Complex Mixture Of Polycyclic Aromatic Hydrocarbons Research Articles

Can environmental factors increase oxidative responses in fish exposed to polycyclic aromatic hydrocarbons (PAHs)?

Relations among polycyclic aromatic hydrocarbons (PAHs), biomarkers of oxidative stress (lipid peroxidation, glutathione, and glutathione S-transferase activity), and the possible influence of environmental factors (temperature, pH, and salinity) were assessed in situ for specimens of Ramnogaster arcuata, a native estuarine fish. PAH levels found in the muscular tissue of R. arcuata ranged from 0.7 to 293.4 ng g−1 wet weight with petrogenic and pyrolytic inputs. Lipid peroxidation in the liver showed positive correlations (P < 0.05) with total PAHs (r = 0.66), 3-ring (r = 0.66) and 4-ring PAHs (r = 0.52) and glutathione in muscle (r = 0.58). Significant positive correlations (P < 0.05) were also evidenced between muscular glutathione with total (r = 0.62) and 3-ring PAHs (r = 0.75). Hepatic glutathione S-transferase negatively correlated with 4-ring PAHs (r = −0.58). These correlations suggest that lipid peroxidation and muscular glutathione could be good biomarkers for complex mixtures of PAHs, and hepatic glutathione S-transferase could be a suitable biomarker for 4-ring PAHs. Furthermore, significant correlations (P < 0.05) of environmental factors with PAH levels and biomarkers were observed, especially pH with 3-ring PAHs (r = −0.65), lipid peroxidation (r = −0.6), glutathione in the liver (r = −0.73) and muscle (r = −0.75); and temperature with 2-ring PAHs (r = −0.75) and glutathione in muscle (r = 0.51). The data suggest an influence of physicochemical parameters which could be driving a shift in PAH toxicity in R. arcuata. These results are essential for an integrated understanding of ecotoxicology and could help to predict environmental effects in present and future scenarios of ocean warming and acidification.

Immunofluorescence Visualization of Polycyclic Aromatic Hydrocarbon Mixtures in the Eastern Oyster Crassostrea virginica.

Bivalve mollusks including oysters have low metabolic potential and are therefore susceptible to accumulating high levels of lipophilic organic contaminants such as polycyclic aromatic hydrocarbons (PAHs). Human exposure to PAHs via consumption of this important commercial shellfish can be a serious public health concern in areas where high PAH contamination exists. Previous PAH immunohistochemical studies have been limited to laboratory-based exposures focusing on one or a few individual PAH compounds. To date, such studies have yet to explore PAH accumulation in oysters, known to have some of the highest levels of PAHs across different food products. Using a monoclonal antibody selective for a range of three- to five-ring PAHs, we present a method to detect and localize complex mixtures of PAHs in oyster tissues via fluorescent immunohistochemistry. Observed immunofluorescence intensity followed a similar trend as measured levels of PAHs in oyster interstitial fluid from PAH-contaminated sites and oysters exposed to the water accommodated fraction of crude oil. This method will be valuable in understanding internal partitioning mechanisms of PAH-exposed oysters and will have important applications in studies on PAH distribution in the tissues of additional organisms for environmental, medical, or veterinary purposes. Environ Toxicol Chem 2023;42:475-480. © 2022 The Authors. Environmental Toxicology and Chemistry published by Wiley Periodicals LLC on behalf of SETAC.

Automated High-Resolution Semi-Preparative Gradient Recycling Liquid Chromatography: Principles, Design, and Applications

A semi-preparative twin-column recycling liquid chromatography (TCRLC) process was extended from isocratic to gradient elution mode. The main separation challenge is when the sample mixture contains early, nearly coeluting, and late impurities, all at the same time. To further improve classical isocratic TCRLC, the gradient TCRLC (GTCRLC) process was implemented with a 2-position 4-port valve in order to better shave the targeted sample from all these impurities. Prior to fully resolving the target compound(s) from the closest impurities by classical isocratic TCRLC, the added valve enabled full elimination by gradient elution mode of not only the early impurities but also any highly retained late impurities that could contaminate the collected fractions of the target compound(s). This GTCRLC process was entirely automated regarding the initial gradient applied, the recycling conditions, and the actuation times of the two valves. The GTCRLC process was applied for the isolation of a single polycyclic aromatic hydrocarbon (PAH), chrysene, present in a complex PAH mixture. In addition, the GTCRLC process was successfully applied to clean vitamins D2 and D3 from a milk extract and to baseline resolve them.

Application of Text Mining in Risk Assessment of Chemical Mixtures: A Case Study of Polycyclic Aromatic Hydrocarbons (PAHs).

Background:Cancer risk assessment of complex exposures, such as exposure to mixtures of polycyclic aromatic hydrocarbons (PAHs), is challenging due to the diverse biological activities of these compounds. With the help of text mining (TM), we have developed TM tools—the latest iteration of the Cancer Risk Assessment using Biomedical literature tool (CRAB3) and a Cancer Hallmarks Analytics Tool (CHAT)—that could be useful for automatic literature analyses in cancer risk assessment and research. Although CRAB3 analyses are based on carcinogenic modes of action (MOAs) and cover almost all the key characteristics of carcinogens, CHAT evaluates literature according to the hallmarks of cancer referring to the alterations in cellular behavior that characterize the cancer cell.Objectives:The objective was to evaluate the usefulness of these tools to support cancer risk assessment by performing a case study of 22 European Union and U.S. Environmental Protection Agency priority PAHs and diesel exhaust and a case study of PAH interactions with silica.Methods:We analyzed PubMed literature, comprising 57,498 references concerning priority PAHs and complex PAH mixtures, using CRAB3 and CHAT.Results:CRAB3 analyses correctly identified similarities and differences in genotoxic and nongenotoxic MOAs of the 22 priority PAHs and grouped them according to their known carcinogenic potential. CHAT had the same capacity and complemented the CRAB output when comparing, for example, benzo[a]pyrene and dibenzo[a,l]pyrene. Both CRAB3 and CHAT analyses highlighted potentially interacting mechanisms within and across complex PAH mixtures and mechanisms of possible importance for interactions with silica.Conclusion:These data suggest that our TM approach can be useful in the hazard identification of PAHs and mixtures including PAHs. The tools can assist in grouping chemicals and identifying similarities and differences in carcinogenic MOAs and their interactions. https://doi.org/10.1289/EHP6702

Heart development in two populations of Atlantic killifish (Fundulus heteroclitus) following exposure to a polycyclic aromatic hydrocarbon mixture

Historic industrial pollution of the Elizabeth River, Virginia resulted in polycyclic aromatic hydrocarbon (PAH) contamination in sediments. Atlantic killifish (Fundulus heteroclitus) inhabiting the Atlantic Wood (AW) industrial site adapted to complex PAH mixture at this Superfund site. Their embryos have proved highly resistant to cardiac abnormalities indicative of PAH toxicity. In this study, embryos spawned from adults collected at AW and King’s Creek (KC), a reference site, were exposed at 24 h post fertilization (hpf) to Elizabeth River Sediment Extract (ERSE), a complex PAH mixture, in a range of concentrations (0, 5.04, 50.45, 100.90, 151.35, or 252.25 µg/L total PAHs). Embryos were processed for histology at 144 hpf to enable evaluations of hearts at tissue and cellular levels. Morphometry and severity scoring were used to evaluate the extent of alterations. Unexposed embryos were similar in both populations. ERSE exposure resulted in multiple changes to hearts of KC embryos but not AW. Alterations were particularly evident in KC embryos exposed to concentrations above 1% ERSE (50.45 µg/L), which had thinner ventricular walls and larger pericardial edema. Individuals with moderate pericardial edema maintained arrangement and proximity of heart chambers, but changes were seen in ventricular myocytes. Severe pericardial edema was prevalent in exposed KC embryos and typically resulted in tube heart formation. Ventricles of tube hearts had very thin walls composed of small, basophilic cells and lacked trabeculae. Edematous pericardial fluid contained small amounts of proteinaceous material, as did controls, and was free of cells. This fluid was primarily unstained, suggesting water influx due to increased permeability. The use of histological approaches provided more specific detail for tissue and cellular effects in hearts of embryos exposed to PAHs and enabled understanding of potential links to later life effects of early life exposure.

Zebrafish CYP1A expression in transgenic Caenorhabditis elegans protects from exposures to benzo[a]pyrene and a complex polycyclic aromatic hydrocarbon mixture

Polycyclic aromatic hydrocarbons (PAHs) are environmental toxicants primarily produced during incomplete combustion; some are carcinogens. PAHs can be safely metabolized or, paradoxically, bioactivated via specific cytochrome P450 (CYP) enzymes to more reactive metabolites, some of which can damage DNA and proteins. Among the CYP isoforms implicated in PAH metabolism, CYP1A enzymes have been reported to both sensitize and protect from PAH toxicity. To clarify the role of CYP1A in PAH toxicity, we generated transgenic Caenorhabditis elegans that express CYP1A at a basal (but not inducible) level. Because this species does not normally express any CYP1 family enzyme, this approach permitted a test of the role of basally expressed CYP1A in PAH toxicity. We exposed C. elegans at different life stages to either the PAH benzo[a]pyrene (BaP) alone, or a real-world mixture dominated by PAHs extracted from the sediment of a highly contaminated site on the Elizabeth River (VA, USA). This site, the former Atlantic Wood Industries, was declared a Superfund site due to coal tar creosote contamination that caused very high levels (in the [mg/mL] range) of high molecular weight PAHs within the sediments. We demonstrate that CYP1A protects against BaP-induced growth delay, reproductive toxicity, and reduction of steady state ATP levels. Lack of sensitivity of a DNA repair (Nucleotide Excision Repair)-deficient strain suggested that CYP1A did not produce significant levels of DNA-reactive metabolites from BaP. The protective effects of CYP1A in Elizabeth River sediment extract (ERSE)-exposed nematodes were less pronounced than those seen in BaP-exposed nematodes; CYP1A expression protected against ERSE-induced reduction of steady-state ATP levels, but not other outcomes of exposure to sediment extracts. Overall, we find that in C. elegans, a basal level of CYP1A activity is protective against the examined PAH exposures.

Genotoxicity and DNA damage signaling in response to complex mixtures of PAHs in biomass burning particulate matter from cashew nut roasting

Approximately 3 billion people world-wide are exposed to air pollution from biomass burning. Herein, particulate matter (PM) emitted from artisanal cashew nut roasting, an important economic activity worldwide, was investigated. This study focused on: i) chemical characterization of polycyclic aromatic hydrocarbons (PAHs) and oxygenated (oxy-) PAHs; ii) intracellular levels of reactive oxygen species (ROS); iii) genotoxic effects and time- and dose-dependent activation of DNA damage signaling, and iv) differential expression of genes involved in xenobiotic metabolism, inflammation, cell cycle arrest and DNA repair, using A549 lung cells. Among the PAHs, chrysene, benzo[a]pyrene (B[a]P), benzo[b]fluoranthene, and benz[a]anthracene showed the highest concentrations (7.8–10 ng/m3), while benzanthrone and 9,10-anthraquinone were the most abundant oxy-PAHs. Testing of PM extracts was based on B[a]P equivalent doses (B[a]Peq). IC50 values for viability were 5.7 and 3.0 nM B[a]Peq at 24 h and 48 h, respectively. At these low doses, we observed a time- and dose-dependent increase in intracellular levels of ROS, genotoxicity (DNA strand breaks) and DNA damage signaling (phosphorylation of the protein checkpoint kinase 1 – Chk1). In comparison, effects of B[a]P alone was observed at micromolar range. To our knowledge, no previous study has demonstrated an activation of pChk1, a biomarker used to estimate the carcinogenic potency of PAHs in vitro, in lung cells exposed to cashew nut roasting extracts. Sustained induction of expression of several important stress response mediators of xenobiotic metabolism (CYP1A1, CYP1B1), ROS and pro-inflammatory response (IL-8, TNF-α, IL-2, COX2), and DNA damage response (CDKN1A and DDB2) was also identified. In conclusion, our data show high potency of cashew nut roasting PM to induce cellular stress including genotoxicity, and more potently when compared to B[a]P alone. Our study provides new data that will help elucidate the toxic effects of low-levels of PAH mixtures from air PM generated by cashew nut roasting.

Comparative mechanisms of PAH toxicity by benzo[a]pyrene and dibenzo[def,p]chrysene in primary human bronchial epithelial cells cultured at air-liquid interface

Current assumption for assessing carcinogenic risk of polycyclic aromatic hydrocarbons (PAHs) is that they function through a common mechanism of action; however, recent studies demonstrate that PAHs can act through unique mechanisms potentially contributing to cancer outcomes in a non-additive manner. Using a primary human 3D bronchial epithelial culture (HBEC) model, we assessed potential differences in mechanism of toxicity for two PAHs, benzo[a]pyrene (BAP) and dibenzo[def,p]chrysene (DBC), compared to a complex PAH mixture based on short-term biosignatures identified from transcriptional profiling. Differentiated bronchial epithelial cells were treated with BAP (100–500 μg/ml), DBC (10 μg/ml), and coal tar extract (CTE 500–1500 μg/ml, SRM1597a) for 48 h and gene expression was measured by RNA sequencing or quantitative PCR. Comparison of BAP and DBC gene signatures showed that the majority of genes (~60%) were uniquely regulated by treatment, including signaling pathways for inflammation and DNA damage by DBC and processes for cell cycle, hypoxia and oxidative stress by BAP. Specifically, BAP upregulated targets of AhR, NRF2, and KLF4, while DBC downregulated these same targets, suggesting a chemical-specific pattern in transcriptional regulation involved in antioxidant response, potentially contributing to differences in PAH potency. Other processes were regulated in common by all PAH treatments, BAP, DBC and CTE, including downregulation of genes involved in cell adhesion and reduced functional measurements of barrier integrity. This work supports prior in vivo studies and demonstrates the utility of profiling short-term biosignatures in an organotypic 3D model to identify mechanisms linked to carcinogenic risk of PAHs in humans.

Assessing Cancer Risk Associated with Aquatic Polycyclic Aromatic Hydrocarbon Pollution Reveals Dietary Routes of Exposure and Vulnerable Populations.

Polycyclic aromatic hydrocarbon (PAH) exposure is widespread, and many PAHs are considered carcinogenic. The PAH-contaminated AWI Superfund site in Virginia provides a model for studying a complex PAH mixture and its extrapolation to cancer risk and PAH exposure in the general population. We examined cancer risk at the Superfund site due to sediment-derived PAHs and then evaluated PAH sources in the general population and potentially vulnerable subpopulations upon PAH mixture exposure. The PAH mixture was assessed for potential carcinogenicity using the US EPA's OncoLogic™ ranking tool and the US EPA list of priority PAHs. Cancer risk due to PAH exposure was calculated for Superfund site users and compared to the US EPA assessment. Human intake and health endpoints of PAHs within the mixture were extracted from USEtox® chemical fate database, while mean intake exposure was calculated for U.S. adults for select PAHs using NHANES database urinary biomarkers. Eleven PAH compounds within the mixture were of carcinogenic concern, and seven PAHs conveyed significant excess cancer risk at the Superfund site and in the general population, wherein PAH-contaminated seafood ingestion was a main contributor. Other dietary sources of PAHs derived from PAH-contaminated soil or water could also play a role in total exposure. Vulnerable populations to PAH exposure and coinciding increased cancer risk may include, in addition to smokers, children and non-Hispanic blacks, which is a public health concern.

Immobilized Laccase Mediator-Catalyzed Oxidation of Aqueous Mixtures of Polycyclic Aromatic Hydrocarbons

ABSTRACTAlthough terrestrial and aquatic environments are polluted with mixtures of polycyclic aromatic hydrocarbons (PAHs), much of the research efforts toward bioremediation of these toxic, mutagenic and/or carcinogenic pollutants have focused on individual compounds. The potential of laccase (E.C. 1.10.3.2) from Trametes versicolor immobilized on soil and kaolinite for in vitro oxidation of equimolar concentration of anthracene (AnT), benzo[a]pyrene (BaP), benz[a]anthracene (BaA) and pyrene (PyR) in sole, binary, ternary and quaternary substrate systems, in the presence of 2, 2-azino-bis (3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) and 1-hydroxybenzotriazole (HBT) as mediator compounds was investigated. Results indicated that HBT was a better mediator compared to ABTS due to favorable redox potential difference (ΔEo) between laccase-HBT and PAH couples. The amount of each PAH oxidized depends on the type and number of PAHs present in the mixture. Due to its low molecular weight and high Eo, AnT inhibited the oxidative transformation of the other PAHs, and appeared to be competing for the same active site of the enzyme with BaP. Except for AnT, the oxidation of all the PAHs decreased with complexity of the mixture, with PyR oxidation inhibited by the presence of BaA. The oxidation of the PAHs was significantly low in the quaternary substrate system, probably due to enzyme inhibition from substrate overload. The results indicated that competitive effect may arise when more than one PAH is present in the reaction solution to interact with the enzyme and offer the possibility of the use of immobilized LMS for remediating complex PAH mixtures in the environment.

Pharmacokinetics of [14C]-Benzo[a]pyrene (BaP) in humans: Impact of Co-Administration of smoked salmon and BaP dietary restriction

Benzo[a]pyrene (BaP), a polycyclic aromatic hydrocarbon (PAH), is a known human carcinogen. In non-smoking adults greater than 95% of BaP exposure is through diet. The carcinogenicity of BaP is utilized by the U.S. EPA to assess relative potency of complex PAH mixtures. PAH relative potency factors (RPFs, BaP = 1) are determined from high dose animal data. We employed accelerator mass spectrometry (AMS) to determine pharmacokinetics of [14C]-BaP in humans following dosing with 46 ng (an order of magnitude lower than human dietary daily exposure and million-fold lower than animal cancer models). To assess the impact of co-administration of food with a complex PAH mixture, humans were dosed with 46 ng of [14C]-BaP with or without smoked salmon. Subjects were asked to avoid high BaP-containing diets and a 3-day dietary questionnaire given to assess dietary exposure prior to dosing and three days post-dosing with [14C]-BaP. Co-administration of smoked salmon, containing a complex mixture of PAHs with an RPF of 460 ng BaPeq, reduced and delayed absorption. Administration of canned commercial salmon, containing very low amounts of PAHs, showed the impacts on pharmacokinetics were not due to high amounts of PAHs but rather a food matrix effect.

Later life swimming performance and persistent heart damage following subteratogenic PAH mixture exposure in the Atlantic killifish (Fundulus heteroclitus).

High-level, acute exposures to individual polycyclic aromatic hydrocarbons (PAHs) and complex PAH mixtures result in cardiac abnormalities in developing fish embryos. Whereas acute PAH exposures can be developmentally lethal, little is known about the later life consequences of early life, lower level PAH exposures in survivors. A population of PAH-adapted Fundulus heteroclitus from the PAH-contaminated Superfund site, Atlantic Wood Industries, Elizabeth River, Portsmouth, Virginia, United States, is highly resistant to acute PAH cardiac teratogenicity. We sought to determine and characterize long-term swimming performance and cardiac histological alterations of a subteratogenic PAH mixture exposure in both reference killifish and PAH-adapted Atlantic Wood killifish embryos. Killifish from a relatively uncontaminated reference site, King's Creek, Virginia, United States, and Atlantic Wood killifish were treated with dilutions of Elizabeth River sediment extract at 24 h post fertilization (hpf). Two proven subteratogenic dilutions, 0.1 and 1.0% Elizabeth River sediment extract (total PAH 5.04 and 50.4 µg/L, respectively), were used for embryo exposures. Then, at 5-mo post hatching, killifish were subjected to a swim performance test. A separate subset of these individuals was processed for cardiac histological analysis. Unexposed King's Creek killifish significantly outperformed the unexposed Atlantic Wood killifish in swimming performance as measured by Ucrit (i.e., critical swimming speed). However, King's Creek killifish exposed to Elizabeth River sediment extract (both 0.1 and 1.0%) showed significant declines in Ucrit. Histological analysis revealed the presence of blood in the pericardium of King's Creek killifish. Although Atlantic Wood killifish showed baseline performance deficits relative to King's Creek killifish, their pericardial cavities were nearly free of blood and atrial and ventricular alterations. These findings may explain, in part, the diminished swimming performance of King's Creek fish. Environ Toxicol Chem 2017;36:3246-3253. © 2017 SETAC.

Early life co-exposures to a real-world PAH mixture and hypoxia result in later life and next generation consequences in medaka (Oryzias latipes)

Acute effects of individual and complex mixtures of polycyclic aromatic hydrocarbons (PAHs) are well documented in vertebrate species. Hypoxia in fish reduces metabolic rate and reproduction. However, less is known about the later life consequences stemming from early-life exposure to PAHs or hypoxia, particularly their co-exposure. To address this, medaka (Oryzias latipes) embryos were exposed to a complex PAH mixture sediment extract from the Elizabeth River, VA (ERSE) at concentrations of 0.1, 0.5, or 1.0% or to one of three different hypoxia scenarios: continuous, nocturnal, or late stage embryogenesis hypoxia. Co-exposures with 0.1% ERSE and each of the hypoxia scenarios were conducted. Results included decreased survival with ERSE, hatching delays with hypoxia, and higher occurrences of deformities with each. The continuous hypoxia scenario caused the most significant changes in all endpoints. These early-life exposures altered later-life growth, impaired reproductive capacity, and reduced the quality of their offspring. ERSE alone resulted in a female-biased sex ratio while continuous or nocturnal hypoxia produced significantly greater numbers of males; and co-exposure produced an equal sex ratio. Exposure to a PAH mixture and hypoxia during early life stages has meaningful later-life and next generational consequences.

Resistance to polycyclic aromatic hydrocarbon toxicity and associated bioenergetic consequences in a population of Fundulus heteroclitus.

Several locations in the Elizabeth River, VA, USA are highly contaminated with polycyclic aromatic hydrocarbons (PAHs) due to the release of creosote mixtures from wood treatment facilities. Interestingly, some populations of Atlantic killifish (Fundulus heteroclitus) inhabiting the Elizabeth River (ER) are resistant to PAH-induced teratogenesis. However, evolutionary resistance to PAHs due to chronic PAH exposure is associated with reduced fitness and increased susceptibility to other environmental stressors in at least one PAH-resistant ER killifish population. More specifically, wild-caught and first generation PAH-resistant juvenile killifish have altered metabolic demands when compared to non-resistant fish. Herein, we investigated this association further by examining a previously under-studied population captured from the creosote-contaminated site Republic Creosoting (Rep). We assessed PAH toxicity and effects on energy metabolism in Rep killifish in comparison with killifish from the reference site Kings Creek (KC). Following exposures to simple and complex PAH mixtures, Rep killifish exhibited several phenotypes associated with PAH resistance including decreased incidences of developmental cardiovascular deformities and recalcitrant cytochrome P450 1A (CYP1A) activity. We evaluated bioenergetics in killifish embryos throughout development and found elevated basal oxygen consumption rates in Rep embryos relative to KC embryos. Furthermore, juvenile F1 Rep fish had significantly lower maximal metabolic rates and aerobic scopes than KC juveniles. These results suggest that populations of killifish that have adapted or evolved to withstand the toxicity associated with PAHs consequently have altered energetic metabolism or demands. Such consequences could result in an enhanced vulnerability to other environmental and anthropogenic stressors in PAH-resistant killifish.

A framework for the use of single-chemical transcriptomics data in predicting the hazards associated with complex mixtures of polycyclic aromatic hydrocarbons

The assumption of additivity applied in the risk assessment of environmental mixtures containing carcinogenic polycyclic aromatic hydrocarbons (PAHs) was investigated using transcriptomics. MutaTMMouse were gavaged for 28 days with three doses of eight individual PAHs, two defined mixtures of PAHs, or coal tar, an environmentally ubiquitous complex mixture of PAHs. Microarrays were used to identify differentially expressed genes (DEGs) in lung tissue collected 3 days post-exposure. Cancer-related pathways perturbed by the individual or mixtures of PAHs were identified, and dose–response modeling of the DEGs was conducted to calculate gene/pathway benchmark doses (BMDs). Individual PAH-induced pathway perturbations (the median gene expression changes for all genes in a pathway relative to controls) and pathway BMDs were applied to models of additivity [i.e., concentration addition (CA), generalized concentration addition (GCA), and independent action (IA)] to generate predicted pathway-specific dose–response curves for each PAH mixture. The predicted and observed pathway dose–response curves were compared to assess the sensitivity of different additivity models. Transcriptomics-based additivity calculation showed that IA accurately predicted the pathway perturbations induced by all mixtures of PAHs. CA did not support the additivity assumption for the defined mixtures; however, GCA improved the CA predictions. Moreover, pathway BMDs derived for coal tar were comparable to BMDs derived from previously published coal tar-induced mouse lung tumor incidence data. These results suggest that in the absence of tumor incidence data, individual chemical-induced transcriptomics changes associated with cancer can be used to investigate the assumption of additivity and to predict the carcinogenic potential of a mixture.

Bioavailability of polycyclic aromatic hydrocarbons (PAHs) and Environmental Risk (ER) Assessment: The case of the Ogbese river, Nigeria

Pollution from PAHs in porewater and surficial sediments of the rapidly contaminated Ogbese River, Ondo State, Nigeria was investigated. Samples were extracted using Hexane/methylene chloride mixture and the complex PAH mixtures were analyzed by gas chromatography-mass spectrometry. There was greater influence of sediment fine particles (R2=0.978) in partitioning of PAHs over other factors. Total concentration of PAHs in the sediments and porewater ranged 14.45 μg g−1 to 26.78 μg g−1 (n=8, dry weight) and 6.25 μg L−1 to 13.93 μg L−1 (n=8) respectively. The measured partition coefficients (i.e., Koc values) of the individual PAHs between sediment organic matter (SOM) and porewater across all locations ranged from 5.027 (±0.157 SD) to 5.074 (±0.169 SD). The correlation in log Koc (observed vs predicted) for high molecular weight/low molecular weight-PAHs suggests variability in specific interactions and unequal partition efficiencies with SOM under natural condition. Based on equilibrium partitioning and narcosis model, three PAHs {benzo(b)fluoranthene, benzo(a)pyrene and dibenz(a,h)anthracene }has toxic unit (TU) values of concern. These results represent a baseline report for future monitoring programs of PAHs.

Seasonal variations and source apportionment of complex polycyclic aromatic hydrocarbon mixtures in particulate matter in an electronic waste and urban area in South China

Complex polycyclic aromatic hydrocarbon (PAH) mixtures including parent PAHs, high molecular weight PAHs (MW 302 PAHs), and halogenated PAHs (HPAHs) were measured in particulate matter (PM) in an urban area and a rural electronic waste area in South China. The concentrations of MW < 302 PAHs at two sites were not significantly different with annual means of 23.2 ± 17.2 and 33.7 ± 29.0 ng/m3, respectively. However the concentrations of both MW 302 PAHs (5.35 ± 3.72 ng/m3) and HPAH (49.9 pg/m3) were significantly higher at the e-waste site than the urban site (2.81 ± 2.36 ng/m3 and 28.2 ± 28.5 pg/m3), suggesting e-waste recycling being a significant source of these PAHs. The majority of PAHs exhibited higher concentrations in winter and spring and lower concentrations in fall and summer. Meteorological conditions and increased emissions of PAHs in northern China due to domestic heating in colder seasons are important factors influencing the PAH seasonal variations. Source apportionment by the chemical mass balance (CMB) model indicated that residential stoves (coal combustion), industrial boilers (coal combustion), biomass burning, and vehicular emission accounted for 38 ± 14%, 30 ± 11%, 22 ± 22%, and 10 ± 7% of the PAHs in the urban PM, respectively. Comparable contributions from these sources were also observed for PM at the e-waste site. PAH emission factors are needed for primitive e-waste recycling to further understand the importance of this source to ambient air.

Identification and quantification of seven fused aromatic rings C26H14peri-condensed benzenoid polycyclic aromatic hydrocarbons in a complex mixture of polycyclic aromatic hydrocarbons from coal tar

A methodology for the characterization of groups of polycyclic aromatic hydrocarbons (PAHs) using a combination of normal phase liquid chromatography with ultraviolet–visible spectroscopy (NPLC/UV–vis) and gas chromatography with mass spectrometry (GC/MS) was used for the identification and quantification of seven fused aromatic rings C26H14peri-condensed benzenoid polycyclic aromatic hydrocarbons, PAHs, in standard reference material (SRM) 1597a, complex mixture of PAHs from coal tar. The NPLC/UV–vis isolated the fractions based on the number of aromatic carbons and the GC/MS allowed the identification and quantification of five of the nine C26H14 PAH isomers; naphtho[1,2,3,4-ghi]perylene, dibenzo[b,ghi]perylene, dibenzo[b,pqr]perylene, naphtho[8,1,2-bcd]perylene, and dibenzo[cd,lm]perylene using a retention time comparison with authentic reference standards. For the other four benzenoid isomers with no available reference standards the following two approaches were used. First, the annellation theory was used to achieve the potential identification of benzo[qr]naphtho[3,2,1,8-defg]chrysene, and second, the elution distribution in the GC fractions was used to support the potential identification of benzo[qr]naphtho[3,2,1,8-defg]chrysene and to reach the tentative identifications of dibenzo[a,ghi]perylene, naphtho[7,8,1,2,3-pqrst]pentaphene, and anthra[2,1,9,8-opqra]naphthacene. It is the first time that naphtho[1,2,3,4-ghi]perylene, dibenzo[b,ghi]perylene, dibenzo[b,pqr]perylene, naphtho[8,1,2-bcd]perylene, and dibenzo[cd,lm]perylene are quantified, and the first time that benzo[qr]naphtho[3,2,1,8-defg]chrysene is potentially identified, in any sample, in any context.

Developmental exposure to a complex PAH mixture causes persistent behavioral effects in naive Fundulus heteroclitus (killifish) but not in a population of PAH-adapted killifish

Acute exposures to some individual polycyclic aromatic hydrocarbons (PAHs) and complex PAH mixtures are known to cause cardiac malformations and edema in the developing fish embryo. However, the heart is not the only organ impacted by developmental PAH exposure. The developing brain is also affected, resulting in lasting behavioral dysfunction. While acute exposures to some PAHs are teratogenically lethal in fish, little is known about the later life consequences of early life, lower dose subteratogenic PAH exposures. We sought to determine and characterize the long-term behavioral consequences of subteratogenic developmental PAH mixture exposure in both naive killifish and PAH-adapted killifish using sediment pore water derived from the Atlantic Wood Industries Superfund Site. Killifish offspring were embryonically treated with two low-level PAH mixture dilutions of Elizabeth River sediment extract (ERSE) (TPAH 5.04μg/L and 50.4μg/L) at 24h post fertilization. Following exposure, killifish were raised to larval, juvenile, and adult life stages and subjected to a series of behavioral tests including: a locomotor activity test (4days post-hatch), a sensorimotor response tap/habituation test (3months post hatch), and a novel tank diving and exploration test (3months post hatch). Killifish were also monitored for survival at 1, 2, and 5months over 5-month rearing period. Developmental PAH exposure caused short-term as well as persistent behavioral impairments in naive killifish. In contrast, the PAH-adapted killifish did not show behavioral alterations following PAH exposure. PAH mixture exposure caused increased mortality in reference killifish over time; yet, the PAH-adapted killifish, while demonstrating long-term rearing mortality, had no significant changes in mortality associated with ERSE exposure. This study demonstrated that early embryonic exposure to PAH-contaminated sediment pore water caused long-term locomotor and behavioral alterations in killifish, and that locomotor alterations could be observed in early larval stages. Additionally, our study highlights the resistance to behavioral alterations caused by low-level PAH mixture exposure in the adapted killifish population. Furthermore, this is the first longitudinal behavioral study to use killifish, an environmentally important estuarine teleost fish, and this testing framework can be used for future contaminant assessment.

Polycyclic Aromatic Hydrocarbon Degradation and Sorption Parameters in Coastal and Open-Sea Sediment

This work describes the experimental deter- mination of the major degradation and sorption param- eters of polycyclic aromatic hydrocarbons (PAHs) in a sensitivemarineenvironment,theNorthernAdriaticSea (Mediterranean Sea). The persistence and sorption of complex PAH mixtures were analysed in the laboratory in conditions mimicking open-sea and coastal sedi- ments, which differ in grain size and organic carbon content and are characterized by different oceanograph- ic conditions including abiotic influences. The study investigated how sediment type and texture and salinity, temperature and solar irradiation conditions affect the partitioning of low molecular weight (LMW) and high molecular weight (HMW) PAHs into aqueous and solid phase, which critically influence their behaviour. With regard tothe changefromoffshoreto coastal conditions, HMW PAHs were found to be more sensitive to the increased salinity (from 21 to <37 parts per thousand), whereas LMW PHAs were more sensitive to the tem- perature increase (from 11 to 22 °C). HMW PAHs were more affected by sediment type changes in terms of distribution coefficient (Kd). Since the physicochemical properties of organic pollutants affect their distribution, transport, bioavailability and toxicity, analysing the ac- cumulation and persistence of dissolved pollutants can provide useful information for environmental risk as- sessment and management.