitable mineral aggregate. ... /Coal tar products/

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment.Use personal protective equipment. Avoid dust formation. Avoid breathing vapours, 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: Soak up with inert absorbent material and dispose of as hazardous waste. Keep in suitable, closed containers for disposal.

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.

Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number U120, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.

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.

Good candidate for rotary kiln incineration, with a temperature range of 820 to 1600 °C and a residence time of seconds for liquids and gases, hours for solids. Also a good candidate for fluidized bed incineration, with a temperature range of 450 to 980 °C and a residence time of seconds for liquids and gases, longer for solids.

The following wastewater treatment technologies have been investigated for Fluoranthene: Activated Carbon.

For more Disposal Methods (Complete) data for FLUORANTHENE (6 total), please visit the HSDB record page.

The employer shall ensure that ... all protective clothing is removed only in the change rooms ... and that contaminated protective clothing that is to be cleaned, laundered, or disposed of is placed in a closed container in the change room. /Coal tar products/

The NIOSH investigators concluded that coal tar pitch fumes during a roofing operation caused acute (short lived) eye and skin disorders in roofers, some of whom were exposed to concentrations of particulate polycyclic organic material (PPOM) greater than 0.2 mg/cu m of air. ... Incidence and severity of eye and skin effects depend on the concn of airborne particulate polycyclic organic material which ... depends on ... type of operation, ... type of pitch used, ... whether the pitch is heated, and ... environmental factors, such as wind. NIOSH recommended that roofers minimize the effects of coal tar pitch fumes by using protective measures. ... They should work upwind of pitch fumes and wash thoroughly at the end of the working day. /Coal tar products/

To prevent skin absorption of coal tar products ... do not use solvents to clean hands. ... /Coal tar products/

Eating and food preparation or dispensing (including vending mechines) shall be prohibited where there is occupational exposure to coal tar products. /Coal tar products/

For more Preventive Measures (Complete) data for FLUORANTHENE (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 FLUORANTHENE (6 total), please visit the HSDB record page.

0.73 [mg/m3]

8.0 [mg/m3]

48 [mg/m3]

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)

Eye and Face protection: Cup type or rubber framed chemical safety goggles shall be worn by employees engaged in activities in which coal tar products may come in contact with the eyes. When employees are exposed to airborne coal tar products in excess of the limits ... a respirator with a full facepiece is required. ... Full length, plastic face shields (20 cm min) shall be worn, in addition to safety goggles. Protective clothing: For employees working with heated coal tar pitch, employers shall require use of protective clothing sufficient to prevent skin contact. Employees handling drums, cans, or other large containers of coal tar products shall wear impervious shoes or boots with safety toe caps. Leather safety shoes shall be protected ... by impervious coverings such as rubbers. /Coal tar products/

Respiratory protection from coal tar products for the following particulate concentration levels: 2 mg/cu m or less: A chemical cartridge respirator with an organic vapor cartridge(s) and with a fume or high efficiency filter or any supplied air respirator or any self contained breathing apparatus; 10 mg/cu m or less: A chemical cartridge respirator with a full facepiece and an organic vapor cartridge(s) and with a fume or high efficiency filter, or a gas mask with a chin style or a front or back mounted organic vapor canister and with a full facepiece and a fume or high efficiency filter, or any supplied air respirator with a full facepiece, helmet, or hood, or any self contained breathing apparatus with a full facepiece; 200 mg/ cu m or less: A type C supplied air respirator operated in pressure demand or other positive pressure or continuous flow mode, or a powered air purifying respirator with an organic vapor cartridge and a high efficiency particulate filter; 400 mg/cu m or less: A type C supplied air respirator with a full facepiece operated in pressure demand or other positive pressure mode, or with a full facepiece, helmet, or hood operated in continuous flow mode; Greater than 400 mg/cu m or entry and escape from unknown concentrations: Self contained breathing apparatus with a full facepiece operated in pressure demand or other positive pressure mode, or a combination respirator which includes a type C supplied air respirator with a full facepiece operated in pressure demand or other positive pressure or continuous flow mode and an auxillary self contained breathing apparatus operated in pressure demand or other positive pressure mode; Escape: Any gas mask providing protection against organic vapors and particulates, including pesticide respirators which meet the requirements of this class, or any escape self contained breathing apparatus. /Coal tar pitch volatiles/

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

Skin protection: Handle with gloves.

For more Personal Protective Equipment (PPE) (Complete) data for FLUORANTHENE (10 total), please visit the HSDB record page.

Our environment is contaminated with a diverse array of chemicals; one of which is polycyclic aromatic hydrocarbons (PAHs). While some PAHs are potent by nature, others undergo interactions such as additivity, synergism, antagonism or potentiation to manifest their toxicity. Therefore, the objective of this study was to investigate whether exposure to benzo(a)pyrene (BaP), a PAH compound influences the cytotoxicity and metabolism of fluoranthene (FLA; another PAH compound) using HT-29 cells. Cells cultured in Dulbecco's Modified Eagle Medium were treated with 1, 5, 10, 25 uM BaP and FLA (0.01% dimethylsulfoxide as vehicle) individually and in combination over the course of 0-96h. At the end of exposure, cells were stained with propidium iodide and the changes in cell cycle were analyzed using FACS analysis. Apoptosis was determined by caspase-3 assay. Post-incubation, samples were extracted and analyzed for FLA metabolites by reverse-phase HPLC with fluorescence detection. Cells exposed to BaP+FLA showed a marginal decrease in growth as compared to FLA alone and vehicle controls. Also, a decline in the percentage of cells in the S and G2 phases compared to G1 phase of cell cycle was noted when cells were treated with BaP and FLA together, compared to individual FLA treatment. The rate of FLA metabolism was more when cells were exposed to FLA in combination with BaP, compared to FLA alone. The enhanced biotransformation of FLA as a result of concomitant exposure to BaP may have implications for colon cancer risks arising from human dietary exposure to PAH mixtures through consumption of barbecued meat.

Polycyclic aromatic hydrocarbons (PAHs) induce developmental defects including cardiac deformities in /Zebra/fish. The aryl hydrocarbon receptor (AHR) mediates the toxicity of some PAHs. Exposure to a simple PAH mixture during embryo development consisting of an AHR agonist (benzo(a)pyrene-BaP) with fluoranthene (FL), an inhibitor of cytochrome p450 1(CYP1)--a gene induced by AHR activation--results in cardiac deformities. Exposure to BaP or FL alone at similar concentrations alters heart rates, but does not induce morphological deformities. Furthermore, AHR2 knockdown prevents the toxicity of BaP+FL mixture. Here, we used a zebrafish microarray analysis to identify heart-specific transcriptomic changes during early development that might underlie cardiotoxicity of BaP+FL. We used AHR2 morphant embryos to determine the role of this receptor in mediating toxicity. Control and knockdown embryos at 36 hr post-fertilization were exposed to DMSO, 100 ug/L BaP, 500 ug/L FL, or 100 ug/L BaP+500 ug/L FL, and heart tissues for RNA were extracted at 2, 6, 12, and 18 hr-post-exposure (hpe), prior to the appearance of cardiac deformities. Data show AHR2-dependent BaP+FL effects on expression of genes involved in protein biosynthesis and neuronal development in addition to signaling molecules and their associated molecular pathways. Ca(2+)-cycling and muscle contraction genes were the most significantly differentially expressed category of transcripts when comparing BaP+FL-treated AHR2 morphant and control embryos. These differences were most prominent at 2 and 6 hpe. Therefore, we postulate that BaP+FL may affect cellular Ca(2+) levels and subsequently cardiac muscle function, potentially underlying BaP+FL cardiotoxicity.

The effect of the cocarcinogen fluoranthene on the DNA binding and metabolism of [3H]benzo[a]pyrene (B[a]P) in vivo in mouse skin has been investigated. In the presence of fluoranthene the level of B[a]]P-DNA binding was increased at each of the time intervals examined (4, 8, 24 and 48 hr) with enhancements ranging from 76% at 4 hr to 36% at 48 hr. The ratio of anti-7,8,-dihydroxy-9,10-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (anti-BPDE)-DNA adducts/syn-BPDE-DNA adducts was also increased in the presence of fluoranthene. This increase was greatest at 8 hr (44%) but by 48 h the ratio was identical in the presence and absence of fluoranthene. The observed increase in anti-BPDE-DNA adducts/syn-BPDE-DNA adducts did not parallel increases in B[a]P-DNA binding suggesting that alteration of the anti-BPDE/syn-BPDE ratio is not a major contributing factor to the cocarcinogenic activity of fluoranthene. The influence of fluoranthene on the metabolism of B[a]P in vivo in mouse skin was also investigated. Fluoranthene was found to have little or no effect on the formation of ethyl acetate extractable metabolites of B[a]P in mouse skin. Specifically, there was no increase in the amount of B[a]P-7,8-diol in the presence of fluoranthene. Fluoranthene also had little or no effect on the levels of beta-glucuronide or sulfate conjugates of B[a]P metabolites formed in vivo in mouse skin. These studies suggest that the effect of fluoranthene is being expressed at some point after B[a]P has been activated to an ultimate carcinogen.

The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that mediates many of the toxic effects of dioxin-like compounds (DLCs) and some polycyclic aromatic hydrocarbons (PAHs). Strong AHR agonists, such as certain polychlorinated biphenyls and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), cause severe cardiac teratogenesis in fish embryos. Moderately strong AHR agonists, such as benzo[a]pyrene and beta-naphthoflavone, have been shown to cause similar cardiotoxic effects when coupled with a cytochrome P450 1A (CYP1A) inhibitor, such as fluoranthene (FL). We sought to determine if weak AHR agonists, when combined with a CYP1A inhibitor (FL) or CYP1A morpholino gene knockdown, are capable of causing cardiac deformities similar to moderately strong AHR agonists. The weak AHR agonists included the following: carbaryl, phenanthrene, 2-methylindole, 3-methylindole, indigo, and indirubin. Danio rerio (zebrafish) embryos were first exposed to weak AHR agonists at equimolar concentrations. The agonists were assessed for their relative potency as inducers of CYP1 enzyme activity, measured by the ethoxyresorufin-O-deethylase (EROD) assay, and cardiac deformities. Carbaryl, 2-methylindole, and 3-methylindole induced the highest CYP1A activity in zebrafish. Experiments were then conducted to determine the individual cardiotoxicity of each compound. Next, zebrafish were coexposed to each agonist (at concentrations below those determined to be cardiotoxic) and FL in combination to assess if CYP1A inhibition could induce cardiac deformities. Carbaryl, 2-methylindole, 3-methylindole, and phenanthrene significantly increased pericardial edema relative to controls when combined with FL. To further evaluate the interaction of the weak AHR agonists and CYP1A inhibition, a morpholino was used to knockdown CYP1A expression, and embryos were then exposed to each agonist individually. In embryos exposed to 2-methylindole, CYP1A knockdown caused a similar level of pericardial edema to that caused by exposure to 2-methylindole and FL. The results showed a complex pattern of cardiotoxic response to weak agonist inhibitor exposure and morpholino-knockdown. However, CYP1A knockdown in phenanthrene and 3-methylindole only moderately increased pericardial edema relative to coexposure to FL. AHR2 expression was also knocked down using a morpholino to determine its role in mediating the observed cardiac teratogenesis. Knockdown of AHR2 did not rescue the pericardial edema as previously observed with strong AHR agonists. While some of the cardiotoxicity observed may be attributed to the combination of weak AHR agonism and CYP1A inhibition, other weak AHR agonists appear to be causing cardiotoxicity through an AHR2-independent mechanism. The data show that CYP1A is protective of the cardiac toxicity associated with weak AHR agonists and that knockdown can generate pericardial edema, but these findings are also suggestive of differing mechanisms of cardiac toxicity among known AHR agonists.

For more Interactions (Complete) data for FLUORANTHENE (6 total), please visit the HSDB record page.

LC50; Species: Mysid shrimp; Conditions: static; Concentration: 40 ug/L for 96 hr

LC50; Species: /Lepomis macrochirus/ (Bluegill); Conditions: static; Concentration: 3,980 ug/L for 96 hr

LC50; Species: Polychaete /worm/; Conditions: static; Concentration: 500 mg/L for 96 hr

EC50; Species: Selenastrum capricornutum (alga); Conditions: static; Concentration: 54,400 ug/L for 96 hr; Effect: cell numbers

For more Ecotoxicity Values (Complete) data for FLUORANTHENE (65 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), a Koc range of 29,500 to 295,000(2) indicates that fluoranthene is expected to be immobile in soil(SRC). Volatilization of fluoranthene from moist soil surfaces is expected to be an important environmental fate process(SRC) given a Henry's Law constant of 9.45X10-6 atm-cu m/mole(3); however, adsorption is expected to attenuate this process. Fluoranthene is not expected to volatilize from dry soil surfaces based on a vapor pressure of 9.22X10-6 mm Hg at 25 C(3). The degradation half-life for fluoranthene applied to Kidman sandy loam and McLaurin sandy loam was determined to be 377 days and 268 days, respectively(4), suggesting that biodegradation is not an important environmental fate process in soil(SRC).

AQUATIC FATE: Based on a classification scheme(1), a Koc range of 29,500 to 295,000 in sediment(2) indicates that fluoranthene is expected to adsorb to suspended solids and sediment in water(SRC). Volatilization from water surfaces is expected(3) based upon a Henry's Law constant of 9.45X10-6 atm-cu m/mole(4). Using this Henry's Law constant and an estimation method(3), estimated volatilization half-lives for a model river and model lake are 4 days and 46 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 was 17 years when adsorption was considered(5). According to a classification scheme(6), BCF values of 380(7) to 6,110(8,9) suggest that the potential for bioconcentration in aquatic organisms is high to very high(SRC). However, it 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). Half-lives for the direct photochemical decomposition of fluoranthene in freshwater ranged from 21.0 hours near the surface of freshwater (simulated latitude, 40 deg N, mid-day, mid-summer) to 200 hours at a depth of 5 m and partitioned to bottom sediment(11). Fluoranthene is not expected to undergo hydrolysis in the environment due to the lack of hydrolyzable functional groups(3). In shake flask studies, an initial fluoranthene concentration of 16.2 ug/mL was reduced to 7.6 ug/mL following 2 weeks incubation in contaminated groundwater from a US Superfund site(12) indicates that biodegradation may be a gradual environmental fate process under certain conditions(SRC).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), fluoranthene, which has a vapor pressure of 9.22X10-6 mm Hg at 25 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase fluoranthene 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 8 hours(SRC) calculated from its rate constant of 5.0X10-11 cu cm/molecule-sec at 25 °C(3). Particulate-phase fluoranthene may be physically removed from the air by wet and dry deposition(SRC). The atmospheric lifetime of vapor-phase fluoranthene due to reaction with nitrate radicals has been calculated as approximately 85 days(4). Fluoranthene absorbs UV light at wavelengths >290 nm(5) and, therefore, may be susceptible to direct photolysis by sunlight(SRC). The photolytic half-life of fluoranthene adsorbed to silica, alumina, fly ash, and carbon black substrates were measured as 74, 23, 44, and >1,000 hours, respectively, following irradiation with a 400 watt mercury lamp(6). Fluoranthene is found both in the free and adsorbed state in both the aqueous and atmospheric compartments and photodegradation is usually different in the sorbed state(7).

Fluoranthene was most frequently found in smoked food, liquid smoke, vegetable oils, wax, charcoal broiled steaks, roasted coffee(1). In the UK, total diet intake was 0.99 ug/day which includes % of total input (average concentration): cereal 32% (1.38 ppb), meat 7% (0.48 ppb), fish 2% (0.81 ppb), oil and fats 14% (1.76 ppb), fruit and sugar 16% (0.93 ppb), root vegetables 5% (0.26 ppb), other vegetables 17% (1.50 ppb), beverages 1% (0.08 ppb), milk 6% (0.15 ppb)(2). Fluoranthene concentrations in food were reported as follows(3-5):[Table#5409]

Fourteen of 25 samples of margarines, butter and vegetable oils contained fluoranthene at concentration ranging from 0.84 to 460 ug/kg(1). The concentration of fluoranthene in bran cereals was determined to range from 0.46-1.8 ug/kg, in puffed cereals: 1.2-3.2 ug/kg, in charbroiled hamburgers: 0.73-14.7 ug/kg and in powdered dairy products: 0.34-8.2 ug/kg(2). Within the Italian diet, fluoranthene was detected in beet greens (5.41 ug/kg), lettuce (0.095 ug/kg), tomatoes (0.095 ug/kg), potatoes (0.053 ug/kg), apples (2.364 ug/kg), beef (1.00 ug/kg), pork (0.545 ug/kg), butter (0.146 ug/kg) and pizza (0.184 ug/kg)(3).

The concentration of fluoranthene in a grilled mesquite wood beef patty 70% lean was determined to be 103 ug/kg(1). The fine aerosol emission rate for fluoranthene from a frying hamburger (extra lean/regular), from a charbroiled hamburger (extra lean) and from a charbroiled hamburger (regular) was determined to be 0.13, 0.12, and 0.35 mg/kg, respectively(2). The level of fluoranthene in seafood collected from Kuwaiti markets in May 1993 revealed an average concentration of 32.1 ug/kg, dry weight(3). The median concentration of fluoranthene in olive oils, safflower oils, sunflower oils, maize germ oils, sesame oil, linseed oil, and wheat germ oil was determined to be 12.9, 0.6, 3.1, 2.4, 1.2, 9.9, and 18.2 ug/kg respectively(4). The concentration of fluoranthene in leaf lettuce was determined to range from 1.1 to 28 ug/kg(5). Fluoranthene was detected in freeze dried carrots at a concentration of 1.59 ug/kg(6).

IDENTIFICATION AND USE: Fluoranthene is a solid. Currently, there is no known production of or use of this compound. Polycyclic aromatic hydrocarbons are a group of chemicals that are formed during the incomplete burning of coal, oil, gas, wood, garbage, or other organic substances, such as tobacco and charbroiled meat. HUMAN EXPOSURE AND TOXICITY: Fluoranthene was mutagenic to cultured human Iymphoblastoid cells in the presence of an exogenous metabolic system. It is confirmed human carcinogen. ANIMAL STUDIES: A 24 week lung adenoma bioassay using newborn mice was employed to determine the tumorigenicity of fluoranthene. A 6.5-fold elevation of lung tumor incidence (58%) and a 12-fold increase in numbers (1.08 tumors/mouse) was observed in animals treated with the highest dose (3.5 mg/mouse), but no increase in tumor incidence was induced by 700 micrograms/mouse. In other experiment, fluoranthene induced lung and liver tumors 6-9 months after intraperitoneal injection of 0.7, 1.75 and 3.5 mg into preweanling mice. Although fluoranthene is mutagenic in bacterial and mammalian in vitro cell systems following metabolic activation, information on in vivo mutagenicity is lacking and studies on tumor initiating activity in mice are equivocal. Fluoranthene can produce behavioral toxicity in rats. Fluoranthene could also compromise B lymphopoiesis. A developmental study was performed in which fluoranthene was administered once via intraperitoneal injection to pregnant C57/B6 mice on gestational day 6, 7, 8 or 9. An increased rate of embryo resorption was observed. ECOTOXICITY STUDIES: The acute and chronic toxicity of fluoranthene was determined for a diverse group of freshwater and saltwater species under both standard laboratory fluorescent light and ultraviolet (UV) light test conditions. Acute tests with 21 species demonstrated that fluoranthene was not lethal within its water solubility limit to most species tested under fluorescent light, but was lethal well below this limit to nearly all of the species tested under UV light. Overall, UV light increased acute fluoranthene toxicity approximately one to three orders of magnitude.

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)

U120; As stipulated in 40 CFR 261.33, when fluoranthene, 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 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).

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 100 lb or 45.4 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.

For the protection of human health from the toxic properties of fluoranthene ingested through water and contaminated aquatic organisms, the ambient water criterion is determined to be 42 ug/L.

For the protection of human health from the toxic properities of fluoranthene ingested through contaminated aquatic organisms alone, the ambient water criterion is determined to be 54 ug/L.

(FL) FLORIDA 280 ug/l

(MN) MINNESOTA 300 ug/l

(WI) WISCONSIN 400 ug/l

Half-life for depuration by Crassostrea virginica (oysters): 5 days from an oil treated enclosure.

The genotoxicity of 15 polycyclic aromatic hydrocarbons was determined with the alkaline version of the comet assay employing V79 lung fibroblasts of the Chinese hamster as target cells. These cells lack the enzymes necessary to convert PAHs to DNA-binding metabolites. ... 11 PAHs, i.e., benzo[a]pyrene (BaP), benz[a]anthracene, 7,12-dimethylbenz[a]anthracene, 3-methylcholanthrene, fluoranthene, anthanthrene, 11H-benzo[b]fluorene, dibenz[a,h]anthracene, pyrene, benzo[ghi]perylene and benzo[e]pyrene caused DNA strand breaks even without external metabolic activation, while naphthalene, anthracene, phenanthrene and naphthacene were inactive. When the comet assay was performed in the dark or when yellow fluorescent lamps were used for illumination the DNA-damaging effect of the 11 PAHs disappeared. White fluorescent lamps exhibit emission maxima at 334.1, 365.0, 404.7, and 435.8 nm representing spectral lines of mercury. In the case of yellow fluorescent lamps these emissions were absent. Obviously, under standard laboratory illumination many PAHs are photo-activated, resulting in DNA-damaging species. This feature of PAHs should be taken into account when these compounds are employed for the initiation of skin cancer. ...

The fungus Cunninghamella elegans ATCC 36112 metabolized approximately 80% of the (3-14)C-labeled fluoranthene (FA) added within 72 hr of incubation. C. elegans metabolized FA to trans-2,3-dihydroxy-2,3-dihydrofluoranthene (trans-2,3-dihydrodiol), 8- and 9-hydroxyfluoranthene trans-2,3-dihydrodiol, 3-fluoranthene-beta-glucopyranoside, and 3-(8-hydroxyfluoranthene)-beta-glucopyranoside. These metabolites were separated by thin-layer and reversed-phase high-performance liquid chromatography and identified by 1H nuclear magnetic resonance, UV, and mass spectral techniques. The major pathway involved hydroxylation to form a glucoside conjugate of 3-hydroxyfluoranthene and a glucoside conjugate of 3,8-dihydroxyfluoranthene which together accounted for 52% of the total ethyl acetate-soluble metabolites. C. elegans initially metabolized FA in the 2,3 position to form fluoranthene trans-2,3-dihydrodiol, which has previously been shown to be a biologically active compound in mammalian and bacterial genotoxicity tests. However, C. elegans formed predominantly glucoside conjugates of the phenolic derivatives of FA, which suggests that this fungus has the potential to detoxify FA.

The 2,3-dihydrodiol has been detected as a metabolite of fluoranthene following incubation of this compound with a rat-liver preparation. The 2,3-dihydriol was found to be mutagenic to bacteria in the presence of a metabolic activation system.

The metabolite of fluoranthene ... obtained upon incubation with liver homogenate from Aroclor pretreated rats ... 2,3-dihydro-2,3-dihydroxyfluoranthene.

Adverse health effects such as cancer and toxicity may be attributed to consumption of chemically contaminated food rich in fat. This leads to a larger intake and retention of lipophilic toxic chemicals in the body with an increase in risks to human health. The objective of this study was to characterize the effect of dietary fat on disposition and metabolism of fluoranthene (FLA), a polycyclic aromatic hydrocarbon compound. FLA was administered to F-344 rats in monounsaturated (peanut oil), polyunsaturated (corn oil) and saturated (coconut oil) fats at doses of 50 and 100 ug/kg via oral gavage. Blood, small intestine, liver, lung, testis, adipose tissue, urine and feces were collected at various time points' post-FLA exposure. Samples were analyzed by reverse-phase high-performance liquid chromatography for FLA parent compound and metabolites. DNA was isolated from the tissues and subjected to (32)P-post labeling to measure FLA-DNA adducts. The concentrations of unchanged FLA (FLA parent compound) and its metabolites showed an increase for the saturated fat treatment group compared with mono- and polyunsaturated fat groups. The FLA-DNA adduct concentrations were high in tissues of rats that received FLA through saturated fat. The toxicokinetic parameters, concentrations of FLA metabolites and FLA-DNA adduct showed a dose-dependent increase, and this increase was statistically significant (P<.05) for saturated fat. These findings clearly demonstrate that the high residence time of FLA parent compound in saturated fat allows extensive metabolism, contributing reactive metabolites of FLA that bind with DNA and causing marked damage in a long-term exposure scenario.

For more Metabolism/Metabolites (Complete) data for FLUORANTHENE (7 total), please visit the HSDB record page.

PAH metabolism occurs in all tissues, usually by cytochrome P-450 and its associated enzymes. PAHs are metabolized into reactive intermediates, which include epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations. The phenols, quinones, and dihydrodiols can all be conjugated to glucuronides and sulfate esters; the quinones also form glutathione conjugates. (L10)

The dose-dependence of hemoglobin binding as well as distribution of fluoranthene and fluoranthene-DNA adducts in various tissues was characterized in male rats 24 hr after a single i.p. injection of (3)H-fluoranthene. Formation and distribution of DNA adducts after chronic administration of fluoranthene in the diet was also studied. Fluoranthene-derived radioactivity was widely distributed throughout the animal after a single dose, and excreta contained the greatest amounts of radioactivity at all dose levels. Fluoranthene binding to globin was proportional to dose over the range of 2 nmol/kg to 177 umol/kg, and the adducted protein was cleared at the same rate as unmodified hemoglobin, indicating that the adducts are stable in vivo. In contrast, fluoranthene-DNA adducts were not present at detectable levels in liver or kidney 24 hr after one dose; low levels of adducts were found only in the lung at the highest dose level. Chronic administration of fluoranthene in the diet, however, resulted in DNA adduct formation in most tissues examined, including liver, kidney, lung, small intestine, heart, spleen and lymphocytes; adducts were not detectable in testes DNA. The major fluoranthene-DNA adduct found in rat tissues was identified by its chromatographic similarity to the major fluoranthene adduct formed in vitro using microsomally-activated fluoranthene and calf thymus DNA, previously identified as a reaction product of anti-2,3-dihydroxy-1,10b-epoxy-1,2,3-trihydro-fluoranthene with N2-deoxyguanosine. The unusual stability of this diol epoxide at physiological pH may allow transport of this ultimate DNA-binding metabolite to virtually all tissues. These results demonstrate the applicability of the HPLC-(32)P-postlabelling procedure to detect and quantify fluoranthene-DNA adducts formed in vivo, and suggest that analysis of these adducts in accessible tissues such as lymphocytes may be a means of assessing chronic, high level exposure to fluoranthene. Our results also indicate that hemoglobin adducts of fluoranthene could be useful dosimeters for detecting short-term or chronic exposure to this compound if a suitable method for their detection were developed.

/MILK/ Polycyclic aromatic hydrocarbons (PAHs) were analyzed in maternal blood and fetuses from Fischer 344 rats exposed to diesel exhaust (DE) during pregnancy, and in breast milk from rats exposed to DE during pregnancy and lactation using high performance liquid chromatography with fluorescence detection. Concentrations of phenanthrene (Phe), anthracene (Ant) and benz[a]anthracene (BaA) were significantly higher in maternal blood of the DE group than those of the control group. Concentration of Phe in fetuses of the DE group was significantly higher than those of the control group. Concentrations of fluorene, Ant, fluoranthene (Flu), pyrene (Pyr), BaA and chrysene (Chr) tended to be higher in fetuses of the DE group. The levels of Ant, Flu, Pyr and Chr in breast milk from the DE group were significantly higher than those of the control group. These results indicate that PAHs taken into mother rat by the inhalation of DE are transferred into fetuses via placenta and into breast milk. ...

Fluoranthene has been found in human urine and feces.

Blood levels of fluoranthene, pyrene, and benz[a]anthracene after oral administration were examined in rats. Fluoranthene, pyrene, or benz[a]anthracene in Tween 80/isotonic saline, was administered orally to rats at a dose of 20 mg/kg. Blood levels after administration indicated that peak concentrations of the three compounds were reached at 1-2 hours after administration. The peak concentration of fluoranthene (approximately 30 mg/cu cm) was twice as high as that of pyrene, and 5 times higher than benz[a]anthracene.

For more Absorption, Distribution and Excretion (Complete) data for FLUORANTHENE (7 total), please visit the HSDB record page.

Occurs in coal tar and petroleum-derived asphalt; Used to make drugs and fluorescent dyes; Also used as a stabilizer in epoxy resins and in electrically insulating oils; [HSDB]

Plastic Composites Manufacturing [Category: Industry]

Currently, there is no known production of or use of this compound.

PAHs are generally not produced commercially in the United States except as research chemicals. /Polycyclic aromatic hydrocarbons/

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)

9.44X10+6 g

2.3X10+3 lb

2023: 781,487 lb

There is no commercial production ... of this compound.

Fluoranthene is a constituent of coal tar and petroleum-derived asphalt. It can be produced by high-temperature pyrolysis of organic raw materials such as coal and petroleum. It is recovered from the fluoranthene fraction boiling between 373 and 385 °C. Redistillation and recrystallization of the fluoranthene fraction from solvent naphtha yields 95% pure fluoranthene. Further refining by recrystallization from xylene with simultaneous partial sulfonation with approximately 1% concentrated sulfuric acid of the impurities or by recrystallization from a pyridine-water mixture.

/Derived/ from coal tar.

Wood Product Manufacturing

Fluoranthene: ACTIVE

Concentration of polycyclic aromatic hydrocarbons are much lower in asphalt linings than they are in coal tar linings. ... Asphalt paint /was analyzed/ for several polycyclic aromatic hydrocarbons ... /fluoranthene among 8 others/ concentration ranging from 0.1 to 10 ug/g.

Triplet fluoranthene was reported to be formed in nearly quantitative yield from reaction of fluoranthene radical anion with the 10-phenyl-phenothiazine radical cation, and an 80% triplet yield was indicated for electrochemiluminescence of fluoranthene by measuring triplet sensitized isomerization of trans- to cis-stilbene.

Fluoranthene occurs ubiquitously in products of incomplete combustion; it also occurs in fossil fuels.

PAHs are a group of chemicals that are formed during the incomplete burning of coal, oil, gas, wood, garbage, or other organic substances, such as tobacco and charbroiled meat. There are more than 100 different PAHs. PAHs generally occur as complex mixtures (for example, as part of combustion products such as soot), not as single compounds. PAHs usually occur naturally, but they can be manufactured as individual compounds for research purposes; however, not as the mixtures found in combustion products. ... Others are contained in asphalt used in road construction. They can also be found in substances such as crude oil, coal, coal tar pitch, creosote, and roofing tar. They are found throughout the environment in the air, water, and soil. They can occur in the air, either attached to dust particles or as solids in soil or sediment. /Polycyclic aromatic hydrocarbons/