Dibenzo(a,h)pyrene

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical, or carbon dioxide.[Sigma-Aldrich; Safety Data Sheet for Dibenzo

Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary.[Sigma-Aldrich; Safety Data Sheet for Dibenzo

Keep container tightly closed in a dry and well-ventilated place.[Sigma-Aldrich; Safety Data Sheet for Dibenzo

PRECAUTIONS FOR "CARCINOGENS": Storage site should be as close as practical 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: Avoid dust formation. Avoid breathing vapors, mist or gas. Environmental precautions: Do not let product enter drains. Methods and materials for containment and cleaning up: Sweep up and shovel. Keep in suitable, closed containers for disposal.[Sigma-Aldrich; Safety Data Sheet for Dibenzo

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/

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

SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.

Product: Offer surplus and non-recyclable solutions to a licensed disposal company. 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 Dibenzo

PRECAUTIONS FOR "CARCINOGENS": There is no universal method of disposal that has been proved satisfactory for all carcinogenic compounds & specific methods of chem destruction ... published have not been tested on all kinds of carcinogen-containing waste. ... summary of avail methods & recommendations ... /given/ must be treated as guide only. /Chemical Carcinogens/

For more Disposal Methods (Complete) data for DIBENZO(A,H)PYRENE (8 total), please visit the HSDB record page.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Avoid dust formation. Avoid breathing vapors, mist or gas. Environmental precautions: Do not let product enter drains.[Sigma-Aldrich; Safety Data Sheet for Dibenzo

Precautions for safe handling: Provide appropriate exhaust ventilation at places where dust is formed.[Sigma-Aldrich; Safety Data Sheet for Dibenzo

Appropriate engineering controls: General industrial hygiene practice.[Sigma-Aldrich; Safety Data Sheet for Dibenzo

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 Dibenzo

For more Preventive Measures (Complete) data for DIBENZO(A,H)PYRENE (17 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 DIBENZO(A,H)PYRENE (6 total), please visit the HSDB record page.

Excerpt from ERG Guide 154 [Substances - Toxic and/or Corrosive (Non-Combustible)]:

Eye/face protection: Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).[Sigma-Aldrich; Safety Data Sheet for Dibenzo

Skin protection: Handle with gloves.[Sigma-Aldrich; Safety Data Sheet for Dibenzo

Body Protection: Choose body protection in relation to its type, to the concentration and amount of dangerous substances, and to the specific work-place.[Sigma-Aldrich; Safety Data Sheet for Dibenzo

Respiratory protection: Respiratory protection is not required. Where protection from nuisance levels of dusts are desired, use type N95 (US) or type P1 (EN 143) dust masks. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).[Sigma-Aldrich; Safety Data Sheet for Dibenzo

For more Personal Protective Equipment (PPE) (Complete) data for DIBENZO(A,H)PYRENE (9 total), please visit the HSDB record page.

Several well-documented examples of human exposure to carcinogens involve complex mixtures of polycyclic aromatic hydrocarbons (PAHs). Although the biological properties of many pure polycyclic aromatic hydrocarbons have been investigated, less is known about their effects when present as components of mixtures. As the ability to form DNA adducts in vivo is generally indicative of carcinogenic activity of polycyclic aromatic hydrocarbons, we have compared the DNA binding potencies of dibenzo(a,e)pyrene (DB(a,e)P), dibenzo(a,h)pyrene (DB(a,h)P), dibenzo(a,i)pyrene (DB(a,i)P), dibenzo(a,l)pyrene (DB(a,l)P) and benzo(a)pyrene (B(a)P), when applied topically, either singly or in combination, to the skin of male Parkes mice. DNA isolated from the skin and lungs was analyzed by (32)P-postlabelling. The adducts formed by each polycyclic aromatic hydrocarbon exhibited markedly different chromatographic mobilities on polyethyleneimine-cellulose TLC plates. The relative binding potencies of the compounds in both skin and lungs were: dibenzo(a,l)pyrene > dibenzo(a,i)pyrene > dibenzo(a,e)pyrene, in good agreement with their reported carcinogenicities in mouse skin. The majority of adducts were removed from DNA within 21 days of treatment, but low levels of adducts were found to persist for at least 3 months in both tissues. When dibenzo(a,l)pyrene, dibenzo(a,e)pyrene and benzo(a)pyrene were applied together to mouse skin, a total binding 31% lower than expected was detected, while with a mixture of dibenzo(a,e)pyrene and benzo(a)pyrene the binding to DNA in skin was 65% higher than expected from the binding levels of the carcinogenes when applied singly. Other binary combinations of these three polycyclic aromatic hydrocarbons gave adduct levels similar to the sum of the binding levels of the individual components when applied singly. The results demonstrate the usefulness of (32)P-post-labelling for the assessment of the DNA binding potencies of polycyclic aromatic hydrocarbons in mouse tissues, and for the detection of interactions between components of mixtures of carcinogens.

Benzo[a]pyrene (B[a]P) is able to inhibit the mutagenicity of 1-nitropyrene (1-NP) through the reduction of nitroreductase activity and formation of adducts with DNA. The relationships between the chemical structure of 9 polycyclic aromatic hydrocarbons (PAHs) and antagonistic effects on the 1-NP-induced mutation were evaluated by the binary mixtures of 1-NP and PAHs with Salmonella typhimurium TA98 in the absence of S9 mix. Remarkably different antagonistic effects of 9 PAHs on the mutagenicity of 1-NP were observed. Among the tested PAHs, coronene demonstrates the most antagonistic potential followed by benzo[g,h,i]perylene (B[g,h,i]P), benzo[e]pyrene (B[e]P), dibenzo[a,h]pyrene (DB[a,h]P), benzo[a]pyrene (B[a]P) and pyrene. Naphthalene, anthracene, and chrysene had only minor inhibitory activity on the 1-NP mutagenicity. The modifying effects of PAHs on the nitroreductase activity of TA98 strains in the presence of 1-NP were further examined from the production of 1-AP. The statistical analytical data showed that the inhibitory effect of PAHs on the mutagenicity of 1-NP significantly correlated with their effects on the nitroreductase activity (r = -0.69, p < 0.05). In addition, the formation of 1-NP-DNA adducts of the binary mixtures of 1-NP and PAH was determined by the (32)P-postlabeling method. The results indicated that the modulatory effects of PAHs on the formation of 1-NP-DNA adducts were correlated well with their antagonistic activity (r = -0.91, P < 0.01). From the above results, the relationships between the chemical structure of PAHs and the antagonistic effects on the 1-NP mutagenicity were revealed by the surface area and electronic parameters of PAHs. The planar molecular area of PAHs was more convincingly correlated with the antagonistic effect on the mutagenicity of 1-NP (r = -0.81, p < 0.01) than that with the difference in energy, delta E, between EHOMO and ELUMO (r = 0.69, p < 0.05). According to the above, two possible mechanisms are involved in the interactive effect of the binary mixtures: (1) a higher binding affinity with nitroreductase for PAHs having a large planar surface area; and (2) a high energy of interaction between 1-NP and PAHs with a low delta E might decrease the nitroreductive capability.

Ferulic, caffeic, chlorogenic, and ellagic acids, four naturally occurring plant phenols, inhibit the mutagenicity and cytotoxicity of (+/-)-7beta,8alpha-dihydroxy-9alpha, 10alpha-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (B[a]P 7,8-diol-9,10-epoxide-2), the only known ultimate carcinogenic metabolite of benzo[a]pyrene. The mutagenicity of 0.05 nmol of B[a]P 7,8-diol-9,10-epoxide-2 in strain TA100 of Salmonella typhimurium is inhibited 50% by incubation of the bacteria and the diol epoxide with 150 nmol of ferulic acid, 75 nmol of caffeic acid, 50 nmol of chlorogenic acid or, most strikingly, 1 nmol of ellagic acid in the 0.5-ml incubation mixture. A 3-nmol dose of ellagic acid inhibits mutation induction by 90%. Ellagic acid is also a potent antagonist of B[a]P 7,8-diol-9,10-epoxide-2 in Chinese hamster V79 cells. Mutations to 8-azaguanine resistance induced by 0.2 uM diol epoxide are reduced by 50% when tissue culture media also contains 2 uM ellagic acid. Similar to results obtained with the bacteria, ferulic, caffeic, and chlorogenic acids are approximately two orders of magnitude less active than ellagic acid in the mammalian cell assay. The antimutagenic effects of the plant phenols result from their direct interaction with B[a]P 7,8-diol-9,10-epoxide-2, because a concentration-dependent increase in the rate of diol epoxide disappearance in cell-free solutions of 1:9 dioxane/water, pH 7.0, is observed with all four phenols. In parallel with the mutagenicity studies, ellagic acid is 80-300 times more effective than the other phenols in accelerating the disappearance of B[a]P 7,8-diol-9,10-epoxide-2. Ellagic acid at 10 uM increases the disappearance of B[a]P 7,8-diol-9,10-epoxide-2 by approximately 20-fold relative to the spontaneous and hydronium ion-catalyzed hydrolysis of the diol epoxide at pH 7.0. Ellagic acid is a highly potent inhibitor of the mutagenic activity of bay-region diol epoxides of benzo[a]pyrene, dibenzo[a,h]pyrene, and dibenzo[a,i]pyrene, but higher concentrations of ellagic acid are needed to inhibit the mutagenic activity of the chemically less reactive bay-region diol epoxides of benz[a]anthracene, chrysene, and benzo[c]phenanthrene. These studies demonstrate that ellagic acid is a potent antagonist of the adverse biological effects of the ultimate carcinogenic metabolites of several polycyclic aromatic hydrocarbons and suggest that this naturally occurring plant phenol, normally ingested by humans, may inhibit the carcinogenicity of polycyclic aromatic hydrocarbons.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 6.3X10+6(SRC), determined from a structure estimation method(2), indicates that dibenzo(a,h)pyrene is expected to be immobile in soil(SRC). Volatilization of dibenzo(a,h)pyrene from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 1.4X10-8 atm-cu m/mole(SRC), using a fragment constant estimation method(2). Dibenzo(a,h)pyrene is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 6.4X10-12 mm Hg at 25 °C(SRC), determined from a fragment constant method(2). Dibenzo(a,h)pyrene showed no biodegradation after a 29-day incubation period in a bioslurry reactor using contaminated soil from a previous gasworks facility(3). In general, polynuclear aromatic hydrocarbons (PAHs) with five or more benzene rings may not biodegrade readily(4). PAHs with four or more rings, such as dibenzo(a,h)pyrene, are expected to be resistant to biodegradation(5). Dibenzo(a,h)pyrene absorbs strongly at wavelengths >290 nm(6) and, therefore, is expected to be susceptible to direct photolysis on soil surfaces exposed to sunlight(SRC).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 6.3X10+6(SRC), determined from a structure estimation method(2), indicates that dibenzo(a,h)pyrene is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 1.4X10-8 atm-cu m/mole(SRC), developed using a fragment constant estimation method(2). According to a classification scheme(4), an estimated BCF of 9600(SRC), from an estimated log Kow of 7.28(2) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is very high, provided the compound is not metabolized by the organism(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(5). In general, polynuclear aromatic hydrocarbons (PAHs) with five or more benzene rings may not biodegrade readily(6). PAHs with four or more rings, such as dibenzo(a,h)pyrene, are expected to be resistant to biodegradation(7). Dibenzo(a,h)pyrene absorbs strongly at wavelengths >290 nm(8) and, therefore, is expected to be susceptible to direct photolysis on water surfaces exposed to sunlight(SRC). Dibenzo(a,h)pyrene is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(3).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), dibenzo(a,h)pyrene, which has an estimated vapor pressure of 6.4X10-12 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist almost entirely in the particulate phase in the ambient atmosphere. Based on an estimated super-cooled vapor pressure of 1.3X10-8 mm Hg at 25 °C(2), a small percentage of dibenzo(a,h)pyrene may exist in the vapor phase in the ambient atmosphere(1). Similar PAHs have been detected in the vapor phase in ambient air(3,4). Vapor-phase dibenzo(a,h)pyrene 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 7.7 hours(SRC), calculated from its rate constant of 5.0X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(2). Particulate-phase dibenzo(a,h)pyrene may be removed from the air by wet and dry deposition(SRC). Dibenzo(a,h)pyrene absorbs strongly at wavelengths >290 nm(5,6) and, therefore, is expected to be susceptible to direct photolysis by sunlight(SRC).

Dibenzo(a,h)pyrene was found in the following Canadian smoked foods (food item, concentration in ppb): bologna, 0.05; sausages, 8.0; ham, 1.0; bacon, 1.0(1). It was not found in meat patties of different fat contents that were grilled over hickory or mesquite wood(2). No dibenzo(a,h)pyrene was found in samples of margarine, spinach and kale from the Netherlands. The vegetables came from a site within 0.5 km of a runway of an international airport(3).

Sources of PAHs in the diet (which includes dibenzo(a,h)pyrene) include barbecued, grilled, broiled, and smoke-cured meats; roasted, baked, and fried foods (prepared by high-temperature processing); breads, cereals, and grains (at least in part from gas or flame drying of grains), and vegetables grown in contaminated soil or with surface contamination from atmospheric deposition of PAH(1).

Eighteen nations in Europe submitted almost 10,000 results (9,714) for PAH levels in different food commodities(1). An evaluation of these data was performed in June 2007 and updated in June 2008. Dibenzo(a,h)pyrene was detected above detection limits (not reported) in 2.2% of 2,341 samples at lower and upper bound mean concentrations of 0.02 and 0.15 ug/kg(1). In a comparison of 1,375 food products for 15 priority PAHS, dibenzo(a,h)pyrene was detected above detection limits in 3.6% of all samples at lower and upper bound mean concentrations of 0.03 and 0.12 ug/kg(1).

IDENTIFICATION AND USE: Dibenzo(a,h)pyrene (DB(a,h)P) forms golden yellow plates. It is used as an experimental carcinogen. HUMAN EXPOSURE AND TOXICITY: DB(a,h)P is reasonably anticipated to be a human carcinogen. DB(a,h)P was mutagenic in human B-lymphoblastoid cells. ANIMAL STUDIES: A group of 24 female mice received a single dermal application of 240 ug DB(a,h)P; a control group of 23 mice was treated with the solvent alone. One week later, all mice received twice weekly dermal applications of 4.26 nmol 12-O-tetradecanoylphorbol-13-acetate in 100 uL acetone for 25 weeks. Papillomas occurred in 18/24 mice treated with DB(a,h)P (5.3 tumors/mouse) compared with 2/23 solvent-treated control mice (0.1 tumors/mouse). One study found 2 tumors in 4 rats dying after 7 to 8 months following im administration of 0.5-1.0 mg of DB(a,h)P. The duration of the experiment was at least 8 months. In another study, 6 female rats were injected with single dose of 0.5 mg DB(a,h)P, and 2 sarcomas appeared at 5.5 and 8 months. DB(a,h)P was not mutagenic in Salmonella typhimurium TM67 with or without metabolic activation. DB(a,h)P was mutagenic in Salmonella typhimurium TA98 and TA100.

Dibenzo(a,h)pyrene was detected in coke plant exhausts(1). Gas exhaust from GTD-5 and D-54A diesel engines were found to contain dibenzo(a,h)pyrene(1). Dibenzo(a,h)pyrene was identified in a coal tar Standard Reference Material (SRM 1597)(2). Bottom ash sampled from four Swedish municipal solid waste incinerators in 1996 contained dibenzo(a,h)pyrene concentrations of less than or equal to 0.4 to 11 ug/kg ash(3). Dibenzo(a,h)pyrene was detected in the exhaust of two diesel and two gasoline-fuelled light-duty vehicles(4).

PRECAUTIONS FOR "CARCINOGENS": Whenever medical surveillance is indicated, in particular when exposure to a carcinogen has occurred, ad hoc decisions should be taken concerning ... /cytogenetic and/or other/ tests that might become useful or mandatory. /Chemical Carcinogens/

Using a structure estimation method based on molecular connectivity indices(1), the Koc of dibenzo(a,h)pyrene can be estimated to be 6.3X10+6(SRC). According to a classification scheme(2), this estimated Koc value suggests that dibenzo(a,h)pyrene is expected to be immobile in soil.

URBAN/SUBURBAN: Dibenzopyrene (isomer not specified) was reported in particulate matter in all seven 24-hr air samples from an industrial site in a town in central Finland in late November at levels ranging from <0.1 to 0.7 ng/cu m; median, 0.2 ng/cu m(1). It was absent in 3 samples collected from the industrial site and in 1 sample from the city center taken in mid May(1). The comparative seasonal concentrations of dibenzo(a,h)pyrene in air (particulate matter) at a site in Sarnia, Ontario in the St. Clair River Basin were: 508 ng/1000 cu m (8.2 ppm) in Apr-June 1975; 81 ng/1000 cu m (1.7 ppm) in July-Sept 1975; 213 ng/1000 cu m (4.1 ppm) in Oct-Dec 1975; and 107 ng/1000 cu m (3.9 ppm) in Jan-March 1976(2). The comparative seasonal concentrations of dibenzo(a,h)pyrene in air (particulate matter) at a site Sudbury, Ontario were: 149 ng/1000 cu m (4.6 ppm) in Apr-June 1975; 47 ng/1000 cu m (1.1 ppm) in July-Sept 1975; 54 ng/1000 cu m (2.4 ppm) in Oct-Dec 1975; and 130 ng/1000 cu m (5.6 ppm) in Jan-March 1976(2). Air particulate samples collected at three different locations in Stockholm, Sweden in 2003 and 2005 contained dibenzo(a,h)pyrene levels 0.39-5.8 pg/cu m(3). Dibenzo(a,h)pyrene was detected in atmospheric air particulates collected in Beijing, China before, during and after the 2008 Beijing Olympic Games(4). Air monitoring conducted at 17 sites in the United Kingdom between 1999 to 2007 detected dibenzo(a,h)pyrene concentrations ranging from 0.00074 to 0.01 ng/cu m(5). Quarterly air monitoring conducted at 8 sites in the United Kingdom during 2009 detected dibenzo(a,h)pyrene concentrations ranging from 0.00065 to 1.4 ng/cu m(5).

/GENOTOXICITY/ C24H14 PAH /is/ a diverse group of five- and six-ring PAH, some of which are present at trace levels in the environment. To better understand the mutagenicity of this class of compounds, 11 C24H14 PAH, including benzo[a]perylene, benzo[b]perylene, dibenzo[a,e]fluoranthene, dibenzo[a,f]fluoranthene, dibenzo[j,l]fluoranthene, dibenzo[a,h]pyrene, dibenzo[a,i]pyrene, dibenzo[e,l]pyrene, naphtho[1,2-b]fluoranthene, naphtho[2,3-a]pyrene, and naphtho[2,3-e]pyrene, were tested in a mutagenicity assay based on human h1A1v2 cells. h1A1v2 cells are a line of human B-lymphoblastoid cells that have been engineered to express cytochrome P4501A1 (CYP1A1), an enzyme capable of metabolizing promutagenic PAH. Mutagenicity was measured at the thymidine kinase (tk) locus following a 72-hr exposure period. Our results show that nine of the compounds were mutagenic. Benzo[a]perylene, dibenzo[a,e]fluoranthene, dibenzo[a,i]pyrene, and naphtho[2,3-a]pyrene were the most potent mutagens, having minimum mutagenic concentrations (MMC) (i.e., the dose at which the induced response was twice that of the negative controls) in the 1-5 ng/mL range. Benzo[b]perylene, dibenzo[a,h]pyrene, dibenzo[a,f]fluoranthene, and naphtho[2,3-e]pyrene were somewhat less potent mutagens, having MMC in the 10-30 ng/mL range. Dibenzo[e,l]pyrene, which had an MMC of 280 ng/mL, was the least potent mutagen. Dibenzo[j,l]fluoranthene and naphtho[1,2-b]fluoranthene were not mutagenic at the doses tested (1-3000 ng/mL). The most mutagenic compounds were also quite toxic. At the highest doses tested, benzo[a]perylene, dibenzo[a,e]fluoranthene, dibenzo[a,i]pyrene, dibenzo[a,h]pyrene, and dibenzo[a,f]fluoranthene induced > 60% killing, and naphtho[2,3-a]pyrene and naphtho[2,3-e]pyrene induced > 50% killing. Benzo[b]perylene, dibenzo[e,l]pyrene, dibenzo[j,l]fluoranthene, and naphtho[1,2-b]fluoranthene induced < 50% killing at the highest doses tested. Comparing these results to a previous study in which nine other C24H14 PAH were tested for mutagenicity in this same assay, it was found that dibenzo[a]pyrene isomers were generally more mutagenic than the other groups of C24H14 PAH tested. ...

/GENOTOXICITY/ The mutagenicity of benzo[a]pyrene (B[a]P), dibenzo[ae]pyrene (DB[ae]P), dibenzo[ah]pyrene (DB[ah]P), dibenzo[ai]pyrene (DB[ai]P), and dibenzo[al]pyrene (DB[al]P) was measured in quantitative forward mutation assays with bacteria (Salmonella typhimurium TM677) and a metabolically competent cell line derived from human B-lymphoblastoid cells (MCL-5) that contained activity for five cytochrome P450s and microsomal epoxide hydrolase found in human liver. DB[al]P and B[a]P, both potent animal carcinogens, were the most mutagenic substances in both assays. DB[al]P was nearly 50-fold more potent than B[a]P in human cells, but only 60% more mutagenic in Salmonella. The carcinogenic isomer DB[ah]P, though nonmutagenic in bacteria, was active in human cells. The following mutagenic potency series, expressed as the minimum detectable mutagen concentration (MDMC) in nmol/ml, was obtained with Salmonella in the presence of rat liver postmitochondrial supernatant (PMS): DB[al]P (3.7), B[a]P (5.8), DB[ae]P (6.9), DB[ai]P (14.9), DB[ah]P (> 100). None of the compounds were mutagenic in the absence of PMS. In human MCL-5 cells the potency series was: DB[al]P (3.1 x 10(-4)), B[a]P (1.5 x 10(-2)), DB[ae]P (2.5 x 10(-2)), DB[ah]P (0.5), DB[ai]P (3.2). The human cell assay thus exhibited over a 10,000-fold range between the most mutagenic and least mutagenic compound, whereas in the bacterial assay there was only a corresponding four-fold difference if the nonmutagenic DB[ah]P was excluded. ...

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/.