Soil PAHs contamination effect on the cellular and subcellular organelle changes of Phragmites australis Cav.

The concentrations of ∑16 priority polycyclic aromatic hydrocarbons (PAHs) for soils, roots, and above-ground parts of reed (Phragmites australis Cav.) were determined on different monitoring plots located near the city of Kamensk-Shakhtinsky, southern Russia, where historically received industrial sewage and sludge. The total PAHs concentration in monitoring soil plots was significantly higher than those in the background site which situated at the distance of 2 km from the contamination source. Accordingly, the maximum accumulation was found for phenanthrene and chrysene among the 16 priority PAHs in most of the plant samples collected in the impact zone. The effects of PAHs' pollution on changes of Phragmites australis Cav. cellular and subcellular organelles in the studied monitoring sites were also determined using optical and electron microscopy, respectively. The obtained data showed that increasing of PAHs contamination negatively affected the ultrastructural changes of the studied plants. Phragmites australis Cav. showed a high level of adaptation to the effect of stressors by using tissue and cell levels. In general, the detected alterations under the PAHs effect were possibly connected to changes in biochemical and histochemical parameters as a response for reactive oxygen species and as a protective response against oxidative stress. The obtained results introduce innovative findings of cellular and subcellular changes in plants exposed to ∑16 priority PAHs as very persistent and toxic contaminants.

The Role of Metabolism in Toxicity of Polycyclic Aromatic Hydrocarbons and their Non-genotoxic Modes of Action.

Polycyclic aromatic hydrocarbons (PAHs) represent a class of widely distributed environmental pollutants that have been primarily studied as genotoxic compounds. Their mutagenicity/genotoxicity largely depends on their oxidative metabolism leading to the production of dihydrodiol epoxide metabolites, as well as additional metabolites contributing to oxidative DNA damage, such as PAH quinones. However, both parental PAHs and their metabolites, including PAH quinones or hydroxylated PAHs, have been shown to produce various types of non-genotoxic effects. These include e.g., activation of the aryl hydrocarbon receptor and/or additional nuclear receptors, activation of membrane receptors, including tyrosine kinases and G-protein coupled receptors, or activation of intracellular signaling pathways, such as mitogen-activated protein kinases, Akt kinase and Ca2+-dependent signaling. These pathways may, together with the cellular DNA damage responses, modulate cell proliferation, cell survival or cell-to-cell communication, thus contributing to the known carcinogenic effects of PAHs. In the present review, we summarize some of the known non-genotoxic effects of PAHs, focusing primarily on those that have also been shown to be modulated by PAH metabolites. Despite the limitations of the available data, it seems evident that more attention should be paid to the discrimination between the potential non-genotoxic effects of parental PAHs and those of their metabolites. This may provide further insight into the mechanisms of toxicity of this large and diverse group of environmental pollutants.

Cell-by-cell estimation of PAH sorption and subsequent toxicity in marine phytoplankton.

Polycyclic Aromatic Hydrocarbons (PAHs) have elicited increasing concern due to their ubiquitous occurrence in coastal marine environments and resultant toxicity in organisms. Due to their lipophilic nature, PAHs tend to accumulate in phytoplankton cells and thus subsequently transfer to other compartments of the marine ecosystem. The intrinsic fluorescence properties of PAHs in the ultraviolet (UV)/blue spectral range have recently been exploited to investigate their uptake modes, localization, and aggregation in various biological tissues. Here, we quantitatively evaluate the sorption of two model PAHs (phenanthrene and pyrene) in three marine phytoplankton species (Chaetoceros tenuissimus, Thalassiosira sp. and Proteomonas sp.) using a combined approach of UV excitation flow cytometry and fluorescence microscopy. Over a 48-h exposure to a gradient of PAHs, Thalassiosira sp. showed the highest proportion of PAH-sorbed cells (29% and 97% of total abundance for phenanthrene and pyrene, respectively), which may be attributed to its relatively high total lipid content (33.87 percent dry weight). Moreover, cell-specific pulse amplitude modulation (PAM) microscope fluorometry revealed that PAH sorption significantly reduced the photosynthetic quantum efficiency (Fv/Fm) of individual phytoplankton cells. We describe a rapid and precise hybrid method for the detection of sorption of PAHs on phytoplankton cells. Our results emphasize the ecologically relevant sub-lethal effects of PAHs in phytoplankton at the cellular level, even at concentrations where no growth inhibition was apparent. This work is the first study to address the cell-specific impacts of fluorescent toxicants in a more relevant toxicant-sorbed subpopulation; these cell-specific impacts have to date been unidentified in traditional population-based phytoplankton toxicity assays.

Comparative toxicity analysis of corannulene and benzo[a]pyrene in mice.

Increasing production of corannulene (COR), a non-planar polycyclic aromatic hydrocarbon (PAH) with promising applications in many fields, has raised a concern about its potential toxic effects. However, no study has been undertaken to evaluate its metabolism and toxicity in mammals. In this study, the acute toxicities of COR in mice were compared with benzo[apyrene (BaP), a typical planar PAH with almost the same molecular weight. After 3-day exposures, the concentrations of COR in both plasma and tissues of mice were higher than that of BaP. However, blood chemistry and tissue weight monitoring showed no observable toxicities in COR-exposed mice. Compared to BaP, exposure to COR resulted in less activation of the aryl hydrocarbon receptor (AhR) and thus less induction of hepatic cytochrome P450 1A(CYP1A) enzymes, which play a critical role in metabolism of both COR and BaP. Additionally, COR also elicited less oxidative stress and microbiota alteration in the intestine than did BaP. RNA-seq analysis revealed that liver transcriptomes are responsive to COR and BaP, with less alterations observed in COR-exposed mice. Unlike BaP, exposure to COR had no effects on hepatic lipid and xenobiotic metabolism pathways. Nonetheless, COR appeared to alter the mRNA expressions of genes involved in carcinogenicity, oxidative stress, and immune-suppression. To conclude, this study for the first time unveils a comparative understanding of the acute toxic effects of COR to BaP in mice, and provides crucial insights into the future safety assessment of COR.

Polycyclic aromatic hydrocarbons and development of respiratory and cardiovascular diseases in workers.

OBJECTIVES: to identify the scientific evidence on the development of cardiovascular and respiratory diseases due to workplace contamination by polycyclic aromatic hydrocarbons. METHODS: integrative literature review. The search for primary articles was held in October 2017 in the Medical Literature Analysis and Retrieval System Online (through Pubmed), Web of Science and Latin American and Caribbean Literature in Health Sciences (LILACS). RESULTS: the 16 studies analyzed showed that exposure to polycyclic aromatic hydrocarbons was associated with cardiovascular diseases, such as increased blood pressure, heart rate variation, and ischemic heart disease; and respiratory disorders, such as decreased lung function, chronic obstructive pulmonary disease, asthma, wheeze, coughing, pulmonary wheezing, chest tightness, effort dyspnea, and sore throat. CONCLUSIONS: polycyclic aromatic hydrocarbons cause deleterious effects on the cardiovascular and respiratory systems through mutations and cellular inflammation, being a risk to exposed individuals.

Risk assessment implications of site-specific oral relative bioavailability factors and dermal absorption fractions for polycyclic aromatic hydrocarbons in surface soils impacted by clay skeet target fragments.

Risk assessment conclusions for a site may differ when using site-specific versus default values for the relative bioavailability factor (RBAF) and dermal absorption fraction (ABS.d), because these inputs affect both surface soil screening levels and risk/hazard estimates. Indeed, our case study demonstrates that different conclusions may be reached as to regulatory need for remedial action to protect human health when evaluating soil sampling data for seven carcinogenic polycyclic aromatic hydrocarbons (PAHs) using site-specific versus default TCEQ and USEPA residential soil screening levels. Use of site-specific RBAF and ABS.d values increased carcinogenicity-based TCEQ and USEPA surface soil screening levels for PAHs by 4.4- and 6-fold on average, respectively. Soil screening levels for PAHs were more sensitive to changes in ingestion exposure route parameters than to changes in dermal exposure route parameters. Accordingly, site-specific RBAF and ABS.d information has important implications for screening chemicals at PAH-impacted sites, and in addition provides more realistic estimates of risks/hazards posed by PAHs in soil with reduced uncertainty compared to estimates based on default RBAF and ABS.d values. Although default values are generally deemed acceptable by regulatory agencies, use of risk/hazard estimates based on these default values may compel insufficiently justified remedial action in some instances.

Derivation of site-specific remediation goals by incorporating the bioaccessibility of polycyclic aromatic hydrocarbons with the probabilistic analysis method.

Incorporating bioaccessibility into human health risk assessment is recognized as a valid way to reduce the conservative properties of conventional results, where the total concentration of a contaminant analysed by exhaustive chemical extraction is applied. Taking a coke production site in Beijing as an example, a mild chemical extraction technology was employed to profile the bioaccessibility of benzo[a]pyrene (BaP), indeno[1,2,3-cd]pyrene (IcP) and dibenz[ah]anthracene (DBA) in soils. The results that were regressed using two bi-phase desorption models (Karickhoff and Weibull) revealed that the rapid desorption fractions of BaP, IcP and DBA, which are taken for bioaccessible fractions, were basically less than half of the total contents in the soils. Probabilistic analysis (PA) was carried out with pre-set distributions of the exposure parameters to characterize the uncertainty in the assessment. The results incorporating bioaccessibility and PA were several times higher than the generic remediation goals which equal to national screening levels, and orders of magnitude higher than the baselines of the region and nation. The results of the Weibull fit were finally recommended as site-specific remediation goals (SSRGs) (10.59 mg/kg, 95.48 mg/kg and 9.24 mg/kg). Over-remediation was avoided while contributing to considerable economic and environmental benefits.

Polycyclic aromatic hydrocarbons (PAHs) in corals of the South China Sea: Occurrence, distribution, bioaccumulation, and considerable role of coral mucus.

Coral reefs have suffered degradation from climate change and water quality deterioration. Studies have shown that PAHs are present widely in some coastal seawater and coral tissues. However, no studies have focused on the PAHs in coastal coral mucus and offshore coral tissues. Targeting the South China Sea, this study for the first time investigated the occurrence, tissue-mucus partitioning, and bioaccumulation of PAHs in coastal and offshore corals. The tissue and mucus of the corals were processed separately. The results indicated that the total concentration of 15 of the 16 PAHs that are prioritized by U.S. EPA (excluding naphthalene) (∑15PAHs) was significantly higher in the coastal tissues (173 ±â€¯314 ng g-1 dw) than in the offshore tissues (71 ±â€¯109 ng g-1 dw), as well as in coastal seawater (196 ±â€¯96 ng L-1) than in the offshore water (54 ±â€¯9 ng L-1). ∑15PAHs is two orders of magnitude higher in the mucus (3200 ±â€¯6470 ng g-1 dw) than in the tissues (128 ±â€¯43 ng g-1 dw). By average, 29% of ∑15PAHs were accumulated in the mucus. The results suggest that mucus plays an important role in the bioaccumulation of PAHs by corals from ambient seawater.

Variability in fish bioconcentration factors: Influences of study design and consequences for regulation.

The fish bioconcentration factor (BCF) is an important aspect within bioaccumulation assessments. Several factors have been suggested to influence BCF values - including species, developmental stage, mixture exposure, and calculation method. However, their exact contribution to variance in BCF values is unknown. Within this study we assessed the relative impact of these test characteristics on BCF values and analyzed the reproducibility of aquatic exposure bioconcentration tests. Linear mixed effects analyses were performed on a newly develop database to investigate the relationship between the response variable (i.e. lipid normalized log BCF values) and several test characteristics as fixed effects. Lower BCF values were observed for substances that were simultaneously applied with high molecular weight polycyclic aromatic hydrocarbons compared to single substance exposure (with an average difference of -0.81 log BCF). Also, lower BCFs upon kinetic determination were observed compared to steady-state BCFs (log BCF -0.27), and lower BCFs for species from the Ostariophysi subcohort level (log BCF -0.17 to -0.15). In addition, data analysis showed high variation within BCF values for single substances (average SD = log BCF 0.21), which questions the robustness of the current bioaccumulation assessments. For example, the 95% confidence range of a BCF value of 2500 ranges from 953 ('not-bioaccumulative') to 6561 ('very bioaccumulative'). Our results show that the use of one single BCF leads to a high uncertainty in bioaccumulation assessments. We strongly recommend that within future bioconcentration studies, the used experimental design and test conditions are described in detail and justified to support solid interpretation.

Metabolism and genotoxicity of polycyclic aromatic hydrocarbons in human skin explants: mixture effects and modulation by sunlight.

Cutaneous exposure to carcinogenic polycyclic aromatic hydrocarbons (PAH) occurs frequently in the industrialized workplace. In the present study, we addressed this topic in a series of experiments using human skin explants and organic extracts of relevant industrial products. PAH mixtures were applied topically in volumes containing either 10 or 1 nmol B[a]P. We first observed that although mixtures were very efficient at inducing expression of CYP450 1A1, 1A2, and 1B1, formation of adducts of PAH metabolites to DNA, like those of benzo[a]pyrene diol epoxide (BPDE), was drastically reduced as the complexity of the surrounding matrix increased. Interestingly, observation of a nonlinear, dose-dependent response with the least complex mixture suggested the existence of a threshold for this inhibitory effect. We then investigated the impact of simulated sunlight (SSL) on the effects of PAH in skin. SSL was found to decrease the expression of CYP450 genes when applied either after or more efficiently before PAH treatment. Accordingly, the level of DNA-BPDE adducts was reduced in skin samples exposed to both PAH and SSL. The main conclusion of our work is that both increasing chemical complexity of the mixtures and co-exposure to UV radiation decreased the production of adducts between DNA and PAH metabolites. Such results must be taken into account in risk management.

Polycyclic aromatic hydrocarbons and development of respiratory and cardiovascular diseases in workers / Hidrocarburos policíclicos aromáticos y desarrollo de enfermedades respiratorias y cardiovasculares en trabajadores / Hidrocarbonetos policíclicos aromáticos e desenvolvimento de doenças respiratórias e cardiovasculares em trabalhadores

ABSTRACT Objectives: to identify the scientific evidence on the development of cardiovascular and respiratory diseases due to workplace contamination by polycyclic aromatic hydrocarbons. Methods: integrative literature review. The search for primary articles was held in October 2017 in the Medical Literature Analysis and Retrieval System Online (through Pubmed), Web of Science and Latin American and Caribbean Literature in Health Sciences (LILACS). Results: the 16 studies analyzed showed that exposure to polycyclic aromatic hydrocarbons was associated with cardiovascular diseases, such as increased blood pressure, heart rate variation, and ischemic heart disease; and respiratory disorders, such as decreased lung function, chronic obstructive pulmonary disease, asthma, wheeze, coughing, pulmonary wheezing, chest tightness, effort dyspnea, and sore throat. Conclusions: polycyclic aromatic hydrocarbons cause deleterious effects on the cardiovascular and respiratory systems through mutations and cellular inflammation, being a risk to exposed individuals.

RESUMEN Objetivos: identificar las evidencias científicas sobre el desarrollo de enfermedades cardiovasculares y respiratorias debido a la contaminación en el ambiente de trabajo por hidrocarburos policíclicos aromáticos. Métodos: revisión integrativa de la literatura. La búsqueda de los artículos primarios se realizó en octubre de 2017 en: Medical Literature Analysis and Retrieval System Online (vía PubMed), Web of Science y Literatura Latinoamericana y del Caribe en Ciencias de la Salud. Resultados: los 16 estudios analizados mostraron que la exposición a los hidrocarburos policíclicos aromáticos estuvo asociada a las enfermedades cardiovasculares, como aumento de la presión arterial, variación de la frecuencia cardíaca y enfermedad cardiaca isquémica; y a la respiración, como disminución de la función pulmonar, enfermedad pulmonar obstructiva crónica, asma, silbido, tos, sibilancia pulmonar, opresión en el pecho, disnea al esfuerzo y dolor de garganta. Conclusiones: los hidrocarburos policíclicos aromáticos causan efecto deletéreo en el sistema cardiovascular y respiratorio por medio de mutaciones e inflamaciones celulares, siendo un riesgo al individuo expuesto.

RESUMO Objetivos: identificar as evidências científicas sobre o desenvolvimento de doenças cardiovasculares e respiratórias devido à contaminação no ambiente de trabalho por hidrocarbonetos policíclicos aromáticos. Métodos: revisão integrativa da literatura. A busca dos artigos primários foi realizada em outubro de 2017 na Medical Literature Analysis and Retrieval System Online (via Pubmed), Web of Science e Literatura Latino-Americana e do Caribe em Ciências da Saúde. Resultados: os 16 estudos analisados mostraram que a exposição aos hidrocarbonetos policíclicos aromáticos esteve associada a doenças cardiovasculares como aumento da pressão arterial, variação da frequência cardíaca e doença cardíaca isquêmica; e respiratórias como diminuição da função pulmonar, doença pulmonar obstrutiva crônica, asma, chiado, tosse, sibilância pulmonar, opressão no peito, dispneia ao esforço e dor de garganta. Conclusões: os hidrocarbonetos policíclicos aromáticos causam efeito deletério no sistema cardiovascular e respiratório por meio de mutações e de inflamações celulares, sendo um risco ao indivíduo exposto.

Influence of exposure dose, complex mixture, and ultraviolet radiation on skin absorption and bioactivation of polycyclic aromatic hydrocarbons ex vivo.

Combined exposure to complex mixtures of polycyclic aromatic hydrocarbons (PAHs) and ultraviolet radiation (UVR) is suspected to enhance PAH skin permeability and skin cancer risk depending on PAH bioactivation. The impact of PAH mixtures (exposure dose, composition, and complexity) and UVR was assessed for PAH cutaneous absorption and metabolism using realistic exposure conditions and human skin explants. PAH complex mixtures were extracted from the industrial products coal tar pitch (CTP-I) and petroleum coke (PC-I). The synthetic mixture (CTP-S) was identically reconstituted using PAH standards. The applied dose was adjusted to 1 (PC-I, CTP-I) or 10 nmol (CTP-I, CTP-S) of benzo[a]pyrene (B[a]P). Unmetabolized PAHs were recovered from the skin surface, skin and medium, and then quantified by HPLC-fluorescence detection. PAH metabolites were collected from the medium and analyzed by GC-MS/MS. B[a]P and PAH penetration was lower for the highest B[a]P dose, industrial mixtures, and CTP-I compared to PC-I. Skin irradiation increased PAH penetration only for CTP-I. PAH uptake was poorly influenced by the different experimental conditions. PAH metabolism markedly decreased in the application of mixtures, leading to unmetabolized PAH accumulation in human skin. PAH metabolism was similar between CTP-I and PC-I, but was lower for the highest dose and the industrial mixtures, suggesting a saturation of xenobiotic metabolizing enzymes, as confirmed in a time-course study. UVR strongly inhibited all PAH metabolism. Altogether, these results underline the necessity to consider the reality of human exposure (PAH complex mixtures and UVR) during in vitro experiments to properly estimate skin absorption and metabolism.

Bioaccumulation of Polycyclic Aromatic Hydrocarbons for Forensic Assessment Using Gas Chromatography-Mass Spectrometry.

Polycyclic aromatic hydrocarbons (PAHs) are considered xenobiotics of a potentially carcinogenic nature, being accumulated in the fatty tissue of the body. The objective of this work was the development and validation of a new analytical method to check the bioaccumulation of these toxic compounds in human organs obtained from autopsies. The contaminants were first isolated from the tissues by salt-assisted liquid-liquid extraction in acetonitrile. Because of the low concentrations of these compounds in the human body, a dispersive liquid-liquid microextraction procedure was included. The preconcentrated samples were analyzed by gas chromatography-mass spectrometry to identify the compounds. Principal component analysis was applied to show the natural clustering of forensic samples and orthogonal partial least-squares discriminant analysis to develop a multivariate regression method, which permitted the classification of samples. The quantification limits for the 13 PAHs (acenaphthylene, fluorene, phenanthrene, anthracene, pyrene, benzo(a)anthracene, chrysene, benzo(b)fluoranthene, benzo(k)fluoranthene, benzo(a)pyrene, dibenz(a,h)anthracene, benzo(g,h,i)perylene, and indeno(1,2,3-cd)pyrene) analyzed were in the 0.06-0.44 ng g-1 range, depending on the compound, while the mean intraday relative standard deviation of about 7% demonstrated the high precision of the method. Linearity was verified in the 0.5-200 ng g-1 range, and the enrichment factors were between 55 and 122. The results provided by the analysis of seven different human organs (brain, liver, kidney, lung, heart, spleen, and abdominal fat) from eight autopsies confirmed the PAH-bioaccumulation capacity of human body, fat showing the highest degree of bioaccumulation. The present work is the first study on PAH contamination in different organs obtained from autopsies, being PAH detected in most human samples at values ranged from 0 to 19 ng g-1.

Arctic marine fish 'biotransformation toxicity' model for ecological risk assessment.

Oil and gas exploration and marine transport in the Arctic region have put the focus on the ecological risk of the possibly exposed organisms. In the present study, the impacts of sea ice, extreme light regime, various polar region-specific physiological characteristics in polar cod (Boreogadus saida) and their effects on xenobiotic distribution and metabolism are studied. A Bayesian belief network is used to model individual fish toxicity. The enzyme activity in the fish liver and other pertinent organs is used as a proxy for cellular damage and repair and is subsequently linked to toxicity in polar cod. Seasonal baseline variation in enzyme production is also taken into consideration. The model estimates the probability of exposure concentration to cause cytotoxicity and circumvents the need to use the traditionally obtained No Observed Effect Concentration (NOEC). Instead, it uses biotransformation enzyme activity as a basis to estimate the probability of individual cell damages.

Tissue distribution of organic contaminants in stranded pregnant sperm whale (Physeter microcephalus) from the Huizhou coast of the South China Sea.

Twelve persistent organic pollutants (POPs) were measured in 11 tissue samples from a pregnant sperm whale stranded on the Huizhou coast of the South China Sea, China, in March 2017. POPs were found to be more concentrated in the irrigated tissues such as placenta, ovary, mammary gland, and liver than the less irrigated tissues such as epidermis. High POP levels detected in the placenta might result in abnormal hormone secretion in the placenta, which would affect the unborn offspring. We hypothesized that ovary is potentially vulnerable to the exposure of higher contaminant levels. The PAH concentrations were higher in the lung than in other tissues, which suggest that PAH levels in the lung were breath-dependent in the sperm whale. The concentrations of POPs except PAHs in the sperm whale blubber were lower than those in the same species in the Northern Hemisphere and were comparable to or lower than those in the same species in the Southern Hemisphere.

Airport emission particles: exposure characterization and toxicity following intratracheal instillation in mice.

BACKGROUND: Little is known about the exposure levels and adverse health effects of occupational exposure to airplane emissions. Diesel exhaust particles are classified as carcinogenic to humans and jet engines produce potentially similar soot particles. Here, we evaluated the potential occupational exposure risk by analyzing particles from a non-commercial airfield and from the apron of a commercial airport. Toxicity of the collected particles was evaluated alongside NIST standard reference diesel exhaust particles (NIST2975) in terms of acute phase response, pulmonary inflammation, and genotoxicity after single intratracheal instillation in mice. RESULTS: Particle exposure levels were up to 1 mg/m3 at the non-commercial airfield. Particulate matter from the non-commercial airfield air consisted of primary and aggregated soot particles, whereas commercial airport sampling resulted in a more heterogeneous mixture of organic compounds including salt, pollen and soot, reflecting the complex occupational exposure at an apron. The particle contents of polycyclic aromatic hydrocarbons and metals were similar to the content in NIST2975. Mice were exposed to doses 6, 18 and 54 µg alongside carbon black (Printex 90) and NIST2975 and euthanized after 1, 28 or 90 days. Dose-dependent increases in total number of cells, neutrophils, and eosinophils in bronchoalveolar lavage fluid were observed on day 1 post-exposure for all particles. Lymphocytes were increased for all four particle types on 28 days post-exposure as well as for neutrophil influx for jet engine particles and carbon black nanoparticles. Increased Saa3 mRNA levels in lung tissue and increased SAA3 protein levels in plasma were observed on day 1 post-exposure. Increased levels of DNA strand breaks in bronchoalveolar lavage cells and liver tissue were observed for both particles, at single dose levels across doses and time points. CONCLUSIONS: Pulmonary exposure of mice to particles collected at two airports induced acute phase response, inflammation, and genotoxicity similar to standard diesel exhaust particles and carbon black nanoparticles, suggesting similar physicochemical properties and toxicity of jet engine particles and diesel exhaust particles. Given this resemblance as well as the dose-response relationship between diesel exhaust exposure and lung cancer, occupational exposure to jet engine emissions at the two airports should be minimized.

Identifying sediment-associated toxicity in rivers affected by multiple pollutants from the contaminant bioavailability.

In this study, we estimated the toxicity risks from river sediments that were affected by multiple pollutants in the Haihe River Basin. We used a range of methods to determine the concentrations, bioavailability, and toxicity of a range of metals and contaminants in sediments and sediment porewater and then assessed the ecological risks and toxicity using various multivariate statistical approaches. We found that more than 70% of the samples were toxic. The concentrations of non-ionic ammonia (0.168-9.295 mg L-1) were generally high in the sediment porewater, while the concentrations of bioavailable chromium (Cr) and polycyclic aromatic hydrocarbons (PAHs) were also high in the porewater samples from NW01 and NW02, respectively. We used the toxic unit (TU) approach, based on the bioavailable pollutant concentrations, to determine the toxicity of PAHs, heavy metals, and non-ionic ammonia in river sediments and sediment porewater. We found that non-ionic ammonia was the main source of toxicity for Daphnia magna, and that Cr and zinc were toxic for Pseudokirchneriella subcapitata and Chironomus dilutus. By combining various indexes, we identified the main contributors to the toxicity in sediments collected from rivers affected by multiple pollutants.

Beyond the obvious: Environmental health implications of polar polycyclic aromatic hydrocarbons.

The genotoxic, mutagenic and carcinogenic effects of polar polycyclic aromatic hydrocarbons (polar PAHs) are believed to surpass those of their parent PAHs; however, their environmental and human health implications have been largely unexplored. Oxygenated PAHs (oxy-PAHs) is a critical class of polar PAHs associated with carcinogenic effects without enzymatic activation. They also cause an upsurge in reactive oxygen species (ROS) in living cells. This results in oxidative stress and other consequences, such as abnormal gene expressions, altered protein activities, mutagenesis, and carcinogenesis. Similarly, some nitrated PAHs (N-PAHs) are probable human carcinogens as classified by the International Agency for Research on Cancer (IARC). Heterocyclic PAHs (polar PAHs containing nitrogen, sulphur and oxygen atoms within the aromatic rings) have been shown to be potent endocrine disruptors, primarily through their estrogenic activities. Despite the high toxicity and enhanced environmental mobility of many polar PAHs, they have attracted only a little attention in risk assessment of contaminated sites. This may lead to underestimation of potential risks, and remediation end points. In this review, the toxicity of polar PAHs and their associated mechanisms of action, including their role in mutagenic, carcinogenic, developmental and teratogenic effects are critically discussed. This review suggests that polar PAHs could have serious toxicological effects on human health and should be considered during risk assessment of PAH-contaminated sites. The implications of not doing so were argued and critical knowledge gaps and future research requirements discussed.

Efficient and stable radiolabeling of polycyclic aromatic hydrocarbon assemblies: in vivo imaging of diesel exhaust particulates in mice.

As a robust radioanalytical method for tracking carbonaceous particulates in vivo, polycyclic aromatic hydrocarbons from diesel exhaust were labeled with a radioactive-iodine-tagged pyrene analogue. Single-photon emission computed tomography and biodistribution studies showed high uptake and slow clearance of this matter in the respiratory system, which may underlie its severe toxicity.

Review: Polycyclic aromatic hydrocarbons (PAHs)-Action on placental function and health risks in future life of newborns.

Polycyclic aromatic hydrocarbons (PAHs) are common environmental pollutants, which are released as products of incomplete combustion processes. Harmful effects of PAHs exposure on human health are observed in increased morbidity of respiratory, cardiovascular and immunological diseases. A particularly sensitive group to PAHs exposure are pregnant women and their developing offspring. PAHs can cross the placental barrier and a lot of published data indicated that prenatal or early postnatal exposure to PAHs can lead to developmental toxicity. Epidemiological data shows increased incidence and prevalence of conditions associated with PAHs exposure, like intrauterine growth retardation. Even more, negative effect of PAHs are observed later in development, low IQ, problems with behavior, allergies or asthma. This review will briefly summarize currently available data on the effects of PAHs on placental function with a specific emphasis on placental differentiation, angiogenesis, hormone signaling and consequences of exposure to PAHs in childhood and adulthood.