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On behalf of Aluminiumindustriens Miljøsekretariat (AMS) and Alcoa Lista, NILU – Norwegian institute for air research has conducted a sampling campaign in the surroundings of the Alcoa Lista aluminium smelter in order to update the knowledge on PAH-concentrations around the smelter today. Samples were taken in the period January – December 2020 and analysed for particle bound PAHs. As a consequence of reduced emissions compared to earlier measurements, the ambient concentrations of benzo(a)pyrene (BaP) were reduced. BaP had an annual average concentration below the target value at both sampling sites. At Huseby, the lower assessment threshold was exceeded. PAH-levels in the area were similar to those observed in Norwegian cities. NILU – Norsk institutt for luftforskning har, på oppdrag fra Aluminiumindustriens Miljøsekretariat (AMS) og Alcoa Lista, tatt PAH-prøver i omgivelsene til Alcoa Lista aluminiums-smelteverk for å oppdatere kunnskapen om PAH-konsentrasjoner rundt smelteverket i dag. Prøvene ble tatt i perioden januar – desember 2020 og analysert for partikkelbundne PAHer. Som en konsekvens av reduserte utslipp sammenlignet med tidligere målinger, er konsentrasjonen av benzo(a)pyren (BaP) redusert. Årsmiddelet av BaP-konsentrasjonen i 2020 var under målsettingsverdien på begge prøvetakingsstedene. På Huseby ble den nedre vurderingsterskelen overskredet. PAH-konsentrasjonen i området på samme nivå som i norske byer.

BACKGROUND Particulate matter 2.5 (PM2.5) in air pollution is regarded as a risk factor for cardiovascular disease (CVDs). Recently, it has become well accepted that polycyclic aromatic hydrocarbons (PAHs) in PM2.5 impacts human CVDs. However, few studies have shown miRNAs affected by PAHs play a critical role in transcriptional regulation related to cardiovascular development and disease. MATERIAL AND METHODS Human umbilical cord vein cells (HUVECs) incubated prior to treatment with PAHs at various concentrations (0, 100, 200, 300, 400, and 500 µg/ml) of PAHs particle solutions were added to the culture medium for 24 h. We performed isolation and sequencing of small RNAs and analysis of small RNA sequences and differential expression. The M3RNA database was used to predict miRNA-miRNA interactions. Tools from the DAVID database were used to perform the GO functional analysis of predicted miRNA target genes. A First-Strand cDNA Synthesis Kit was used to synthesis cDNA. RESULTS miRNA155 was revealed as a key regulator in PAHs treatment. The putative targets of upregulated miRNA in PAHs treatment indicated that the downregulated genes were enriched in biological pathways such as Wnt signaling and ErbB signaling, which are crucial for the development of vasculature. CONCLUSIONS In general, our results suggest that PAHs taken by PM2.5 can decrease cardiovascular-related gene expression through upregulating miRNA, which may be a new target for therapy in the future.

OBJECTIVES: Workers' exposure to diesel exhaust in a bus depot, a truck repair workshop and an underground tunnel was determined by the measuring of elemental carbon (EC) and 15 carcinogenic polycyclic aromatic compounds (PACs) proposed by the US Department of Health and Human Services/National Toxicology Program (NTP). Based on these concentration data, the genotoxic PAC contribution to the diesel-exhaust particle (DEP) lung-cancer risk was calculated. METHOD: Respirable particulate matter was collected during the summer and winter of 2001 (except for in the underground situation) and analysed by coulometry for EC and by GC-MS methods for PACs. The use of potency equivalence factors (PEFs) allowed the studied PAC concentrations to be expressed as benzo[a]pyrene equivalents (B[a]P(eq)). We then calculated the lung-cancer risk due to PACs and DEPs by multiplying the B[a]P(eq) and EC concentrations by the corresponding unit risk factor. The ratio of these two risks values has been considered as an estimate of the genotoxic contribution to the DEP cancer risk. RESULTS: For the bus depot and truck repair workshop, exposure to EC and PACs has been shown to increase by three to six times and ten times, respectively, during winter compared to summer. This increase has been attributed mainly to a decrease in ventilation during the cold. With the PEF approach, the B[a]P(eq) concentration is five-times higher than if only benzo[ a]pyrene (B[a]P) is considered. Dibenzopyrenes contribute an important part to this increase. A simple calculation based on unit risk factors indicates that the studied PAC contribution to the total lung-cancer risk attributed to DEPs is in the range of 3-13%. CONCLUSIONS: The 15 NTP PACs represent a small but non-negligible part of lung-cancer risk with regard to diesel exposure. From this point of view, the dibenzopyrene family are important compounds to be considered.

Harbours are important hubs for economic growth in both tourism and commercial activities. They are also an environmental burden being a source of atmospheric pollution often localized near cities and industrial complexes. The aim of this study is to quantify the relative contribution of maritime traffic and harbour activities to atmospheric pollutant concentration in the Venice lagoon. The impact of ship traffic was quantified on various pollutants that are not directly included in the current European legislation for shipping emission reduction: (i) gaseous and particulate PAHs; (ii) metals in PM10; and (iii) PM10 and PM2.5. All contributions were correlated with the tonnage of ships during the sampling periods and results were used to evaluate the impact of the European Directive 2005/33/EC on air quality in Venice comparing measurements taken before and after the application of the Directive (year 2010). The outcomes suggest that legislation on ship traffic, which focused on the issue of the emissions of sulphur oxides, could be an efficient method also to reduce the impact of shipping on primary particulate matter concentration; on the other hand, we did not observe a significant reduction in the contribution of ship traffic and harbour activities to particulate PAHs and metals. Graphical abstract Impact of maritime traffic on polycyclic aromatic hydrocarbons, metals and particulate matter and evaluation of the effect of an European Directive on air quality in Venice.

There has been limited study of the removal of polycyclic aromatic hydrocarbons (PAHs) from inorganic clay minerals. Determining the amount of PAH removal is important in predicting their environmental fate. This study was carried out to the degradation and evaporation of PAHs from bentonite, which is an inorganic clay mineral. UV apparatus was designed specifically for the experiments. The impacts of temperature, UV, titanium dioxide (TiO2), and diethylamine (DEA) on PAH removal were determined. After 24 h, 75 and 44 % of Sigma(12) PAH in the bentonite were removed with and without UV rays, respectively. DEA was more effective as a photocatalyst than TiO2 during UV application. The Sigma(12) PAH removal ratio reached 88 % with the addition of DEA to the bentonite. It was concluded that PAHs were photodegraded at high ratios when the bentonite samples were exposed to UV radiation in the presence of a photocatalyst. At the end of all the PAH removal applications, higher evaporation ratios were obtained for 3-ring compounds than for heavier ones. More than 60 % of the amount of Sigma(12) PAH evaporated consisted of 3-ring compounds.

Near-ground air (26 substances) and surface seawater (55 substances) concentrations of persistent toxic substances (PTS) were determined in July 2012 in a coordinated and coherent way around the Aegean Sea based on passive air (10 sites in 5 areas) and water (4 sites in 2 areas) sampling. The direction of air–sea exchange was determined for 18 PTS. Identical samplers were deployed at all sites and were analysed at one laboratory. hexachlorobenzene (HCB), hexachlorocyclohexanes (HCHs) as well as dichlorodiphenyltrichloroethane (DDT) and its degradation products are evenly distributed in the air of the whole region. Air concentrations of p,p′-dichlorodiphenyldichloroethylene (p,p′-DDE) and o,p′-DDT and seawater concentrations of p,p′-DDE and p,p′-DDD were elevated in Thermaikos Gulf, northwestern Aegean Sea. The polychlorinated biphenyl (PCB) congener pattern in air is identical throughout the region, while polybrominated diphenylether (PBDE)patterns are obviously dissimilar between Greece and Turkey. Various pollutants, polycyclic aromatic hydrocarbons (PAHs), PCBs, DDE, and penta- and hexachlorobenzene are found close to phase equilibrium or net-volatilisational (upward flux), similarly at a remote site (on Crete) and in the more polluted Thermaikos Gulf. The results suggest that effective passive air sampling volumes may not be representative across sites when PAHs significantly partitioning to the particulate phase are included., Granting Agency of the Czech Republic (312334); Czech Ministry of Education (LO1214--LM2011028); European Social Fund (CZ.1.07/2.3.00/30.0037); European Commission FP7 (262254 ACTRIS)

The Nador Lagoon holds a major interest in present-day Moroccan socioeconomic development. This environment is exposed to a number of potential polluting sources, such as mine tailings, urban and industrial dumping, and untreated wastewater inputs from surrounding cities. The aim of this study was to assess concentrations and trends of persistent contaminants such as PCBs and PAHs and to identify their origin. The non-Aroclor PCB-11 was determined for the first time in the lagoon sediments. Chronology and source assessment helped identifying the timing and nature of inputs and post-depositional processes controlling the two classes of contaminants: PAHs present a typical mixed petrogenic signature, with the exception of sediments deposited in the period 1930-1960 near the city of Nador, when pyrogenic inputs prevailed; PCBs show signs of microbial anaerobic degradation from 1950 to 1990, probably linked to changing hydrodynamic conditions in the South-Western part of the lagoon where agricultural inputs are dominant. The presence of PCB-11 is linked to specific productions and might be affected by degradation processes. Presently, different land uses (e.g., urban and agricultural areas) appear to be the key factors in controlling the level and composition of PAHs and PCBs in lagoon sediments. Total PAH and PCB levels are low (from 21.6 to 108ngg-1 and from 2.50 to 20.7ngg-1, respectively) but recent increasing values and the potential threat to humans and biota require continuous and constant monitoring.

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous air pollutants generated by combustion sources that include diesel- and gasoline-powered motor vehicles, coal-fired power plants, residential heating, cooking, and tobacco smoking (Bostrom et al. 2002). An estimated > 80% of airborne PAHs results from the combustion of fossil fuels and biomass (Bostrom et al. 2002). There is growing concern about the adverse effects of air pollution from fossil fuel combustion on public health (Bostrom et al. 2002; Brunekreef and Holgate 2002) and the global climate (National Academy of Sciences 2001). PAHs are human mutagens and carcinogens (Bostrom et al. 2002) and are potentially significant reproductive and developmental toxicants (Dejmek et al. 2000; Perera et al. 2003). For example, prenatal exposure of rats to 25–100 μg/m3 of the representative PAH, benzo[a]pyrene (BaP), through maternal inhalation significantly decreased the fetal survival rate and birth weight in a dose-dependent manner (Archibong et al. 2002). In humans, associations between PAHs or PAH–DNA damage and fetal growth reduction have been reported in some but not all studies (Dejmek et al. 2000; Perera et al. 1998, 2003; Sram et al. 2005). In the Czech Republic, ambient PAHs significantly increased the risk of intrauterine growth retardation (IUGR) both in Teplice and Prachatice (Dejmek et al. 2000). An earlier study in Poland found that the infants who had higher than median leukocyte PAH–DNA adduct level had significantly reduced birth weight, length, and head circumference (Perera et al. 1998). In New Jersey, USA, the risk of fetal death, premature birth, and low birth weight was significantly higher for those with a high prenatal polycyclic organic matter exposure (Vassilev et al. 2001). However, the limitations of most prior studies [retrospective or cross-sectional design, reliance on ambient air monitoring data, failure to account for co-exposure to other sources of PAHs such as environmental tobacco smoke (ETS)] have prevented definitive causal inferences regarding airborne PAHs and impaired fetal growth (Sram et al. 2005). We conducted two parallel prospective cohort studies in Krakow, Poland, and New York City (NYC), USA, using identical eligibility criteria, study design, and personal air monitoring methodology. Here we examined effects across the entire range of PAH exposure in each cohort separately, to understand the relationship between in utero exposure to airborne PAHs and fetal growth within each population. We also conducted exploratory analyses comparing the magnitude of PAH-related effects between the two different populations within the exposure range common to both, recognizing the limitations of such international, interethnic comparisons. The U.S. and Polish cohorts represent a wide range of exposure, experienced in many other urban areas; therefore, study results in Krakow and NYC are relevant to other populations worldwide. In the Krakow cohort, the average PAH concentration estimated by personal air monitoring was 39.0 ng/m3 (range, 1.8–272.2 ng/m3), compared with 3.3 ng/m3 (range, 0.3–36.5 ng/m3) in NYC. Comparable personal air monitoring data on PAHs are not available for other populations, but stationary ambient air monitoring data for BaP can be used for comparison. The mean ambient BaP level in Krakow was 3.8 ng/m3 in 2000. Annual mean ambient BaP level in various locations within Krakow ranged from 4 to 10 ng/m3 during 2002. This level is comparable to the winter means reported in Teplice (7.42 ng/m3) and Prachatice (5.37 ng/m3), Czech Republic, between 1993 and 1994 (Binkova et al. 1999) but lower than that measured in Tongliang, China, between 2002 and 2003 (15 ng/m3) (Chow et al. 2006). In an ongoing prospective study in NYC, personal exposure to BaP among the cohort of pregnant women was 0.49 ± 0.65 ng/m3 (Tonne et al. 2004). In U.S. cities, as well as in many urban areas of Europe, ambient BaP concentrations are generally < 1 ng/m3, but may range between 1 and 5 ng/m3 during winter or in areas with heavy traffic (Naumova et al. 2002; Tonne et al. 2004).

This study investigated host factors and environmental factors as potential determinants of polychlorinated aromatic hydrocarbons (PCAHs) in serum of adolescents. We recruited 200 participants (80 boys and 120 girls), with a mean age of 17.4 years (SD, 0.8), in Belgium from a rural control area (Peer) and from two polluted suburbs of Antwerp where a nonferrous smelter (Hoboken) and waste incinerators (Wilrijk) are located. We quantified polychlorinated biphenyls (PCBs; congeners 138, 153, and 180) in serum by gas chromatography and obtained the toxic equivalents (TEQs) of PCAHs in serum with the chemically activated luciferase gene expression bioassay (CALUX). Serum PCB concentration was higher in boys than in girls (1.67 vs. 1.02 nmol/L or 377 vs. 210 pmol/g serum lipids; p< 0.001). In the whole adolescent group, multiple regression showed that serum PCB concentration decreased 0.06 nmol/L per 1% increase in body fat content (p< 0.001) and increased 0.39 nmol/L and 0.14 nmol/L per 1 mmol/L increase in serum concentrations of triglycerides (p < 0.001) and cholesterol (p = 0.002), respectively. Host factors explained 44% of the serum PCB variance. In the same model, serum PCB concentration increased 0.14 nmol/L with 10 weeks of breast-feeding (p< 0.001) and 0.06 nmol/L with intake of 10 g animal fat per day (p < 0.001), and was associated with residence in the waste incinerator area (9% higher; p = 0.04); 11% of the variance could be explained by these environmental factors. The geometric mean of the serum TEQ value was similar in boys and girls (0.15 TEQ ng/L or 33.0 pg/g serum lipids). In multiple regression, TEQ in serum decreased 0.03 ng/L per centimeter increase in triceps skinfold (p = 0.006) and was 29% higher in subjects living close to the nonferrous smelter (p < 0.001). This study showed that in 16- to 18-year-old teenagers host factors are important determinants of serum concentrations of PCAHs, whereas environmentally related determinants may to some extent contribute independently to human exposure to these persistent chemicals in the environment. ispartof: Environmental health perspectives vol:110 issue:6 pages:583-9 ispartof: location:United States status: published

Occupational exposures to wood dust have been associated with an elevated risk of sinonasal cancer (SNC). Wood dust is recognized as a human carcinogen but the specific cancer causative agent remains unknown. One possible explanation is a co-exposure to; wood dust and polycyclic aromatic hydrocarbons (PAHs). PAHs could be generated during incomplete combustion of wood due to heat created by use of power tools. To determine if PAHs are generated from wood during common woodworking operations, PAHs concentrations in wood dust samples collected in an experimental chamber operated under controlled conditions were analyzed. In addition, personal air samples from workers exposed to wood dust (n=30) were collected. Wood dust was generated using tree different power tools: vibrating sander, belt sander, and saw; and six wood materials: fir, Medium Density Fiberboard (MDF), beech, mahogany, oak and wood melamine. Monitoring of wood workers was carried out by means of personnel sampler device during wood working operations. We measured 21 PAHs concentrations in wood dust samples by capillary gas chromatographic-ion trap mass spectrometric analysis (GC-MS). Total PAH concentrations in wood dust varied greatly (0.24 – 7.95 ppm) with the lowest being in MDF dust and the highest in wood melamine dust. Personal exposures to PAHs observed were between 37.5-119.8 ng m-3 among workers during wood working operations. Our results suggest that PAH exposures during woodworking operation are present and hence could play a role in the mechanism of cancer induction related to wood dust exposure.

We have developed and validated a sandwich chemiluminescence immunoassay (SCIA) which measures polycyclic aromatic hydrocarbon (PAH)-DNA adducts combining high throughput and adequate sensitivity, appropriate for evaluation of adduct levels in human population studies. Fragmented DNA is incubated with rabbit antiserum elicited against DNA modified with r7,t8-dihydroxy-t-9,10-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (BPDE) and subsequently trapped by goat anti-rabbit IgG bound to a solid surface. Anti-single-stranded (ss) DNA antibodies binds in a quantity proportional to the adduct levels and is detected by chemiluminescence. The BPDE-DNA SCIA has a limit of detection of 3 adducts per 10(9) nucleotides with 5 μg DNA per well. We have validated the BPDE-DNA SCIA using DNA modified in vitro, DNA from benzo[a]pyrene (BP)-exposed cultured cells and mice. The levels of adduct measured by SCIA were lower (30-60%) than levels of bulky DNA adducts measured in the same samples by (32)P-postlabelling. The BPDE-DNA SCIA also detected adducts produced in vivo by PAHs other than BP. When blood DNA samples from maternal/infant pairs were assayed by BPDE-DNA SCIA, the adduct levels obtained were significantly correlated. However, there was no correlation between (32)P-postlabelling and SCIA values for the same samples. The SCIA can be extended to any DNA adduct and is expected to provide, when fully automated, a valuable high-throughput approach in large-scale population studies. This work was supported by contracts from the European Union (to S.A.K): Network of Excellence ECNIS—‘Environmental cancer risk, nutrition and individual susceptibility’ and Integrated Project NewGeneris—‘Newborns and genotoxic exposure risks’ (contract numbers FOOD-CT-2005-513943, FOOD-CT-2005-016320). The work was also supported in part by the intramural program of the Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA (to M.C.P.).

Polycyclic aromatic hydrocarbons (PAH) are an important class of environmental contaminants many of which require metabolic activation to DNA-reactive bay or fjord region diolepoxides (DE) in order to exert their mutagenic and carcinogenic effects. In this study, the mutagenicity of the bay region diolepoxides (+)-anti-7,8-dihydroxy-9,10-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (BPDE) and (±)-anti-1,2-dihydroxy-3,4-epoxy-1,2,3,4-tetrahydrodibenzo[a,h]anthracene (DBADE) and the fjord region diolepoxides (±)-anti-11,12-dihydroxy-13,14-epoxy-11,12,13,14-tetrahydrodibenzo[a,l]-pyrene (DBPDE) and (±)-anti-3,4-dihydroxy-1,2-epoxy-1,2,3,4-tetrahydrobenzo[c]-phenanthrene (BPhDE) was compared in nucleotide excision repair (NER) proficient and deficient hamster cell lines. The (32)P-postlabelling assay was applied to analyze DNA adduct levels and the Hprt gene mutation assay for monitoring mutations. Previously, we found that the mutagenicity per adduct was four times higher for DBPDE compared to BPDE in NER proficient cells. In these same cells, the mutagenicity of DBADE and BPhDE adducts was now found to be significantly lower compared to that of BPDE. In NER deficient cells the highest mutagenicity per adduct was found for BPDE and there was a tenfold and fivefold difference when comparing the BPDE data with the DBADE and BPhDE data, respectively. In order to investigate to what extent the mutagenicity of the different adducts in NER proficient cells was influenced by repair or replication bypass, we measured the overall NER incision rate, the rate of adduct removal, the rate of replication bypass and the frequency of induced recombination in the Hprt gene. Since NER turned out to be an important pathway for the yield of mutations, we further analyzed the role of transcription coupled NER versus global genome NER. However, our data demonstrate that neither of these pathways seems to be the sole factor determining the mutation frequency of the four PAH-DE and that the differences in the repair efficiency of these compounds could not be related to the presence of a bay or fjord region in the parent PAH. This work was supported by The European Commission; projects AMBIPAH (QLK4-CT-2002-02402), DIEPHY (FOOD-CT-2003-505609), ECNIS (FOOD-CT-2005-513943) and The Swedish Research Council Formas.

Historical records of total organic carbon (TOC), black carbon (BC), and polycyclic aromatic hydrocarbons (PAHs) were reconstructed in dated sediment cores from four nearby lakes in central Switzerland. In the sub-Alpine Lake Thun, located at 558 m a.s.l., the proximity to anthropogenic emission sources is reflected in higher input of BC and PAHs into sediments with fluxes only slightly decreasing during the last decades. PAH/BC ratios are relatively high and correlation between levels of total PAHs and BC is almost inexistent in Lake Thun, probably due to the presence of less condensed forms of the BC spectrum (char BC) that is underestimated with the chemothermal oxidation method applied in this study. The sediment profiles of TOC, BC, and PAHs are noticeably different in the mountain lakes located around 2000 m a.s.l. In Lake Engstlen, the PAH/BC ratios, as well as the correlation between PAHs and BC, point towards appreciable amounts of predominantly light soot particles. Light soot particles have higher mobility and can, therefore, be efficiently transported to this remote site. The proglacial Lake Oberaar is shown to be a receptor of BC and PAHs released by the fast melting adjacent glacier acting as a secondary source for these conservative species temporarily stored in the glacier ice. Finally, Lake Stein is in strong contrast to all other lakes. High flux of BC into Lake Stein, combined with constant temporal evolutions of BC and PAHs, and in particular BC/TOC ratios approaching 100% are all strong indications for a geogenic presence of graphite in its catchment area.

A phenyl-based hybrid organic -inorganic coating has been synthesized and processed by hard X-ray lithography. The overall lithography process is performed in a two-step process only (X-rays exposure and chemical etching). The patterns present high aspect ratio, sharp edges, and high homogeneity. The coating has been doped with a variety of polycyclic aromatic hydrocarbon functional molecules, such as anthracene, pentacene, and fullerene. For the first time, hard X-rays have been combined with thick hybrid functional coatings, using the sol-gel thick film directly as resist. A new technique based on a new material combined with hard X-rays is now available to fabricate optical devices. The effect due to the high-energy photon exposure has been investigated using FT-IR and Raman spectroscopy, laser scanner, optical profilometer, and confocal and electron microscope. Highquality thick hybrid fullerene-doped microstructures have been fabricated. © 2011 American Chemical Society.

Samples of PM(2.5) were gravimetrically collected during the winter 2005/2006 in the urban area of Milan (North Italy). Samples were chemically characterized and the particles were detached from filters to determine their cytotoxic effects on the A549 cell line. Based on the potential toxicological relevance of its components, Milan winter PM(2.5) contained high concentrations of pro-oxidant transition metals and PAHs, while re-suspended particles showed a relatively high frequency of dimensional classes ranging from 40 nm to 300 nm. A549 cells exposed to particle suspensions showed a concentration-dependent decrease in viability, starting from 10 microg/cm(2). Phagocytosis of particles by A549 cells and particle aggregates were morphologically characterized and seemed to depend on both particle concentration and exposure time, with the majority of particles being engulfed in membrane-bound vacuoles after 24h of exposure. The ability of ultrafine particles to penetrate and spread throughout the cells was also verified. Cell membrane lysis and mitochondrial ultrastructural disruption appeared to be the main modifications induced by PM(2.5) on A549 cells. Concomitantly to the adverse effects observed in terms of cell mortality and ultrastructural lesions, a significant intracellular production of reactive oxygen species (ROS) was observed, suggesting that the cytotoxicity, exerted by the winter PM(2.5) in Milan, derived also from its oxidative potential, probably associated with particle-adsorbed metals and PAHs.

Although exposure to polycyclic aromatic hydrocarbons (PAHs) occurs mostly through mixtures, hazard and risk assessment are mostly based on the effects caused by individual compounds. The objective of the current study was to investigate whether interactions between PAHs occur, focusing on gene expression (as measured by cDNA microarrays) and DNA adduct formation. The effects of benzo[a]pyrene or dibenzo[a,h]anthracene (DB[a,h]A) alone and in binary mixtures with another PAH (DB[a,h]A, benzo[b]fluoranthene, fluoranthene or dibenzo[a,l]pyrene) were investigated using precision-cut rat liver slices. All compounds significantly modulated the expression of several genes, but overlap between genes affected by the mixture and by the individual compounds was relatively small. All mixtures showed an antagonistic response on total gene expression profiles. Moreover, at the level of individual genes, mostly antagonism was evident, with additivity and synergism observed for only a few genes. As far as DNA adduct formation is concerned, the binary mixtures generally caused antagonism. The effects in liver slices suggest a lower carcinogenic potency of PAH mixtures than estimated based on additivity of individual compounds. © The Author 2008. Published by Oxford University Press on behalf of the UK Environmental Mutagen Society. All rights reserved.

The aim of this study was to determine airborne polycyclic aromatic hydrocarbons (PAHs) and biphenyl at an airport by gas chromatography–mass spectrometry and to evaluate occupational exposure by environmental monitoring. A total of 12 samplings were carried out in three areas: (1) a handling area where baggage was unloaded manually from vehicles onto conveyor belts ( n = 5); (2) the runway with plane and motor vehicle traffic ( n = 5) and (3) a departure lounge ( n = 2). PAHs levels were in most cases low. The higher levels found refer to naphthalene (130–13,050 ng/m 3 ) and to its methyl-substitutes 2-methylnaphthalene (64–28,500 ng/m 3 ) and 1-methylnaphtalene (24–35,300 ng/m 3 ), and biphenyl (24–1610 ng/m 3 ). A method was used to quantify twenty-four airborne PAHs, and biphenyl, and to detect a variety of other chemical compounds by means of the deconvolution program AMDIS. After sampling air on quartz filter and PUF and XAD-2 sorbents; extraction with dichloromethane, and concentration and purification on silica cartridges, analyses were carried out by gas chromatography–ion trap mass spectrometry. We used 20 deuterated PAHs to quantify both the 24 native PAHs and biphenyl. The native substances had been subdivided into small groups and in this way, their volatility was adequately reflected by the D-PAH present in each group. The limit of detection was 0.1 ng/m 3 for all the PAHs, and a linear range of at least about three-fold the maximum level studied (naphthalene) was obtained both for D-PAHs and the native PAHs. A good recovery pattern was obtained for D-PAHs on quartz filters, PUF and XAD-2.

Concern regarding the hazardous health effects from exposure to chemicals in bitumen fumes has been expressed and there is a great deal of interest for data on profile of individual compounds in the gas and particulate phases. The purpose of the study was to evaluate a method for the determination of volatile organic compounds (VOC), semi-volatile and particulate polycyclic aromatic compounds (PAH) and sulfur poly-heterocylic (PASH) compounds in bitumen fumes. The methylated derivatives of PAH are of particular interest since many of them exhibit carcinogenic activities while the parent compound does not. Bitumen fumes were laboratory generated at 170°C using a fume generator with controlled characteristics. Sampling of bitumen fumes was carried out with XAD-2 Orbo tubes for the gas phase chemicals and semi-volatile PAH or PASH. Glass Fiber GF/B were used to sample the fumes aerosol particulates at a flow rate of 1.2 L/min. PAH profiles and PASH in bitumen fumes were determined by GC-MS further to a multi-step sample treatment and automatic clean-up procedure. The internal standard was added to 0.1 to 0.3 g of raw bitumen or bitumen fumes filter samples which were then extracted twice with 25 mL toluene by sonication for 10 min each. The reduced extract was partitioned between cyclohexane and dimethylformamide before elution on a SiO2 micro column. The eluent was reduced and fractionated by HPLC. The PAH fraction of interest which also contained PASH was separated by capillary column GC-ion trap MS. Quantification was made relative to the respective calibration curves between compounds of interest and the internal standard. The semi-volatile SVPAH and SVPASH were determined by separate desorption of the two distinct parts of the XAD-2 by 5mL CS2 and sonication for 30 min. Microliters of the combined filtered extract were then injected into a GC column and quantified by ion trap MS. Standard reference compounds were used for comparisons of respective spectra. The purified extract enables the determination of PAH profile from 2 to 7 rings including their methyl derivatives and 3 carcinogenic benzonaphthothiophene isomers. The reproducibility of the method was estimated by analyzing 6 bitumen replicates and is around the 30% overall uncertainty or less. In bitumen fumes generated at 170°C under standardized conditions, VOC and semi-volatile PAH were sampled with XAD-2 tubes and were also determined in six replicates. The VOCs are mainly monoaromatic derivatives (4% of fumes) and aliphatics essentially from C6 to C17 (27%). With regards to the particulate phase PAC, the coefficients of variation from 6 replicates are 5-24 % for PAH and 6-10% for PASH. Data on VOC and PASH represent new contribution in the characterization of bitumen fumes.

Polycyclic aromatic hydrocarbons (PAHs) cover a wide range of structurally related compounds which differ greatly in their carcinogenic potency. PAH exposure usually occurs through mixtures rather than individual compounds. Therefore, we assessed whether the effects of binary PAH mixtures on gene expression, DNA adduct formation, apoptosis and cell cycle are additive compared with the effects of the individual compounds in human hepatoma cells (HepG2). Equimolar and equitoxic mixtures of benzo[a]pyrene (B[α]P) with either dibenzo[a,l]pyrene (DB[a,l]P), dibenzo[a,h]anthracene (DB[a,h]A), benzo[b]fluoranthene (B[b]F), fluoranthene (FA) or 1-methylphenanthrene (1-MPA) were studied. DB[a,l]P, B[α]P, DB[a,h]A and B[b]F dose-dependently increased apoptosis and blocked cells cycle in S-phase. PAH mixtures showed an additive effect on apoptosis and on cell cycle blockage. DNA adduct formation in mixtures was higher than expected based on the individual compounds, indicating a synergistic effect of PAH mixtures. Equimolar mixtures of B[α]P and DB[a,l]P (0.1, 0.3 and 1.0 μM) were assessed for their effects on gene expression. Only at 1.0 μM, the mixture showed antagonism. All five compounds were also tested as a binary mixture with B[α]P in equitoxic concentrations. The combinations of B[α]P with B[b]F, DB[a,h]A or FA showed additivity, whereas B[α]P with DB[a,l]P or 1-MPA showed antagonism. Many individual genes showed additivity in mixtures, but some genes showed mostly antagonism or synergism. Our results show that the effects of binary mixtures of PAHs on gene expression are generally additive or slightly antagonistic, suggesting no effect or decreased carcinogenic potency, whereas the effects on DNA adduct formation show synergism, which rather indicates increased carcinogenic potency. © The Author 2007. Published by Oxford University Press. All rights reserved.

Background The highest rates of esophageal squamous cell carcinoma (ESCC) in Brazil occur in Rio Grande do Sul, the most southern state, which has incidence rates of 20.4/100,000/year for men and 6.5/100,000/year for women. Exposure to carcinogenic polycyclic aromatic hydrocarbons (PAHs) through tobacco smoke and other sources may increase the risk of ESCC. The aims of the current study were to investigate the degree and sources of PAH exposure of the inhabitants of this region of southern Brazil. Methods Two hundred healthy adults (half smokers, half non smokers, half male and half female) were recruited, given a standardized questionnaire, and asked to provide a urine sample for measurement of 1-hydroxypyrene glucuronide (1-OHPG), a PAH metabolite). Urine 1-OHPG concentrations were measured using immunoaffinity chromatography and synchronous fluorescence spectroscopy and urine cotinine was measured using a dipstick test. We examined factors associated with 1-OHPG concentration using Wilcoxon tests and multiple linear regression. Results Urine 1-hydroxypyrene glucuronide (1-OHPG) was successfully measured on 199 subjects. The median (interquartile range) of urine 1-OHPG in the 199 participants was 2.09 pmol/mL (0.51, 5.84). Tobacco smoke exposure and maté drinking were statistically significantly associated with higher urine 1-OHPG concentrations in the multivariate linear regression model. Conclusion Tobacco smoke and maté both contribute to high levels of benzo[a]pyrene exposure in the people of southern Brazil. This high PAH exposure may contribute to the high rates of ESCC observed in this population. The increased urine 1-OHPG concentrations associated with maté suggest that contaminants, not just thermal injury, may help explain the increased risk of ESCC previously reported for maté consumption.

In order to study microbial diversity in a polycyclic aromatic hydrocarbon-impacted soil, 14 bacterial strains were analyzed by 16S rRNA gene sequencing and amplified fragment length polymorphism (AFLP) analysis. Bacterial strains isolated from two different hydrocarbon-polluted sites were identified to the species level by 165 rRNA full-gene sequencing using MicroSeq 16S rRNA gene sequencing. Their genome was subsequently analyzed by high-resolution genotyping with AFLP analysis, in order to monitor species variability and to differentiate closely related strains. Cluster analysis based on AFLP fingerprinting showed intraspecific polymorphism, even among strains with 100% 16S rRNA gene sequence identity. The results show that AFLP is a powerful, highly reproducible and discriminatory toot for revealing genetic relationships in bacterial populations. The ability to differentiate and track related closely microbes is fundamental for studying structure and dynamics of microbial communities in contaminated ecosystems. (C) 2005 Elsevier GmbH. All rights reserved.

The aim of this study was to use environmental monitoring to evaluate occupational exposure to polycyclic aromatic hydrocarbons (PAHs) and biphenyl in an Italian airport. Air was sampled using a quartz fiber filter, a polyurethane foam, and an XAD-2 layer. After extraction with dichloromethane, concentration and purification analyses of 25 PAHs (including biphenyl) were carried out by gas chromatography-ion trap mass spectrometry. In winter 2005, 12 air samples were taken at 120 L/min for 24 hours in three different areas of the airport. PAH levels were found to be generally low. In all investigated areas, the higher levels refer to naphthalene (130-13,050 ng/m 3 ), 2-methylnaphthalene (64-28,500 ng/m 3 ), 1-methylnaphtalene (24-35,300 ng/m 3 ), and biphenyl (24-1610 ng/m 3 ). However, in some instances, for compounds such as benzo [b+j+k] fluoranthene and benzo[a]pyrene, two high-boiling PAHs, the levels found (54.2 ng/ m 3 and 8.6 ng/m 3 , respectively) can be considered of some concern.

Airport personnel can be exposed to several polycyclic aromatic hydrocarbons (PAHs) from jet fuel vapours, jet fuel combustion products and diesel exhaust. The aim of this study was to characterize the exposure and to evaluate genotoxic and oxidative effects in airport personnel (n=41) in comparison with a selected control group (n=31). Environmental monitoring of exposure was carried out analysing 23 PAHs on air samples collected from airport apron, airport building and terminal/office area during 5 working days. The urinary 1-hydroxy-pyrene (1-OHP) following 5 working days, was used as biomarker of exposure. Genotoxic effects and early direct-oxidative DNA damage were evaluated by micronucleus (MN) and Fpg-modified comet assay on lymphocytes and exfoliated buccal cells, and by chromosomal aberrations (CA) and sister chromatid exchange (SCE) analyses. For comet assay, tail moment (the product of comet relative tail intensity and length) values from Fpg-enzyme treated cells (TMenz) and from untreated cells (TM) were used as parameters of oxidative and direct DNA damage, respectively. We found 27,703 microg/m(3) total PAHs in airport apron, 17,275 microg/m(3) in airport building and 9,494 microg/m(3) in terminal/office area. Urinary OH-pyrene did not show differences between exposed and controls. The exposed group showed a higher mean value of SCE frequency in respect to controls (4.6 versus 3.8) and an increase (1.3-fold) of total structural CA in particular breaks (up to 2.0-fold) and fragments (0.32% versus 0.00%), whereas there were no differences of MN frequency in both cellular types. Comet assay evidenced in the exposed group a higher value in respect to controls of mean TM and TMenz in both exfoliated buccal cells (TM 118.87 versus 68.20, p=0.001; TMenz 146.11 versus 78.32, p0.001) and lymphocytes (TM 43.01 versus 36.01, p=0.136; TMenz 55.86 versus 43.98, p=0.003). An oxidative DNA damage was found, for exfoliated buccal cells in the 9.7% and for lymphocytes in the 14.6% of exposed in respect to the absence in controls. Our findings furnish a useful contribution to the characterization of civil airport exposure and suggest the use of comet assay on exfoliated buccal cells to assess the occupational exposure to mixtures of inhalable pollutants at low doses since these cells represent the target tissue for this exposure and are obtained by non-invasive procedure.

Polychlorinated aromatic hydrocarbons (PCAHs) have been described as endocrine disruptors in animals and in accidentally or occupationally exposed humans. In the present study we examined the effect of moderate exposure to PCAHs on sexual maturation. Two hundred adolescents (mean age, 17.4 years) who resided in two polluted suburbs and a rural control area in Flanders (Belgium) participated. We measured the serum concentration of polychlorinated biphenyl (PCB) congeners 138, 153, and 180 and dioxin-like compounds [chemically activated luciferase expression (CALUX) assay] as biomarkers of exposure. School physicians assessed the pubertal development of boys and girls and measured testicular volume. In one suburb near two waste incinerators, compared with the other suburb and the control area, fewer boys (p < 0.001) had reached the adult stages of genital development (62% vs. 92% and 100%, respectively) and pubic hair growth (48% vs. 77% and 100%). Also, in the same suburb, fewer girls (p = 0.04) had reached the adult stage of breast development (67% vs. 90% and 79%). In individual boys, a doubling of the serum concentration of PCB congener 138 increased the odds of not having matured into the adult stage of genital development by 3.5 (p = 0.04); similarly for PCB congener 153 in relation to male pubic hair growth, the odds ratio was 3.5 (p = 0.04). In girls, a doubling of the serum dioxin concentration increased the odds of not having reached the adult stage of breast development by 2.3 (p = 0.02). Left plus right testicular volume was lower in both polluted areas than in the control area (42.4 mL vs. 47.3 mL, p = 0.005) but was not related to the current exposure of the adolescents to PCAHs. Through endocrine disruption, environmental exposure to PCAHs may interfere with sexual maturation and in the long-run adversely affect human reproduction. ispartof: Environmental health perspectives vol:110 issue:8 pages:771-6 ispartof: location:United States status: published

Occupational exposure to polycyclic aromatic hydrocarbons (PAH) increases the risk of developing lung cancer. Human exposure is often demonstrated by increased internal levels of PAH metabolites and of markers for early biological effects, like DNA adducts and cytogenetic aberrations. Objective: This study aimed to assess whether the current exposure to PAH of coke oven workers in a Dutch plant induced biological effects, and to determine if these effects are influenced by tobacco smoking and by genetic polymorphisms for the glutathione S-transferase genes GSTM1 and GSTT1. Methods: Urinary 1-hydroxypyrene (1-OHpyr) levels were used to monitor the internal dose, while the internal effective dose was assessed by monitoring PAH-DNA adducts, DNA strand breaks (Comet assay), sister-chromatid exchanges (SCE) and cells with a high frequency of SCE (HFC) in lymphocytes together with micronuclei (MN) in exfoliated urothelial cells. Results: Occupational exposure to PAH resulted in statistically significant increased 1-OHpyr levels (P

Three different in vitro mutation assays were used to investigate the involvement of cytochrome P450 enzymes in the activation of the nitro- polycyclic aromatic hydrocarbons (nitroPAHs) 1-nitropyrene and 2- nitrofluorene and their reduced metabolites amino-polycyclic aromatic hydrocarbons (aminoPAHs) 1-aminopyrene and 2-aminofluorene. Mutagenicity was investigated at the HPRT locus in Chinese hamster V79 cells with (V79-NH) or without (V79-MZ) endogenous acetyltransferase activity, stably expressing human cytochrome P450 cDNAs; in NIH/3T3 control or stably expressing human CYP1A2 cells, in combination with a shuttle vector containing a reporter gene; and in Salmonella typhimurium TA98, by inhibition of cytochrome P450 enzymes in rat liver S9 mix. Both the HPRT assay and the Ames test did not show any involvement of CYP3A in the activation of 1-nitropyrene to a mutagenic metabolite. In addition, a clear involvement of CYP1A2 in the activation of the nitroPAH 1-nitropyrene was demonstrated in both mutation assays using eukaryotic cells. However, no activation of 1-nitropyrene was seen in the eukaryotic cell lines when expressing only CYP1A2 (V79-MZ1A2) or acetyltransferase (V79-NH, 3T3-LNCX). The reduced metabolite of 1- nitropyrene, 1-aminopyrene, was also shown to be activated to a mutagenic metabolite by CYP1A2, using 3T3-1A2 cells in combination with a shuttle vector, and the Amestest in combination with the specific CYP1A2 inhibitor furafylline. No clear involvement of cytochrome P450 could be demonstrated for activation of 2-nitrofluorene to a mutagenic metabolite, whereas a role for CYP1A2 in the bioactivation of 2-aminofluorene is suggested. In the present study, we have demonstrated the complementary value of the three in vitro mutation assays in the examination of promutagen activation pathways. (C) 2000 Elsevier Science B.V. Chemicals/CAS: 1-nitropyrene, 5522-43-0; 2-aminofluorene, 153-78-6; 2-nitrofluorene, 607-57-8; Cytochrome P-450 Enzyme System, 9035-51-2; Enzyme Inhibitors; Ethyl Methanesulfonate, 62-50-0; Fluorenes; furafylline, 80288-49-9; Hypoxanthine Phosphoribosyltransferase, EC 2.4.2.8; Ketoconazole, 65277-42-1; Mutagens; Polycyclic Hydrocarbons, Aromatic; Pyrenes; Recombinant Fusion Proteins; Theophylline, 58-55

The previous studies from our laboratory reported that benzo(a)pyrene (Bap) influenced efflux transport of rhodamine 123 (Rho-123) by induction of P-glycoprotein (P-gp) in Caco-2 cells. The present study investigated whether induction of P-gp and the enhanced efflux transport of Rho-123 were caused by benzo(e)pyrene (Bep), which has a structure similar to Bap, but is not a carcinogenic compound. In Caco-2 monolayer exposed to 50 microM Bep for 72 h, the ratio of the apparent permeability coefficient (P(app)) of Rho-123 efflux increased significantly compared to that of the control monolayer. Similarly, a significant increase in expression of MDR1 mRNA and of P-gp at the protein level were detected by RT-PCR and by Western blot analysis, respectively, in Caco-2 cells exposed to Bep, compared to that of the control. Caco-2 cells exposed to Bep showed oxidative stress that was detected by fluorescence microscopy using aminophenyl fluorescein. However, the oxidative stress was weaker compared with that of Bap. The cellular GSH content was decreased to 80% or 59% of control cells, respectively, in Caco-2 cells exposed to either Bep or Bap. Our results further show that Bep or Bap-induced P-gp in Caco-2 cells might have been the result of oxidative stress rather than DNA damage.

An investigation is presented of occupational exposure to polycyclic aromatic hydrocarbons (PAH) in a carbon-electrode manufacturing plant, as assessed by three monitoring methods, viz, environmental monitoring of the external dose by analysis of personal air samples, biological monitoring of the internal dose by analysis of urinary 1-hydroxypyrene (1-OHpyrene), and biological effect monitoring by dosimetry of PAH-DNA adducts in blood lymphocytes. On the basis of job conditions, workers at the plant were divided into three groups with presumed low, intermediate and high exposure to air-borne PAH, respectively. All air samples showed levels of total PAH below the current MAC-value in the Netherlands, which is 200 μg/m3, whereas the benzo[a]pyrene level was occasionally higher than the recommended concentration of 2 μg/m3. The values of 1-OHpyrene in urine from the intermediate and high exposure groups were significantly higher than those of the low exposure group, namely 3.6- and 8.2-fold, respectively. Clear external and internal exposure was thus demonstrated for workers of the high and intermediate exposure groups, but this did not result in a measurable effect at the DNA level in blood lymphocytes. Tobacco smoking, on the other hand, caused a significant increase of the levels of PAH-DNA adducts but did not affect 1-OHpyrene values. These data suggest that smoking is a more important risk factor for adverse health effects, i.e. cancer, than occupational exposure to PAH in this plant.

Study objective - To evaluate the influence of occupational exposure to carcinogens in explaining the association between socioeconomic status and lung cancer. Design - A prospective cohort study. Data on diet, other lifestyle factors, sociodemographic characteristics and job history were collected by means of a self administered questionnaire. Follow up for incident cancer was established by record linkage with a national pathology register and with regional cancer registries. Setting - Population originating from 204 municipalities in The Netherlands. Participants - These comprised 58,279 men aged 55-69 years in September 1986. After 4.3 years of follow up there were 470 microscopically confirmed incident lung cancer cases with complete data on dietary habits and job history. Measurements and main results - Estimation of occupational exposure to asbestos, paint dust, polycyclic aromatic hydrocarbons, and welding fumes was carried out by two experts, using information on job history from the baseline questionnaire. Socioeconomic status was measured by means of highest attained level of education and two indicators based on occupation. In the initial multivariate analyses of socioeconomic status and lung cancer, adjustment was made for age, smoking habits, intake of vitamin C, betacarotene and retinol, and history of chronic obstructive pulmonary disease or asthma. Additional adjustment for occupational exposure to the four carcinogens mentioned above did not change the inverse association between the level of education and lung cancer risk (initial model: RR highest/lowest level of education = 0.53; 95% CI 0.34,0.82; additional model: RR highest/lowest level of education = 0.53; 95% CI 0.34,0.84). Nor was the association between the two occupation based indicators of socioeconomic status and lung cancer risk influenced by occupational exposure to carcinogens. The effect of occupational exposure on the association between the level of education and lung cancer risk did not differ between ex-smokers and current smokers. Conclusions - Occupational exposure to asbestos, paint dust, polycyclic aromatic hydrocarbons, and welding fumes could not explain the inverse association between socioeconomic status and lung cancer risk. More research which explicitly addresses possible explanations for the association between socioeconomic status and lung cancer risk is needed.

A coordinated study was carried out on the development, evaluation and application of biomonitoring procedures for populations exposed to environmental genotoxic pollutants. The procedures used involved both direct measurement of DNA or protein damage (adducts) and assessment of secondary biological effects (mutation and cytogenetic damage). Adduct detection at the level of DNA or protein (haemoglobin) was carried out by 32P-postlabelling, immunochemical, HPLC or mass spectrometric methods. Urinary excretion products resulting from DNA damage were also estimated (immunochemical assay, mass spectrometry). The measurement of adducts was focused on those from genotoxicants that result from petrochemical combustion or processing, e.g. low-molecular-weight alkylating agents, PAHs and compounds that cause oxidative DNA damage. Cytogenetic analysis of lymphocytes was undertaken (micronuclei, chromosome aberrations and sister chromatid exchanges) and mutation frequency was estimated at a number of loci including the hprt gene and genes involved in cancer development. Blood and urine samples from individuals exposed to urban pollution were collected. Populations exposed through occupational or medical sources to larger amounts of some of the genotoxic compounds present in the environmental samples were used as positive controls for the environmentally exposed population. Samples from rural areas were used as negative controls. The project has led to new, more sensitive and more selective approaches for detecting carcinogen-induced damage to DNA and proteins, and subsequent biological effects. These methods were validated with the occupational exposures, which showed evidence of DNA and/or protein and/or chromosome damage in workers in a coke oven plant, garage workers exposed to diesel exhaust and workers exposed to ethylene oxide in a sterilization plant. Dose response and adduct repair were studied for methylated adducts in patients treated with methylating cytostatic drugs. The biomonitoring methods have also demonstrated their potential for detecting environmental exposure to genotoxic compounds in nine groups of non-smoking individuals, 32P-postlabelling of DNA adducts being shown to have the greatest sensitivity. Chemicals/CAS: Antineoplastic Agents, Alkylating; Blood Proteins; Carcinogens, Environmental; DNA Adducts; Epichlorohydrin, 106-89-8; Ethylene Oxide, 75-21-8; Methylene Chloride, 75-09-2; Mutagens; Nitrogen Oxides; Petroleum; Polycyclic Hydrocarbons, Aromatic; Styrene, 100-42-5; Styrenes