56-55-3c1ccc2cc3c(ccc4ccccc43)cc2c1DXBHBZVCASKNBY-UHFFFAOYSA-NBenz[a]anthracene can cause cancer according to an independent committee of scientific and health experts.
56-55-3DTXSID5023902CHEMBL1873684CHEBI:51348Carcinogens
Semi-Volatile Organic Compound (SVOC)
Other Classes -> Polycyclic Aromatic Hydrocarbons
Polycyclic aromatic hydrocarbon
log Kow = 5.76
5.61
5.93
Plates from glacial acetic acid or alcohol
Greenish-yellow fluorescence
less than 1 mg/mL at 68 °F (NTP, 1992)
In water, 9.4X10-3 mg/L at 25 °C
Insoluble in water
soluble in ether, alcohol, acetone, benzene
Soluble in most organic solvents; difficulty solubilizing in boiling alcohol
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Danger
H350: May cause cancer [Danger Carcinogenicity]
P203, P273, P280, P318, P391, P405, and P501 (click each P-code to see the statement)
Danger
H350 (100%): May cause cancer [Danger Carcinogenicity]
P203, P273, P280, P318, P391, P405, and P501 (click each P-code to see the statement)
Hazard Traits - Bioaccumulation; Carcinogenicity; Environmental Persistence
Benz[a]anthracene is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of Benz[a]anthracene 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)
Substance: Benz[a]anthracene
Benz[a]anthracene: Does not have an individual approval but may be used under an appropriate group standard
The New Jersey Worker and Community Right to Know Act requires public and private employers to provide information about hazardous substances at their workplaces. (N.J.S.A. 34:5A-1 et. seq.)
Flash point data for this chemical are not available. It is probably combustible. (NTP, 1992)
Combustible. Finely dispersed particles form explosive mixtures in air.
Disruption of cell proliferation control by polycyclic aromatic hydrocarbons (PAHs) may contribute to their carcinogenicity. We investigated role of the aryl hydrocarbon receptor (AhR) in disruption of contact inhibition in rat liver epithelial WB-F344 'stem-like' cells, induced by the weakly mutagenic benz[a]anthracene (BaA), benzo[b]fluoranthene (BbF) and by the strongly mutagenic benzo[a]pyrene (BaP). There were significant differences between the effects of BaA and BbF, and those of the strongly genotoxic BaP. Both BaA and BbF increased percentage of cells entering S-phase and cell numbers, associated with an increased expression of Cyclin A and Cyclin A/cdk2 complex activity. Their effects were significantly reduced in cells expressing a dominant-negative AhR mutant (dnAhR). Roscovitine, a chemical inhibitor of cdk2, abolished the induction of cell proliferation by BbF. However, neither BaA nor BbF modulated expression of the principal cdk inhibitor involved in maintenance of contact inhibition, p27(Kip1), or pRb phosphorylation. The strongly mutagenic BaP induced apoptosis, a decrease in total cell numbers and significantly higher percentage of cells entering S-phase than either BaA or BbF. Given that BaP induced high levels of Cyclin A/cdk2 activity, downregulation of p27(Kip1) and hyperphosphorylation of pRb, the accumulation of cells in S-phase was probably due to cell proliferation, although S-phase arrest due to blocked replication forks can not be excluded. Both types of effects of BaP were significantly attenuated in dnAhR cells. Transfection of WB-F344 cells with siRNA targeted against AhR decreased induction of Cyclin A induced by BbF or BaP, further supporting the role of AhR in proliferative effects of PAHs. This suggest that activation of AhR plays a significant role both in disruption of contact inhibition by weakly mutagenic PAHs and in genotoxic effects of BaP possibly leading to enhanced cell proliferation. Thus, PAHs may increase proliferative rate and the likelihood of fixation of mutations.
Activation of the aryl hydrocarbon receptor (AhR)-mediated activity is one of key events in toxicity of polycyclic aromatic hydrocarbons (PAHs). Although various classes of AhR ligands may differentially activate human and rodent AhR, there is presently a lack of data on the human AhR-inducing relative potencies (REPs) of PAHs. Here, we focused on estimation of the AhR-mediated activities of a large set of environmental PAHs in human gene reporter AZ-AhR cell line, with an aim to develop the human AhR-based REP values with potential implications for risk assessment of PAHs. The previously identified weakly active PAHs mostly failed to activate the AhR in human cells. The order for REPs of individual PAHs in human cells largely corresponded with the available data from rodent-based experimental systems; nevertheless, we identified differences up to one order of magnitude in REP values of PAHs between human and rodent cells. Higher REP values were found in human cells for some important environmental contaminants or suspected carcinogens, such as indeno[1,2,3-cd]pyrene, benz[a]anthracene or benzo[b]fluoranthene, while lower REP values were determined for methyl-substituted PAHs. Our results also indicate that a different rate of metabolism for individual PAHs in human vs. rodent cells may affect estimation of REP values in human cell-based assay, and potentially alter toxicity of some compounds, such as benzofluoranthenes, in humans. We applied the AZ-AhR assay to evaluation of the AhR-mediated activity of complex mixtures of organic compounds associated with diesel exhaust particles, and we identified the polar compounds present in these mixtures as being particularly highly active in human cells, as compared with rodent cells. The present data suggest that differences may exist between the AhR-mediated potencies of PAHs in human and rodent cells ... .
Wird geladen…
Slightly sol in acetic acid
815 °F at 760 mmHg (sublimes) (NTP, 1992)
437.6 °C
815 °F
437.6 °C @760 [mm Hg]
Hazardous decomposition products formed under fire conditions - Carbon oxides.[Sigma-Aldrich; Safety Data Sheet for Benz
When heated to decomposition it emits acrid smoke and irritating fumes.
315 to 318 °F (NTP, 1992)
155-157 °C
162 °C
315-318 °F
160.5 °C
Kuroki T; Comparative Mutagenicity of Diol Epoxides of Benzo(a)pyrene and Benz(a)anthracene in V79 Chinese Hamster Cells and Salmonella Typhimurium; Polycyclic Hydrocarbons Cancer 2: 123-34 (1978) Review: Mutagenicity of diol epoxides of benzo(a)pyrene and benz(a)anthracene in cultured hamster cells and Salmonella typhimurium are reviewed.
Health & Welfare Canada; Polycyclic Aromatic Hydrocarbons (1979) Report No. 80-EHD-50
USEPA; Ambient Water Quality Criteria Doc: Polynuclear Aromatic Hydrocarbons (Draft) (1980)
USEPA; Health Assessment Document: Polycyclic Organic Matter (1979) EPA-600/9-79-008
For more Special Reports (Complete) data for BENZ(A)ANTHRACENE (8 total), please visit the HSDB record page.
U018; As stipulated in 40 CFR 261.33, when benz(a)anthracene, 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).
BENZ[A]ANTHRACENE may react vigorously with strong oxidizing agents. 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.
Fires involving this chemical can be controlled using a dry chemical, carbon dioxide or Halon extinguisher. (NTP, 1992)
Use water spray, powder, carbon dioxide, foam. In case of fire in the surroundings, use appropriate extinguishing media.
Fresh air.
Remove contaminated clothes. Rinse and then wash skin with water and soap.
Rinse with plenty of water (remove contact lenses if easily possible).
Rinse mouth. Seek medical attention if you feel unwell.
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.
Biological Exposure Indices (BEI) [ACGIH] - 1-Hydroxypyrene (1-HP) in urine = 2.5 ug/L at end of shift at end of workweek; (Adjusted for the Pyrene to Benzo(a)pyrene ratio); 3-Hydroxybenzo(a)pyrene (3-HBAP) in urine = Nq at end of shift at end of workweek; [TLVs and BEIs]
Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.[Sigma-Aldrich; Safety Data Sheet for Benz
Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary.[Sigma-Aldrich; Safety Data Sheet for Benz
Use dry chemical, carbon dioxide, water spray, or foam extinguishers. ... If material or contaminated runoff enters waterways, notify downstream users of potentially contaminated waters. Notify local health and fire officials and pollution control agencies. From a secure, explosion-proof location, use water spray to cool exposed containers. If cooling streams are ineffective (venting sound increases in volume and pitch, tank discolors, or shows any signs of deforming), withdraw immediately to a secure position. ... The only respirators recommended for firefighting are self-contained breathing apparatuses that have full face-pieces and are operated in a pressure-demand or other positive-pressure mode.
Keep container tightly closed in a dry and well-ventilated place.[Sigma-Aldrich; Safety Data Sheet for Benz
Store in a secure poison location. Store in a cool, dry place away from oxidizers. A regulated, marked area should be established where this chemical is handled, used, or stores in compliance with OSHA Standard 1910.1045.
PRECAUTIONS FOR "CARCINOGENS": Storage site should be as close as practicable to lab in which carcinogens are to be used, so that only small quantities required for ... expt need to be carried. Carcinogens should be kept in only one section of cupboard, an explosion-proof refrigerator or freezer (depending on chemicophysical properties ...) that bears appropriate label. An inventory ... should be kept, showing quantity of carcinogen & date it was acquired ... Facilities for dispensing ... should be contiguous to storage area. /Chemical Carcinogens/
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. Evacuate personnel to safe areas. 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.[Sigma-Aldrich; Safety Data Sheet for Benz
Evacuate and restrict persons not wearing protective equipment from area of spill or leak until cleanup is complete. Remove all ignition sources. Collect powdered material in the most convenient and safe manner and deposit in sealed containers. Ventilate area of spill or leak after cleanup is complete. It may be necessary to contain and dispose of this chemical as a hazardous waste. If material or contaminated runoff enters waterways, notify downstream users of potentially contaminated waters.
PRECAUTIONS FOR "CARCINOGENS": A high-efficiency particulate arrestor (HEPA) or charcoal filters can be used to minimize amt of carcinogen in exhausted air ventilated safety cabinets, lab hoods, glove boxes or animal rooms. ... Filter housing that is designed so that used filters can be transferred into plastic bag without contaminating maintenance staff is avail commercially. Filters should be placed in plastic bags immediately after removal. ... The plastic bag should be sealed immediately. ... The sealed bag should be labelled properly ... Waste liquids ... should be placed or collected in proper containers for disposal. The lid should be secured & the bottles properly labelled. Once filled, bottles should be placed in plastic bag, so that outer surface ... is not contaminated ... The plastic bag should also be sealed & labelled. ... Broken glassware. ... should be decontaminated by solvent extraction, by chemical destruction, or in specially designed incinerators. /Chemical Carcinogens/
The particle-bound portion of polycyclic aromatic hydrocarbons (PAH) can be removed by sedimentation, flocculation, and filtration processes. The remaining one-third dissolved PAH usually requires oxidation for partial removal/transformation.
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 U018, 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.
Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber; Contaminated packaging: Dispose of as unused product.[Sigma-Aldrich; Safety Data Sheet for Benz
Atomize into incinerator with a flammable liquid.
For more Disposal Methods (Complete) data for BENZ(A)ANTHRACENE (14 total), please visit the HSDB record page.
Personal protection: complete protective clothing including self-contained breathing apparatus. Wet powder to prevent dusting and ignition. Do NOT let this chemical enter the environment. Vacuum spilled material with specialist equipment. Sweep spilled substance into sealable containers. Then store and dispose of according to local regulations.
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. Evacuate personnel to safe areas. 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.[Sigma-Aldrich; Safety Data Sheet for Benz
Precautions for safe handling: Avoid formation of dust and aerosols. Provide appropriate exhaust ventilation at places where dust is formed.[Sigma-Aldrich; Safety Data Sheet for Benz
Appropriate engineering controls: Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of workday.[Sigma-Aldrich; Safety Data Sheet for Benz
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.[Sigma-Aldrich; Safety Data Sheet for Benz
For more Preventive Measures (Complete) data for BENZ(A)ANTHRACENE (18 total), please visit the HSDB record page.
Benz(a)anthracene was analyzed in blood serum and skin oil collected from roofing workers. Although range of 0.05 to 36 ng was observed in skin oil samples, none was detected in serum, at detection limits of 1.0 to 175 pg/mL(1).
Benzo(a)pyrene and benz(a)anthracene levels were 0.528 and 0.546 ug/L respectively in the urine in 451 and 437 samples collected in the northwest of the Ruhr area, whereas 35 and 34 urine samples collected in an uncontaminated area contained 0.395 and 0.416 ug/L of benzo(a)pyrene and benz(a)anthracene. Smoking did not affect the urinary ... levels.
The study was conducted in a Chinese population with occupational or environmental exposures to polycyclic aromatic hydrocarbons (PAHs). A total of 106 subjects were recruited from coke-oven workers (workers), residents in a metropolitan area (residents) and suburban gardeners (gardeners). All subjects were monitored twice for their personal exposures to PAHs. The biological samples were collected for measurements of 1-hydroxypyrene (1-OHP) and cotinine in urine. The geometric means of personal exposure levels of pyrene, benz(a)anthracene (BaA) and benzo(a)pyrene (BaP) in workers were 1.470, 0.978 and 0.805 ug/cu m, respectively. The corresponding levels in residents were 0.050, 0.034 and 0.025 ug/cu m; and those in gardeners were 0.011, 0.020 and 0.008 ug/cu m, respectively. The conjugate of 1-OHP with glucuronide (1-OHP-G) is the predominant form of pyrene metabolite in urine and it showed strong associations with exposures not only to pyrene, but also to BaA, BaP and total PAHs. Most importantly, a significant difference in 1-OHP-G was even detected between the subgroups with exposures to BaP at < 0.010 and > 0.010 but < 0.020 ug/cu m, suggesting that 1-OHP-G is a good marker that can be used for the risk assessment of BaP exposure at levels currently encountered in ambient air. Furthermore, multiple regression analyses of 1-OHP-G on PAHs exposure indicated that cigarette smoke was a major confounding factor and should be considered and adjusted for while using 1-OHP to estimate PAHs exposure.
Co-exposure to environmental polycyclic aromatic hydrocarbons (PAHs) and interleukin (IL)-1beta induces expression of the tumor-promoting cytokine IL-6 in cancer cells. The present study was designed to determine whether such an IL-6 up-regulation also occurs in response to co-treatment by PAHs and tumor necrosis factor (TNF)-alpha, an inflammatory cytokine commonly found in tumor microenvironment. Co-exposure to the prototypical PAH benzanthracene (BZA) and TNF-alpha was found to markedly induce mRNA expression and secretion of IL-6 in human breast cancer cells MCF-7, whereas exposure to either BZA or TNF-alpha alone was without significant effect. Co-treatment by BZA and TNF-alpha-containing conditioned media from human inflammatory macrophages similarly up-regulated IL-6 expression in MCF-7 cells. BZA/TNF-alpha-mediated IL-6 induction in MCF-7 cells was counteracted by silencing aryl hydrocarbon receptor (AhR), known to mediates most of PAH effects. IL-6 up-regulation was moreover associated with NF-kappaB activation and was abolished by using chemical NF-kappaB inhibitors or knocking-down expression of the p65/RelA NF-kappaB subunit. Taken together, these data indicate that co-exposure to BZA/TNF-alpha induces IL-6 expression by AhR- and NF-kappaB-dependent pathways in MCF-7 cancer cells. This regulation of IL-6 by environmental PAHs, that is dependent of inflammatory cytokine microenvironment, may contribute to the well-known carcinogenic properties of these organic pollutants.
Human colon tumor cells (cell line LS174T) retain a cytochrome P-450-containing drug metabolism system capable of hydroxylating polycyclic hydrocarbons and the anticancer drug cyclophosphamide. The hydroxylation of benzo(a)pyrene by human colon tumor cells is highly inducible. Phenobarbital plus hydrocortisone induce benzo(a)pyrene hydroxylation activities 10-fold, while benz(a)anthracene induces the rate of hydroxylation 30-fold. Cytochrome P-450 specific content is increased 2- to 3-fold by treatment with phenobarbital plus hydrocortisone and benz(a)anthracene, respectively. Addition of cyclophosphamide alone results in no increase in hydroxylation activities but causes a decrease in cell growth rate. The combination of cyclophosphamide with either of the inducers phenobarbital plus hydrocortisone or benz(a)anthracene results in markedly enhanced inhibition of cell growth as judged both by a decrease in the number of cells per plate and in the incorporation of [3H]thymidine into DNA. Thus, these data show that cyclophosphamide is cytotoxic to human colon tumor cells and that the cytotoxicity is enhanced by simultaneous administration of benz(a)anthracene or phenobarbital plus hydrocortisone to the tissue cultures.
The mutagenic activity of ethyl acetate extracts of culture medium from Cunninghamella elegans incubated 72 hr with various polycyclic aromatic hydrocarbons (PAHs) was evaluated in the Salmonella typhimurium reversion assay. All of the PAH extracts were assayed in tester strains TA98 and TA100 both with and without metabolic activation using a liver fraction from Aroclor 1254-treated rats. None of the extracts from fungal incubations with the mutagenic PAHs, benzo[a]pyrene, 7,12-dimethylbenz[a]anthracene, 3-methylcholanthrene and benz[a]anthracene, as well as the non-mutagenic PAHs, naphthalene, phenanthrene and anthracene, displayed any appreciable mutagenic activity. In addition, time course experiments indicated that the rate of decrease in mutagenic activity in the extracts from cultures incubated with benzo[a]pyrene or 7,12-dimethylbenz[a]anthracene was coincident with the rate of increase in total metabolism. The results demonstrated the ability of the fungus C. elegans to detoxify known carcinogens and mutagens and suggests that this organism may play an important role in the metabolism and inactivation of PAHs in the environment.
Ip admin of 40 mg/kg benz(a)anthracene to Wistar rats can reduce the potency of synthetic estrogen triphenylethylene, presumably as a result of benz(a)anthracene hydroxylase induction.
For more Interactions (Complete) data for BENZ(A)ANTHRACENE (16 total), please visit the HSDB record page.
LC50; Species: Daphnia pulex (Crustacean); Concentration: 0.01 mg/L for 96 hr /Conditions of bioassay not specified in source examined/
EC50; Species: Chlorella fusca var. vacuolata (Green Algae) strain 21115, 75000 cells/mL; Conditions: freshwater, static, 28 °C, pH 6.9; Concentration: 0.06 umol/L for 24 hr (95% confidence interval: 0.0555-0.0655 umol/L); Effect: population growth rate /99% purity/
LC50; Species: Daphnia magna (Water Flea) age <24 hr neonate; Conditions: freshwater, static, 25 °C, pH 7.9-8.3, hardness 80-100 mg/L CaCO3, alkalinity 57-64 mg/L CaCO3; Concentration: 97.5 ug/L for 48 hr /99% purity/
TERRESTRIAL FATE: Based on a recommended classification scheme(1), an experimental Koc range of 545,000 to 1,870,000 in sediment(2) indicates that benz(a)anthracene is expected to be immobile in soil(SRC). Volatilization of benz(a)anthracene from moist soil surfaces is expected(SRC) given a Henry's Law constant of 1.20X10-5 atm-cu m/mole(4); however, volatilization will be attenuated by adsorption to soil(SRC). Benz(a)anthracene is not expected to volatilize from dry soil surfaces based on an experimental vapor pressure of 2.1X10-7 mm Hg(5). The degradation half-life for benz(a)anthracene applied to Kidman sandy loam and McLaurin sandy loam was determined to be 261 days and 162 days, respectively, suggesting that biodegradation is not an important environmental fate process in soil(6).
TERRESTRIAL FATE: The overall mineralization of benz(a)anthracene in soil collected from an abandoned coal tar refinery in Dover, Ohio ranged from 0 to 40 percent after 64 days using an indigenous soil microbial population(1). The half-life of benz(a)anthracene in a DAF sludge soil was determined to be 40.5 days, from an initial concentration of 670 mg/kg and a final concentration of 127 mg/kg after 97 days(2).
AQUATIC FATE: Based on a recommended classification scheme(1), an experimental Koc range of 545,000 to 1,870,000 in sediment(2) indicates that benz(a)anthracene is expected to adsorb to suspended solids and sediment in water(SRC). Benz(a)anthracene may volatilize from water surfaces(SRC) based on a Henry's Law constant of 1.20X10-5 atm-cu m/mole(3). Using this Henry's Law constant and an estimation method(4) volatilization half-lives for a model river and model lake are 3 days and 39 days, respectively(SRC); however, volatilization will be attenuated by adsorption to suspended solids and sediment in the water column(SRC). The volatilization half-life from a model pond was estimated as 12 years when adsorption was considered(5). According to a classification scheme(6), an estimated BCF of 2,940(SRC), from its log Kow of 5.76(7) and a regression-derived equation(8), suggests the potential for bioconcentration in aquatic organisms is very high(SRC). Hydrolysis is not expected to be an important environmental fate process since this compound lacks functional groups that hydrolyze under environmental conditions(4). Benz(a)anthracene had half-lives ranging from 199-252 days in three seawater-sediment slurries(9), suggesting that biodegradation is not an important environmental fate process in water(SRC).
AQUATIC FATE: When benz(a)anthracene is released into water it will rapidly sorb to the sediment and particulate matter in the water column including phytoplankton and zooplankton. Therefore, high initial concentrations are rapidly reduced (few hours). However low concentrations caused by desorption can last almost indefinitely(1). The dissolved benz(a)anthracene will undergo photolysis (half-life hours to a few days) and in eutrophic bodies of water, oxidation by alkylperoxy radicals may be important. The relative contribution of sorption and photolysis to benz(a)anthracene removal will depend on the type of aquatic system(4). In a microcosm experiment which simulated shallow coastal waters of the northeast US, 29 percent of the benz(a)anthracene had respired to CO2 while 21 percent was unchanged(2). When a crude oil dispersion was placed on top of a water column in a controlled ecosystem enclosure in Saanich Inlet, Canada, the benz(a)anthracene concentration in the water column decreased exponentially, declining to half its initial concentration in 4 to 5 days(3). Another study determined a half-life for benz(a)anthracene of 290 days in sediment from an oil-contaminated stream but a half-life of 10 to 400 times as long in an uncontaminated stream(5). Benz(a)anthracene was found to absorb light beyond 480 nm and photolyze in sunlight(6). The photolysis half-life of benz(a)anthracene in water measured in early March at 40 N latitude was determined to be 5 hours(6). Another investigator estimated that the midsummer photolysis half-life for benz(a)anthracene was 0.6 hours(4). The photolysis rate for benz(a)anthracene was reduced in humic waters due to light screening and quenching. Photolysis was also inhibited in anaerobic waters. In addition, 7,12-benzanthracene quinone and 2 unidentified products were observed in aerobic waters(6). When modeled for various environmental systems, the photolysis half-life of benz(a)anthracene was 10 hours for an oligotrophic lake, 20 hours for a stream and 50 hours for a eutrophic pond or lake(1). Although the rate of loss due to oxidation by peroxyl radicals is about four times slower than for photolysis, this process is dominant in a eutrophic lake or pond (half-life of 38 hours)(6). In an experiment in which crude oil was added to a large salt-water tank with simulated natural conditions, 55 percent of the benz(a)anthracene photo-decomposed in 5 hours and 100 percent photo-decomposed in 10 hours(7).
Benz(a)anthracene has been identified in many food sources (ug/kg): smoked beef (chipped), 0.4; smoked ham, 2.8; barbecued beef, 13.2; smoked hot sausage, 0.5; smoked frankfurters, 1.5; smoked salami, 1.5, pepperoni, 0.2; charcoal-broiled steak, 1.0; charcoal-broiled hamburger, 50.0; charcoal-broiled frankfurter, 2.0; vegetable oils, 0.8 to 1.1; spinach, 16; kale, 43 to 230; cereals, 0.4 to 6.8; very dark roast coffee, 2; soots, 16 to 150; and Japanese horse mackerel, gas broiler, 0.6 to 2.9(1). The concentration of benz(a)anthracene in lettuce and rye grown at varying distances from a highway in Sweden were determined to range from 0.4 to 1.9 ug/kg fresh weight and 0.2 ug/kg fresh weight, respectively(2). The fine aerosol emission rate for benz(a)anthracene from a frying hamburger (extralean/regular), from a charbroiled hamburger (extralean), and from a charbroiled hamburger (regular) was determined to be 0.02, 0.30, and 0.29 mg/kg, respectively(3). Benz(a)anthracene was identified in bolted wheat flour, bolted rye flour, rolled oats, milled oats, milled wheat, and bran in concentrations of <0.1, 0.1, 0.2, <0.1, <0.1, and 11 ug/kg, respectively(4). The concentration of benz(a)anthracene in bread and margarine was determined to be 0.2 and 5.8 ug/kg, respectively(5).
Benz(a)anthracene was detected in charcoal-broiled steaks (4.5 ug/kg); different broiled & smoked foods (up to 189 ug/kg); fresh foods (up to 230 ug/kg); edible oils (0.1 to 98.3 ug/kg)(1).
The substance can be absorbed into the body by inhalation, through the skin, by ingestion and through the eyes.
Oral (L10) ; inhalation (L10)
IDENTIFICATION AND USE: Benz(a)anthracene (BA) is a solid. There is no commercial production 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: It is reasonably anticipated to be a human carcinogen. Benz(a)anthracene induced arylhydrocarbon hydroxylase in two human hepatoma cell lines. The percent of lymphoblasts was higher in benz(a)anthracene-treated cultures of peripheral blood mononuclear cells than in control cultures. ANIMAL STUDIES: 2 mg BA induced 17 carcinomas and 1 papilloma in the bladders of 52 mice surviving 40 or more weeks. The incidence of tumors in the controls was 3.8%. Single administration of 0.5 mg BA by stomach tube produced no tumors among 13 mice observed for 16 months. Eight or 16 administrations at three- to seven-day intervals produced a papilloma of the forestomach in 2/27 mice, whereas no tumors appeared among 16 controls. Benz(a)anthracene was mutagenic in an in vitro L5178Y mouse lymphoma assay with metabolic activation. Benz(a)anthracene showed unequivocal mutagenic activity with metabolic activation in Salmonella typhimurium TA98 and TA100 as determined by Ames assay. Postnatal exposure to BA altered ovarian ERbeta expression, disturbed morphological development of the ovaries and caused ovarian dysfunction in immature rats. ECOTOXICITY STUDIES: BA induced alterations in metabolic enzyme activity in northern bobwhite quail. An increase in mixed-function oxygenase and cytochrome p450 was found in intestinal homogenates from Nereis virens fed food contaminated with benz(a)anthracene. The lowest tested and observed effect concentration (LOEC) for Japanese medaka early life stages was equivalent to 0.92 ug/g dryw of BA. weight
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)
/BIRDS and MAMMALS/ ... Acute toxicity of naphthalene, pyrene, and benz[a]anthracene (BAA) was examined in adult northern bobwhite quail (Colinus virginianus). Additionally, subacute (8 d) and subchronic (60 d) studies were conducted to assess alterations in metabolic enzyme activity. Neither naphthalene, nor pyrene, nor BAA exposure via oral gavage produced acute toxicity up to the limit dose of 2 g/kg body weight. In the subacute study, quail provided feed containing the highest concentration of BAA for 5 d had significantly increased renal ethoxyresorufin O-deeththylase (EROD) activity compared to controls. Following a 3-d recovery period, significant increases between 10 and 100 mg/kg of BAA in feed existed for both hepatic EROD and pentoxyresorufin O-deethylase (PROD) activity compared to controls. Subchronic exposure to BAA (ranging from 0.1 to 10 mg/kg) also resulted in a significant rise of EROD and PROD in both kidney and liver tissue compared to controls. Though the individual polycyclic aromatic hydrocarbons (PAHs) used in this study were not acutely toxic, these results confirm that these individual PAHs induce alterations in metabolic enzyme activity in northern bobwhite quail.
/BIRDS and MAMMALS/ The potency of tetrachlorodibenzo-p-dioxin (TCDD) and 18 polycyclic aromatic hydrocarbons (PAHs) for induction of ethoxyresorufin-O-deethylase (EROD) activity was assessed in primary hepatocyte cultures prepared from chicken (Gallus domesticus), Peking duck (Anas platyrhynchos domesticus), and greater scaup (Aythya marila). TCDD and 8 of the PAHs induced EROD activity in a concentration-dependent manner. Seven of these were previously shown to be acutely toxic to avian embryos, while the 10 congeners that did not produce an EROD response caused limited mortality. The rank order potency of the EROD-active congeners in all three species was as follows: TCDD > dibenz[ah]anthracene > benzo[k]fluoranthene > indeno[1,2,3-cd]pyrene > benzo[a]pyrene > chrysene ... /approximately equal to/ benz[a]anthracene ... /approximately equal to/ benz[ghi]perylene > benzo[b]naphtho[2,3-d]thiophene. Chicken hepatoctyes were more sensitive than duck hepatocytes to EROD induction by all test compounds, but the gap in species sensitivity was 100-fold for TCDD, and generally </= 10-fold for PAHs. ...
/AQUATIC SPECIES/ The toxicity of benz(a)anthracene and fluoranthene (polycyclic aromatic hydrocarbons, PAHs) was evaluated on seven species of marine algae in culture belonging to pico-, nano-, and microphytoplankton, exposed to increasing concentrations of up to 2 mg/L. The short-term (24 hr) toxicity was assessed using chlorophyll a fluorescence transients, linked to photosynthetic parameters. The maximum quantum yield Fv/Fm was lower at the highest concentrations tested and the toxicity thresholds were species-dependent. For acute effects, fluoranthene was more toxic than benz(a)anthracene, with LOECs of 50.6 and 186 ug/L, respectively. After 72 hr exposure, there was a dose-dependent decrease in cell density, fluoranthene being more toxic than benz(a)anthracene. The population endpoint at 72 hr was affected to a greater extent than the photosynthetic endpoint at 24 hr. EC50 was evaluated using the Hill model, and species sensitivity was negatively correlated to cell biovolume. The largest species tested, the dinoflagellate Alexandrium catenella, was almost insensitive to either PAH. The population endpoint EC50s for fluoranthene varied from 54 ug/L for the picophytoplankton Picochlorum sp. to 418 ug/L for the larger diatom Chaetoceros muelleri. ...
U018; As stipulated in 40 CFR 261.33, when benz(a)anthracene, 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 10 lb or 4.54 kg. The toll free number of the NRC is (800) 424-8802. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV.D.3.b).
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/.
Ah locus controls induction by such cmpd as 3-methylcholanthrene, benzo(a)anthracene, and TCDD of many drug-metab enzyme activities. The Ah system is believed to comprise regulatory, structural and probably temporal genes which may or may not be linked. Multiple forms of cytochrome p450 are among many structural gene products "turned on" during sequence of events following exposure of animals or cultured cells to polycyclic aromatic inducers. Cytosolic receptor for these inducers in genetically "responsive" mice is believed to be major product of aryl hydrocarbon hydroxylase (ah) regulatory genes. Cytosolic receptor with specifically bound inducer appears to translocate into nucleus during cytochrome p450 induction by polycyclic aromatic cmpd in intact liver of Ah-responsive mice and cultured cells.
... For aquatic species, polycyclic aromatic hydrocarbons (PAHs) are generally accepted as acting through either of two modes of action: (1) "dioxin-like" toxicity mediated by activation of the aryl hydrocarbon receptor (AHR), which controls a battery of genes involved in PAH metabolism, such as cytochrome P4501A (CYP1A) and (2) "nonpolar narcosis", in which tissue uptake is dependent solely on hydrophobicity and toxicity is mediated through non-specific partitioning into lipid bilayers. ...
The cytochrome P450 isoforms responsible for the regio-selective metabolism of benz[a]anthracene (BA) are poorly defined but as with other polycyclic aromatic hydrocarbons (PAHs) may include members of the CYP2C sub-family. Since the expression of some of these is regulated in a gender-specific manner and may be altered by age, rat strain or by phenobarbital treatment, the effects of these variables on metabolism of BA to diols was investigated. These studies used hepatic, microsomal membranes from immature and adult Long-Evans rats and adult Hooded Lister rats. BA-diols were resolved by normal phase HPLC into three discrete peaks identified as benz[a]anthracene-5,6-diol (BA-5,6-diol), benz[a]anthracene-10, 11-diol (BA-10,11-diol) and a mixture of benz[a]anthracene-3,4- and -8,9-diols (BA-3,4-diol and BA-8,9-diol and termed Peak(3/8)). Significant gender-related differences were found in the rates of diol formation in adults of both the Long-Evans and Hooded Lister rat strains. Formation of BA-10,11-diol and to a lesser extent the components of Peak(3/8) were greater in the male compared to female animals by factors of at least 14 and two, respectively. An age-dependent effect is also observed in the Long-Evans rat since these differences are still apparent in prepubertal animals but to a lesser extent (gender ratio male:female BA-10,11-diol 9X; Peak(3/8) 1.4X). In contrast BA-5,6-diol was formed at similar rates by membranes from female and male rats whether mature (Long-Evans and Hooded Lister) or immature (Long-Evans). Phenobarbital treatment of the adult Long-Evans rats resulted in a moderate increase in the formation of each diol other than at the 10,11-position and the induction was not gender specific. The rate of formation of BA-10, 11-diol was decreased in phenobarbital-treated male rats suggesting modulation of a male specific isoform. Measurement of microsomal epoxide hydrolase revealed no gender or age differences and suggests that this enzyme is not rate limiting in BA-diol formation and thus is not responsible for the differences in BA-diol formation observed. The results suggest that CYP2C11 along with a male-specific isoenzyme not regulated by age are important in the formation of BA-10,11-diol and a component(s) of Peak(3/8) in males. CYPs 2B2 and/or 2C6 appear to be involved in formation of BA-5,6-diol in male and female. ...
Benz[a]anthracene (BA) is one of the most abundant polycyclic aromatic hydrocarbons (PAHs) that are ubiquitous environmental pollutants. PAH carcinogenesis is explained by DNA adduct formation by PAH diol epoxide and oxidative DNA damage by PAH o-quinone. Benz[a]anthracene-trans-3,4-dihydrodiol (BA-3,4-dihydrodiol) is a minor metabolite but shows higher mutagenicity and tumorigenicity than parent BA. We confirmed that a BA o-quinone type metabolite, benz[a]anthracene-3,4-dione (BA-3,4-dione), induced oxidative DNA damage in the presence of cytochrome P450 reductase. ... We found that BA-3,4-dihydrodiol nonenzymatically caused Cu(II)-mediated DNA damage including 8-oxo-7,8-dihydro-2'-deoxyguanosine formation and the addition of NADH enhanced DNA damage. BA-3,4-dihydrodiol induced a double-base lesion of C and G at the 5'-ACG-3' sequence complementary to codon 273 of the human p53 tumor suppressor gene, which is known as a hotspot. The DNA damage was inhibited by catalase and bathocuproine, indicating the involvement of H(2)O(2) and Cu(I). Time-of-flight mass spectroscopic study suggested that BA-3,4-dihydrodiol undergoes Cu(II)-mediated autoxidation leading to the formation of its hydroxylated form of BA-3,4-dihydrodiol, capable of causing oxidative DNA damage. It is noteworthy that BA-3,4-dihydrodiol can nonenzymatically induce DNA damage more efficiently than BA-3,4-dione with metabolic activation. In conclusion, oxidative DNA damage induced by BA-3,4-dihydrodiol not only via quinone-type redox cycle but also via a new type of redox cycle participates in the expression of carcinogenicity of BA and BA-3,4-dihydrodiol.
Cultures of Mycobacterium vanbaalenii strain PYR-1 grown in mineral salts medium and nutrients in the presence of benz[a]anthracene metabolized 15% of the added benz[a]anthracene after 12 days of incubation. Neutral and acidic ethyl acetate extractable metabolites were isolated and characterized by high performance liquid chromatography (HPLC) and uv-visible absorption, gas chromatography/mass (GC/MS) and nuclear magnetic resonance (NMR) spectral analysis. Trimethylsilylation of the metabolites followed by GC/MS analysis facilitated identification of metabolites. The characterization of metabolites indicated that M. vanbaalenii initiated attack of benz[a]anthracene at the C-1,2-, C-5,6-, C-7,12- and C-10,11-positions to form dihydroxylated and methoxylated intermediates. The major site of enzymatic attack was in the C-10, C-11 positions. Subsequent ortho- and meta-cleavage of each of the aromatic rings led to the accumulation of novel ring-fission metabolites in the medium. The major metabolites identified were 3-hydrobenzo[f]isobenzofuran-1-one (3.2%), 6-hydrofuran[3,4-g]chromene-2,8-dione (1.3%), benzo[g]chromene-2-one (1.7%), naphtho[2,1-g]chromen-10-one (48.1%), 10-hydroxy-11-methoxybenz[a]anthracene (9.3%), and 10,11-dimethoxybenz[a]anthracene (36.4%). Enzymatic attack at the C-7 and C-12 positions resulted in the formation of benz[a]anthracene-7,12-dione, 1-(2-hydroxybenzoyl)-2-naphthoic acid, and 1-benzoyl-2-naphthoic acid. A phenyl-naphthyl metabolite, 3-(2-carboxylphenyl)-2-naphthoic acid, was formed when M. vanbaalenii was incubated with benz[a]anthracene cis-5,6-dihydrodiol, indicating ortho-cleavage of 5,6-dihydroxybenz[a]anthracene. A minor amount of 5,6-dimethoxybenz[a]anthracene was also formed. The data extend and propose novel pathways for the bacterial metabolism of benz[a]anthracene.
Cultures of the ligninolytic fungus Irpex lacteus incubated in a nutrient liquid medium degraded more than 70% of the initially applied benz[a]anthracene within 14 days. At the first step of metabolization, benz[a]anthracene was transformed via a typical pathway of ligninolytic fungi to benz[a]anthracene-7,12-dione (BaAQ). The product was further transformed by at least two ways, whereas one is complied with the anthracene metabolic pathway of I. lacteus. Benz[a]anthracene-7,12-dione was degraded to 1,2-naphthalenedicarboxylic acid and phthalic acid that was followed with production of 2-hydroxymethyl benzoic acid or monomethyl and dimethylesters of phthalic acid. Another degradation product of BaAQ was identified as 1-tetralone. Its transformation via 1,4-naphthalenedione, 1,4-naphthalenediol and 1,2,3,4-tetrahydro-1-hydroxynaphthalene resulted again in phthalic acid. None of the intermediates were identified as dead-end metabolites. ...
For more Metabolism/Metabolites (Complete) data for BENZ(A)ANTHRACENE (21 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)
Benz(a)anthracene undergoes intestinal transport by passive diffusion.
... Benz(a)anthracene was not detected in /human/ liver, but was present in fatty tissues.
Benzo(a)pyrene and benz(a)anthracene levels were 0.528 and 0.546 ug/L respectively in the urine in 451 and 437 samples collected in the northwest of the Ruhr area, whereas 35 and 34 urine samples collected in an uncontaminated area contained 0.395 and 0.416 ug/L of benzo(a)pyrene and benz(a)anthracene. Smoking did not affect the urinary ... levels.
The time for uptake and metabolism of benz(a)anthracene is approximately 24 hours in Daphnia pulex.
Used as a research chemical; Not commercially used or produced; [HSDB]
There is no ... known use of this compound.
PAHs are generally not produced commercially in the United States except as research chemicals. /Polycyclic aromatic hydrocarbons/
Substance listed with specific concentration in tattoo ink and/or permanent make up according to EU Commission Regulation 2020/2081. The concentration limit (by weight) is 0.00005%.
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)
2023: 640,745 lb
(1977) NOT PRODUCED COMMERCIALLY IN USA
(1982) NOT PRODUCED COMMERCIALLY IN USA
There is no commercial production ... of this compound.
Wood Product Manufacturing
Benz[a]anthracene: ACTIVE
Benz(a)anthracene occurs ubiquitously in products of incomplete combustion; it is also found 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/
ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), Benz(a)anthracene, which has an experimental vapor pressure of 2.1X10-7 mm Hg at 25 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase benz(a)anthracene 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 5X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase benz(a)anthracene may be physically removed from the air by wet and dry deposition(SRC). Benz(a)anthracene irradiated with light at wavelengths greater than 290 nm was found to be 25.3 percent degraded after 17 hours(4). Benz(a)anthracene is found in the atmosphere both as the free vapor and adsorbed to particulate matter. Polyaromatic hydrocarbons are found concentrated in submicron particles and aerosols. These particles will be transported but are subject to gravitational settling and scavenging by rain and snow. The estimated half-lives of these particles in the atmosphere has been estimated to be 5 to 30 days during which time they can be transported to remote regions(5,6).
/AQUATIC SPECIES/ ... The present study ... reports the toxicity of several alkylated derivatives of chrysene and benz[a]anthracene to the embryos of Japanese medaka (Oryzias latipes) using the partition controlled delivery (PCD) method of exposure. The PCD method maintained the desired exposure concentrations by equilibrium partitioning of hydrophobic test compounds from polydimethylsiloxane (PDMS) films. Test concentrations declined by only 13% over a period of 17 days. Based on the prevalence of signs of blue sac disease (BSD), as expressed by median effective concentrations (EC50s), benz[a]anthracene (B[a]A) was more toxic than chrysene. Alkylation generally increased toxicity, except at position 2 of B[a]A. Alkylated polycyclic aromatic hydrocarbons (alkyl-PAHs) substituted in the middle region had a lower EC50 than those substituted at the distal region. Except for B[a]A and 7-methylbenz[a]anthracene (7-MB), estimated EC50 values were higher than their solubility limits, which resulted in limited toxicity within the range of test concentrations. The regression between log EC50s and logKow values provided a rough estimation of structure-activity relationships for alkyl-PAHs, but Kow alone did not provide a complete explanation of the chronic toxicity of alkyl PAHs.
For more Ecotoxicity Excerpts (Complete) data for BENZ(A)ANTHRACENE (10 total), please visit the HSDB record page.