Potential Of Polycyclic Aromatic Hydrocarbons Research Articles

Voltammetric behavior of benzo[a]pyrene at boron-doped diamond electrode: A study of its determination by adsorptive transfer stripping voltammetry based on the enhancement effect of anionic surfactant, sodium dodecylsulfate

Benzo[a]pyrene (BaP), a member of the polycyclic aromatic hydrocarbon (PAH) class, is one of the most potent PAH carcinogens. The electrochemical oxidation of BaP was first studied by cyclic voltammetry at the boron-doped diamond electrode in non-aqueous solvent (dimethylsulphoxide with lithium perchlorate). The compound was irreversibly oxidized in a single step at high positive potential, resulting in the well-resolved formation of a couple with a reduction and re-oxidation wave at much lower potentials. Special attention was given to the use of adsorptive stripping voltammetry together with a medium exchange procedure in aqueous and aqueous/surfactant solutions over the pH range of 2.0–8.0. The technique in aqueous solutions had little value in practice because of too small oxidation peak current. This problem was solved when surfactants were added into the sample solution, by which the oxidation peak currents of BaP were found enhanced dramatically. The employed surfactants were sodium dodecylsulfate (anionic, SDS), cetyltrimethylammonium bromide (cationic, CTAB) and Tween 80 (non-ionic). Using square-wave stripping mode, the compound yielded a well-defined voltammetric response in Britton–Robinson buffer, pH 2.0 containing 2.5×10−4M SDS at +1.07V (vs. Ag/AgCl) (after 120s accumulation at +0.10V). The process could be used to determine BaP in the concentration range of 16–200nM (4.04–50.46ngmL−1), with a detection limit of 2.86nM (0.72ngmL−1). This method was also applied to determine BaP in model water sample prepared by adding its different concentrations into tap water.

Assessment of carcinogenic risk due to inhalation of polycyclic aromatic hydrocarbons in PM 10 from an industrial city: A Korean case-study

This study investigated the effects of meteorological conditions and spatial variations on the toxicity of polycyclic aromatic hydrocarbons (PAHs) in airborne PM 10 in Ulsan, the largest industrial city in Korea. Daily PM 10 samples were collected on quartz microfiber filters using high volume samplers located in a downtown area, a residential area and an industrial area of Ulsan during spring and summer sampling periods. Sixteen individual PAHs were extracted into a mixture solution of dichloromethane and n-hexane (1:1, v/v) in an ultrasonic bath and were analyzed using a high performance liquid chromatography system with an ultra-violet detector (HPLC-UVD). The average total PAH concentrations from the three representative sampling sites of Ulsan ranged from 16.15 to 57.12 ng/m 3 in spring and from 11.11 to 34.56 ng/m 3 in summer. The toxicity equivalent concentrations (TEQs) of the PAHs in PM 10 of Ulsan ranged from 1.82 to 13.1 ng/m 3, with an average level of 4.17 ng/m 3. The highest TEQs were found in the downtown area, which had an average value of 6.30 ng/m 3 in spring and 5.52 ng/m 3 in summer. BaP and DahA were identified as the major carcinogenic PAHs that contributed to 34.8 and 59.4% of the total carcinogenic potency of PAHs in PM 10 in Ulsan. The identified TEQs were highly correlated ( r 2 = 0.73–0.90, p < 0.01) with the total PAH concentrations for each area. The TEQs showed a significant correlation ( p < 0.01) with the concentration of air pollutants, including PM 10, PM 2.5 and NO 2.

대도시의 주거/도로변 지역 및 배경 지역의 대기 중 입자상 다환 방향족 탄화수소의 특성

The present study aims to evaluate the characteristics of atmospheric polycyclic aromatic hydrocarbons (PAHs) pollution in roadside and residential areas of two Korean metropolitan cities (Seoul and Incheon) and a background area (Seokmolee). This purpose was established by analyzing temporal and spacial concentration distribution of total and 7 individual PAHs, which were extracted from ambient particulate matters, and by utilizing a multivariate statistical method (principal component analysis, PCA) for the qualitative determination of potential PAH sources. Target PAHs included benzo(a)anthracene (BaA), benzo(a)pyrene (BaP), benzo(b)fluoranthene (BbF), benzo(k)fluoranthene (BkF), chrysene (Chr), dibenzo(a,h)anthracene (DahA), and indeno(1,2,3-cd)pyrene (IcdP). For all surveyed sites, the concentrations of total PAHs were higher in winter season than in other seasons. However, the concentrations of individual PAHs varied with surveyed sites. In both residential and roadside sites of Seoul and Incheon, BbF revealed the highest atmospheric levels. For all 7 target PAHs, the ambient concentrations were higher in Seoul and Incheon than in a background area (Seokmolee). In both residential and roadside areas, the concentrations of 4 target PAHs (BaA, BbF, BkF, DahA) were higher in Incheon than in Seoul. However, both the residential and roadside Chr concentrations were comparable in Seoul and Incheon. In addition, the residential IcdP concentrations were higher in Incheon than in Seoul, whereas the roadside concentrations were higher in Seoul. The roadside and residential BaP concentrations exhibited the reverse result to the IcdP concentrations. An PCA analysis suggested that atmospheric PAHs in both residential and roadside areas would be due to combined effects of several potential sources such as gasoline- and diesel-fueled vehicles, coal/oil combustion, and waste incineration.

Abstract 3456: Characterization of dibenzo[a,l]pyrene-trans-11,12-diol glucuronidation by UDP-glucuronosyltransferases

Abstract A procarcinogen found most notably in tobacco smoke is dibenzo[a,l]pyrene (DB[a,l]P), which can be further metabolized into its epoxide, diol, and carcinogenic diol-epoxide forms. DB[a,l]P metabolites are some of the most potent carcinogens of the polycyclic aromatic hydrocarbon (PAH) family of compounds due to a structural feature called the fjord region. The activated metabolites of DB[a,l]P bind mostly to deoxyadenosine in DNA to form stable adducts, which can potentially lead to DNA damage. UDP-glucuronosyltransferase (UGT) enzymes mediate the attachment of a UDP-glucuronic acid to a wide variety of endogenous and exogenous substrates including several carcinogens, resulting in increases in water solubility and elimination of the carcinogen from the body. The focus of the current study was to examine the detoxification of the carcinogenic diol form (DB[a,l]P-trans-11,12-diol) by glucuronidation. In order to understand the metabolism of this potent PAH by human UGT enzymes, HEK293 cell lines over-expressing individual UGTs were screened for glucuronidation activity toward DB[a,l]P-11,12-diol. Glucuronide products were quantified using an ultra-performance liquid chromatography (UPLC) method. Six UGTs (UGTs 1A1, 1A7, 1A8, 1A9, 1A10 and UGT2B7) were found to be highly active. Three glucuronide conjugates were observed in activity assays with UGT1A1 and 1A10, while only two glucuronides were formed with UGTs 1A7, 1A8, 1A9, and 2B7. Enzyme kinetic analysis indicated that UGT1A9 is the most active isoform among all the UGTs, exhibiting the highest Vmax/Km for the two glucuronide products it formed. These results suggest that multiple UGTs are involved in stereospecific glucuronidation of DB[a,l]P metabolites in humans. In addition to the further characterization of (DB[a,l]P-trans-11,12-diol) glucuronide conjugates, studies examining the role of polymorphisms in active UGTs on cancer risk are currently on-going. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3456.

Characterization of contaminant migration potential in the vicinity of an in-place sand cap

Purpose This study characterized the chemical transport potential of polycyclic aromatic hydrocarbons (PAHs) and total petroleum hydrocarbons (TPH) in the vicinity of a sand cap placed in the nearshore zone of a tidal marine embayment.

Polycyclic aromatic hydrocarbons in the atmosphere of Shanghai, China

Shanghai is the largest industrial and commercial city in China, and its air quality has been concerned for several years. However, scarce study had been made on the seasonal levels of atmospheric polycyclic aromatic hydrocarbons (PAHs), together with their gas-particle partitioning and potential emission sources. Based on an intensive sampling campaign at urban and suburban areas in Shanghai during four seasons of 2005-2006, this study presented the measurement of PAH concentrations in both particulate and gaseous phases, as well as seasonal and spatial variability. The results showed that the annual PAH levels (gas + particle) were 167 ± 109 ng m⁻³ at the urban site and 216 ± 86.5 ng m⁻³ at the suburban site. Gaseous PAHs (>70%) dominated the total PAH mass at both sites, while particulate PAHs contributed more than 90% of the toxic power according to benzo(a)pyrene-equivalent carcinogenic parameter. Different seasonal trend of PAH concentrations was observed between the two sites, and it may be explained by complicated factors such as sampling heights, local/regional emission sources, and climatic conditions. The gas-particle partitioning of PAHs in all samples was calculated, and strong linear correlations between log K (p) and log P(L)° were observed, with shallower slopes (m(r)) at the suburban site than the urban one and in warm season than the cold months, indicating the different equilibrium conditions of PAHs in spatial and seasonal scales in Shanghai. The slope (m(r) = - 0.96) and correlation coefficient (R² = 0.81) for four-ring PAHs were closest to theoretical equilibrium conditions among compounds with various aromatic rings. Finally, the potential PAH sources were estimated based on principal factor analysis with multiple linear regressions. Ground volatilization dominated the PAH pollutions at both sites, while vehicles and coal consumption were the other main emission sources, which totally contributed 32.0% (suburban) to 49.2% (urban) of PAH mass in Shanghai atmosphere. The effects of wood and biomass burning were also detected, but their contributions to PAHs were negligible.

An experimental study of the influence of biofuel origin on particle-associated PAH emissions

The chemical speciation of the 16 polycyclic aromatic hydrocarbons associated to the particulate matter of conventional diesel fuel, rapeseed methyl esters, waste cooking oil methyl esters, waste cooking oil ethyl esters and their conventional fuel blends has been carried out. The speciation of these individual compounds was made by a combination of thermal extraction, solid phase micro-extraction and GC/MS analysis. This PAH speciation method was applied to a real samples obtained from a diesel engine under two different operating modes, urban and extraurban modes. The purpose of this work was to study the relationship between the amount, type and carcinogenic potency of polycyclic aromatic hydrocarbons in engine emissions and the multi-component biodiesel fuel composition.

The thermodynamic landscape of methanogenic PAH degradation

SummaryMethanogenic degradation of polycyclic aromatic hydrocarbons (PAHs) has long been considered impossible, but evidence in contaminated near surface environments and biodegrading petroleum reservoirs suggests that this is not necessarily the case. To evaluate the thermodynamic constraints on methanogenic PAH degradation we have estimated the Gibbs free energy values for naphthalene, phenanthrene, anthracene, pyrene and chrysene in the aqueous phase, and used these values to evaluate several possible routes whereby PAHs may be converted to methane. Under standard conditions (25°C, solutes at 1 M concentrations, and gases at 1 atm), methanogenic degradation of these PAHs yields between 209 and 331 kJ mol−1. Per mole of methane produced this is 27–35 kJ mol−1, indicating that PAH‐based methanogenesis is exergonic. We evaluated the energetics of three potential PAH degradation routes: oxidation to H2/CO2, complete conversion to acetate, or incomplete oxidation to H2 plus acetate. Depending on the in situ conditions the energetically most favourable pathway for the PAH‐degrading organisms is oxidation to H2/CO2 or conversion into acetate. These are not necessarily the pathways that prevail in the environment. This may be because the kinetic theory of optimal length of metabolic pathways suggests that PAH degraders may have evolved towards incomplete oxidation to acetate plus H2 as the optimal pathway.

Crosstalk between activated forms of the aryl hydrocarbon receptor and glucocorticoid receptor

Pyrene, benzo[ a]pyrene (BaP), and indeno[1,2,3-cd]pyrene (IND) are poly cyclic aromatic hydrocarbons (PAHs) with four to six annealed phenyl rings. Dexamethasone (Dex) is a synthetic agonist of glucocorticoids. The aryl hydrocarbon receptor (AhR) ligands, BaP and IND, did not directly activate the glucocorticoid receptor (GR), and Dex did not activate the AhR either. Whenever BaP and IND were added to Dex-treated cultures, they were present with Dex for longer periods, and higher enhancement of Dex-induced transactivation of the GR was found, which indicates that the freshly activated AhR is essential for synergistic interactions with the activated GR. The degree of enhancement of Dex-induced transactivation of the GR by PAHs, BaP ≈ IND > pyrene, paralleled the potency of PAHs in activating the AhR. This synergistic interaction was more distinct in ovarian granulosa cells (HO23) than in HepG2, 293T, or HeLa cells. In contrast, Dex suppressed AhR-mediated expressions, including AhR and cytochrome P450 (CYP) 1 A1 expressions. Dex also counteracted the BaP-induced decrease in cell viability. Crosstalk between the AhR and GR was independent of their expression levels. We concluded that the AhR functionally cross-reacts with the GR, through which transactivation activity of the GR is further enhanced, and in contrast, transactivation activity of the AhR is inhibited. This report shows the significance of in vitro endocrine-related results, which provide a clue for molecular studies of an interactive mechanism between the AhR and GR, and should be confirmed by future in vivo studies.

Biodegradation of soil-applied polycyclic aromatic hydrocarbons by sulfate-reducing bacterial consortium

In the present study, the potential of polycyclic aromatic hydrocarbons (PAHs) biodegradation by sulfate-reducing bacterial consortium enriched from piggery wastewater was investigated. The batch experiments of soil-applied PAH biodegradation were conducted with a mixture of PAHs, i.e., naphthalene, fluorene, phenanthrene, fluoranthene and pyrene, at a concentration of 50 μ g of each PAH per g of soil. A central composite design (CCD) was applied to determine the experimental conditions of each batch assay. The pH, biomass and ethanol concentrations were selected as independent variables and the PAH removal percentage was considered as a dependent variable. The optimal conditions for PAH biodegradation were found to be a pH between 4 and 6.5, an ethanol concentration less than 35 mg/L and a biomass concentration greater than 65 mg/L. Bench scale experiments were carried out at the optimal conditions. At the end of experiment (27 d), total PAH removals by biodegradation and volatilization were around 74% and 20%, respectively. The order of PAH removal was naphthalene, phenanthrene, fluorene, fluoranthene, and pyrene. Throughout the study, PAH biodegradation was in good correlation with sulfate reduction. Results of the kinetics study indicated a competitive inhibition between PAHs investigated.

Quantification of Benzo[a]pyrene-Guanine Adducts in in vitro Samples by LC Tandem Mass Spectrometry with Stable Isotope Internal Standardization

Benzo[a]pyrene, after metabolic activation, is known as one of the most potent polycyclic aromatic hydrocarbons that cause a carcinogenic effect. When benzo[a]pyrene is activated by one-electron oxidation to its radical cation, it binds to either the C-8 or N-7 of guanine on DNA and forms depurinated adducts. A sensitive liquid chromatography/tandem mass spectrometry method coupled with a stable isotope internal standard was developed for detection and quantitative analysis of benzo[a]pyrene with DNA adducts. In vitro samples were analyzed by our method. The method provides structural confirmation of the adduct, as well as quantitative analysis with accuracy, confidence, isomeric specificity, and precision to measure biologically relevant levels in small sample sizes.

Differential response of human and rat epoxide hydrolase to polycyclic aromatic hydrocarbon exposure: Studies using precision-cut tissue slices

The potential of polycyclic aromatic hydrocarbons (PAHs) to modulate microsomal epoxide hydrolase activity, determined using benzo[a]pyrene 5-oxide as substrate, in human liver, was evaluated and compared to rat liver. Precision-cut liver slices prepared from fresh human liver were incubated with six structurally diverse PAHs, at a range of concentrations, for 24h. Of the six PAHs studied, benzo[a]pyrene, dibenzo[a,h]anthracene and fluoranthene gave rise to a statistically significant increase in epoxide hydrolase activity, which was accompanied by a concomitant increase in epoxide hydrolase protein levels determined by immunoblotting. The other PAHs studied, namely dibenzo[a,l]pyrene, benzo[b]fluoranthene and 1-methylphenanthrene, influenced neither activity nor enzyme protein levels. When rat slices were incubated under identical conditions, only benzo[a]pyrene and dibenzo[a,h]anthracene elevated epoxide hydrolase activity, which was, once again accompanied by a rise in protein levels. At the mRNA level, however, all six PAHs caused an increase, albeit to different extent. In rat, epoxide hydroxylase activity in lung slices was much lower than in liver slices. In lung slices, epoxide hydrolase activity was elevated following exposure to benzo[a]pyrene and dibenzo[a,l]pyrene and, to a lesser extent, 1-methylphenanthrene; similar observations were made at the protein level. At both activity and protein levels extent of induction was far more pronounced in the lung compared with the liver. It is concluded that epoxide hydrolase activity is an inducible enzyme by PAHs, in both human and rat liver, but induction potential by individual PAHs varies enormously, depending on the nature of the compound involved. Marked tissue differences in the nature of PAHs stimulating activity in rat lung and liver were noted. Although in the rat basal lung epoxide hydrolase activity is much lower than liver, it is more markedly inducible by PAHs.

Estrogenic status modulates aryl hydrocarbon receptor—mediated hepatic gene expression and carcinogenicity

Estrogenic status is thought to influence the cancer risk in women and has been reported to affect toxicity of carcinogenic polycyclic aromatic hydrocarbons (PAHs) in animals. The objective of this study was to examine the influence of estradiol (E2) on hepatic gene expression changes mediated by 7,12-dimethylbenz(a)anthracene (DMBA), a potent PAH. Sprague-Dawley rats were ovariectomized on postnatal day 50 and infused with E2 (5 mug/kg/day) or polyethylene glycol using osmotic pumps and 14 days later gavaged with DMBA (50 mg/kg) or sesame oil and killed 24 h thereafter. To understand the mechanism of DMBA-mediated hepatocarcinogenicity in the presence of E2, microarray analysis (Rat 230 2.0 Affymetrix-GeneChip) was performed. Two hundred and sixteen genes were downregulated; whereas, 106 genes were upregulated significantly (+/-1.5-fold, P < 0.05) by DMBA treatment. Hierarchical clustering revealed that the expression profile of 39 genes, regulated by DMBA, was significantly modified by E2 supplementation. Interestingly, 71 genes were uniquely modulated in the combined treatment of DMBA and E2, but not by either treatment alone. Results from chromatin immunoprecipitation assay demonstrate that in animals cotreated with E2 and DMBA, there was enhanced recruitment of estrogen receptor-alpha to the regulatory regions of CYP1A1 and aryl hydrocarbon receptor (AhR) genes compared with that observed in animals treated with DMBA alone. E2 supplementation leads to increased DMBA-induced CYP1A1 transcription, while the AhR gene was upregulated in the presence of E2 +DMBA only. Our data suggest that estrogenic status is (i) important in AhR regulation and can influence the effects of xenobiotics and (ii) may be an important factor in DMBA-mediated carcinogenicity.

&lt;b&gt;CARCINOGENIC POTENCY OF POLYCYCLIC AROMATIC HYDROCARBONS IN SOIL&lt;/b&gt;

Carcinogenic potency of polycyclic aromatic hydrocarbons (PAHs) in soils obtained from seven different sampling locations in Effurun metropolis and its environs of Niger Delta Area of Nigeria were evaluated. The 16 US EPA priority PAHs were determined with GC-MS. The concentrations of individual PAHs observed were used to compute the carcinogenic risk potency of the PAHs relative to benzo(a)pyrene (reference carcinogen). Benzo(a)pyrene equivalent concentration in soils from industrial sites, possess about 22 times carcinogenic potencies than soils from residential areas. KEY WORDS: Benzo(a)pyrene, Carcinogen, Carcinogenic risk potency, Tumours, Soil Bull. Chem. Soc. Ethiop. 2007, 21(3), 437-443.

DNA adducts formation and induction of apoptosis in rat liver epithelial ‘stem-like’ cells exposed to carcinogenic polycyclic aromatic hydrocarbons

The bipotent liver progenitor cells, so called oval cells, may participate at the early stages of hepatocarcinogenesis induced by chemical carcinogens. Unlike in mature parenchymal cells, little is known about formation of DNA adducts and other genotoxic events in oval cells. In the present study, we employed spontaneously immortalized rat liver WB-F344 cell line, which is an established in vitro model of oval cells, in order to study genotoxic effects of selected carcinogenic polycyclic aromatic hydrocarbons (PAHs). With exception of dibenzo[ a, l]pyrene, and partly also benzo[ g]chrysene and benz[ a]anthracene, all other PAHs under the study induced high levels of CYP1A1 and CYP1B1 mRNA. In contrast, we observed distinct genotoxic and cytotoxic potencies of PAHs. Dibenzo[ a, l]pyrene, and to a lesser extent also benzo[ a]pyrene, benzo[ g]chrysene and dibenzo[ a, e]pyrene, formed high levels of DNA adducts. This was accompanied with accumulation of Ser-15 phosphorylated form of p53 protein and induction of apoptosis. Contrary to that, benz[ a]anthracene, chrysene, benzo[ b]fluoranthene and dibenzo[ a, h]anthracene induced only low amounts of DNA adducts formation and minimal apoptosis, without exerting significant effects on p53 phosphorylation. Finally, we studied effects of 2,4,3′,5′-tetramethoxystilbene and fluoranthene, inhibitors of CYP1B1 activity, which plays a central role in metabolic activation of dibenzo[ a, l]pyrene. In a dose-dependent manner, both compounds inhibited apoptosis induced by dibenzo[ a, l]pyrene, suggesting that it interferes with the metabolic activation of the latter one. The present data show that in model cell line sharing phenotypic properties with oval cells, PAHs can be efficiently metabolized to form ultimate genotoxic metabolites. Liver progenitor cells could be thus susceptible to this type of genotoxic insult, which makes WB-F344 cell line a useful tool for studies of genotoxic effects of organic contaminants in liver cells. Our results also suggest that, unlike in mature hepatocytes, CYP1B1 might be a primary enzyme responsible for formation of DNA adducts in liver progenitor cells.

Modulation of TCDD-mediated induction of cytochrome P450 1A1 by mercury, lead, and copper in human HepG2 cell line

Co-contamination with complex mixtures of heavy metals and polycyclic aromatic hydrocarbons (PAHs) is a common environmental problem with multiple biological consequences. In this study, we tested in human hepatoma HepG2 cells the potential effects of three prominent environmental heavy metals, mercury (Hg 2+), lead (Pb 2+), and copper (Cu 2+), on the induction of cytochrome P450 1A1 (CYP1A1) by 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD), the most potent PAH. Our results show that TCDD in the absence and presence of heavy metals did not significantly affect HepG2 cell viability using MTT and LDH leakage assays. Exposure of HepG2 cells with either Hg 2+ or Pb 2+ significantly decreased, whereas Cu 2+ potentiated the CYP1A1 induction mediated by TCDD at the activity levels. In a manner similar to CYP1A1 activity, both Hg 2+ and Pb 2+ significantly down-regulated, while Cu 2+ up-regulated, the induction of CYP1A1 protein mediated by TCDD, suggesting that the modulations of CYP1A1 by heavy metals are mediated at least in part at the translational level. Based on these results, exposure to metal/PAH mixtures would differentially modulate PAHs-mediated carcinogenicity.

Using Semipermeable Membrane Devices, Bioassays, and Chemical Analysis for Evaluation of Bioavailable Polycyclic Aromatic Hydrocarbons in Water

Meiliang Bay is a sublake of Taihu Lake and has been polluted by domestic and industrial effluents. As part of a comprehensive risk assessment project in this region, semipermeable membrane devices (SPMDs) were applied to evaluate the levels and potential toxic potency of polycyclic aromatic hydrocarbons (PAHs) in lakewater, in combination with chemical analysis and in vitro bioassay using H4IIE rat hepatoma cells. In addition, induction of hepatic ethoxyresorufin-O-deethylase (EROD) activity, in crucian carp (Carassius auratus), caged in the vicinity of SPMD sampling sites was also used as a biomarker of exposure to PAHs and related chemicals. The caged crucian carp accumulated similar PAH profile patterns (p < 0.001) but at lower levels compared with SPMDs on a wet-weight basis. Total concentrations of PAHs in crucian carp muscle tissues ranged from 35.6 to 69.1 ng/g after the 32-day exposure, whereas total PAHs in SPMDs ranged from 716.9 to 1007.8 ng/g. Dialysates from SPMDs exposed to Meiliang Bay water caused marked EROD activity in H4IIE cells. Toxic potency of dialysates expressed as bioassay-derived 2,3,7,8-tetrachlorodibenzo-p-dioxin equivalents (TCDD-EQ) ranged from 3.8 to 6.2 pg TCDD-EQ/g SPMD for 32-day exposure samples. A linear correlation of total amount of PAHs and in vitro TCDD-EQ of SPMD dialysates yielded an R (2) of 0.82. Empirical evidence suggests that aryl hydrocarbon receptor-active PAHs can account for about 42-56% of the potency observed. Significant induction of liver EROD activity was also observed in crucian carp caged alongside SPMDs and there was a good correlation between the results of EROD assays in vivo and in vitro (R (2) = 0.62, p = 0.02). It is, therefore, suggested that the SPMD technique in connection with chemical analysis and specific in vitro bioassays might be a valuable tool to assess the levels and effects of bioavailable hydrophobic pollutants in water.

Identification and Determination of Highly Carcinogenic Dibenzopyrene Isomers in Air Particulate Samples from a Street Canyon, a Rooftop, and a Subway Station in Stockholm

This study presents determined levels of the highly carcinogenic dibenzopyrene isomers dibenzo(a,l)pyrene, dibenzo(a,e)pyrene, dibenzo(a,l)pyrene, and dibenzo(a,h)pyrene as well as three other polycyclic aromatic hydrocarbons (PAHs)--benzo(a)pyrene, perylene and coronene--in ambient particulate material samples from a street canyon, a rooftop, and an underground subway station in Stockholm, Sweden. To our knowledge, these are the first reported determinations of dibenzopyrene isomers in air particles from either Stockholm or a subway station. Taking into account both concentration and toxic equivalence factors (TEFs), the PAH with the highest carcinogenic potency in the analyzed samples was dibenzo(a,l)pyrene, and the sum carcinogenic potency of the determined dibenzopyrenes was about 1-4 times higher than that of benzo(a)pyrene in the analyzed samples. These findings indicate that it is important to analyze the dibenzopyrene isomers as well as benzo(a)pyrene; the common approach of using benzo(a)pyrene as an indicator substance could lead to underestimates of the potential carcinogenic potency of PAHs in ambient air. The results also indicate that the relative carcinogenic potency of the determined dibenzopyrenes and benzo(a)pyrene in air particles from Stockholm is similar to that of air particles sampled in Washington in 1976-1977, despite general improvements in air quality in the intervening period. However, more data are needed to characterize temporal variations in dibenzopyrene levels in locations such as subway stations, suburbs, road tunnels, and metropolitan areas. There is also a need to identify and characterize both stationary and mobile PAH sources with respect to emission of dibenzopyrene isomers.

The electron affinity of phenanthrene

Phenanthrene is studied by photodetachment-photoelectron spectroscopy. Due to the absence of a parent ion peak in the anion mass spectrum the electron affinity could not be determined directly. However, this absence is the first indication that this molecule has a negative electron affinity. The first three water complexes of phenanthrene were studied, supplying insights into its microsolvation property. Moreover, the electron affinity of the bare molecule could be determined to be -0.01+/-0.04 eV by an extrapolation method using the water cluster data. The experimental work is supported by ab initio calculations for determining the structure of the water complexes. Finally a correlation between the electron affinity and the reduction potential of polycyclic aromatic hydrocarbons is investigated.

Urban Dust Particulate Matter Alters PAH-Induced Carcinogenesis by Inhibition of CYP1A1 and CYP1B1

The polycyclic aromatic hydrocarbons (PAHs) benzo[a]pyrene (B[a]P) and dibenzo[a,l]pyrene (DB[a,l]P) are well-studied environmental carcinogens, however, their potency within a complex mixture is uncertain. We investigated the influence of urban dust particulate matter (UDPM) on the bioactivation and tumor initiation of B[a]P and DB[a,l]P in an initiation-promotion tumorigenesis model. SENCAR mice were treated topically with UDPM or in combination with B[a]P or DB[a,l]P, followed by weekly application of the promoter 12-O-tetradecanoylphorbol-13 acetate. UDPM exhibited weak tumor-initiating activity but significantly delayed the onset of B[a]P-induced tumor initiation by two-fold. When cotreated with UDPM, DB[a,l]P-treated animals displayed no significant difference in tumor-initiating activity, compared with DB[a,l]P alone. Tumor initiation correlated with PAH-DNA adducts, as detected by (33)P-postlabeling and reversed-phase high-performance liquid chromatography. Induction of cytochrome P450 (CYP)1A1 and 1B1 proteins was also detected following UDPM treatment or cotreatment with B[a]P or DB[a,l]P, indicating PAH bioactivation. Further genotoxicity analyses by the comet assay revealed that cotreatment of UDPM plus B[a]P or DB[a,l]P resulted in increased DNA strand breaks, compared with PAH treatment alone. The metabolizing activities of CYP1A1 and CYP1B1, as measured by the 7-ethoxyresorufin O-deethylation (EROD) assay, revealed that UDPM noncompetitively inhibited CYP1A1 and CYP1B1 EROD activity in a dose-dependent manner. Overall, these data suggest that components within complex mixtures can alter PAH-induced carcinogenesis by inhibiting CYP bioactivation and influence other genotoxic effects, such as oxidative DNA damage. These data further suggest that in addition to the levels of potent PAH, the effects of other mixture components must be considered when predicting human cancer risk.