Urinary 1-hydroxypyrene as a biomarker of exposure to polycyclic aromatic hydrocarbons: biological monitoring strategies and methodology for determining biological exposure indices for various work environments

This article reviews the published studies on urinary 1-hydroxypyrene (1-OHP) as a biomarker of exposure to polycyclic aromatic hydrocarbons (PAHs) in work environments. Sampling and analysis strategies as well as a methodology for determining biological exposure indices (BEIs) of 1-OHP in urine for different work environments are proposed for the biological monitoring of occupational exposure to PAHs. Owing to the kinetics of absorption of pyrene by different exposure routes and excretion of 1-OHP in urine, in general, 1-OHP urinary excretion levels increase during the course of a workday, reaching maximum values 3-9 h after the end of work. When the contribution of dermal exposure is important, post-shift 1-OHP excretion can however be lower than pre-shift levels in the case where a worker has been exposed occupationally to PAHs on the day prior to sampling. In addition, 1-OHP excretion levels in either pre-shift, post-shift or evening samples increase during the course of a work-week, levelling off after three consecutive days of work. Consequently, ideally, for a first characterization of a work environment and for an indication of the major exposure route, considering a 5-day work-week (Monday to Friday), the best sampling strategy would be to collect all micturitions over 24 h starting on Monday morning. Alternatively, collection of pre-shift, post-shift and evening urine samples on the first day of the work-week and at the end of the work-week is recommended. For routine monitoring, pre-shift samples on Monday and post-shift samples on Friday should be collected when pulmonary exposure is the main route of exposure. On the other hand, pre-shift samples on Monday and Friday should be collected when the contribution of skin uptake is important. The difference between beginning and end of work-week excretion will give an indication of the average exposure over the workweek. Pre-shift samples on the first day of the work-week will indicate background values, and, hence, reflect general environment exposure and body burden of pyrene and/or its metabolites. On the other hand, since PAH profile can vary substantially in different work sites, a single BEI cannot apply to all workplaces. A simple equation was therefore developed to establish BEIs for workers exposed to PAHs in different work environments by using a BEI already established for a given work environment and by introducing a correction factor corresponding to the ratio of the airborne concentration of the sum of benzo(a)pyrene (BaP) equivalent to that of pyrene. The sum of BaP equivalent concentrations represents the sum of carcinogenic PAH concentrations expressed as BaP using toxic equivalent factors. Based on a previously estimated BEI of 2.3 μmol 1-OHP mol^-1 creatinine for coke-oven workers, BEIs of 4.4, 8.0 and 9.8 μmol 1-OHP mol^-1 creatinine were respectively calculated for vertical pin Söderberg workers, anode workers and pre-bake workers of aluminium plants and a BEI of 1.2 μmol 1-OHP mol^-1 creatinine was estimated for iron foundry workers. This approach will allow the potential risk of cancer in individuals occupationally exposed to PAHs to be assessed better.     

Sensitive biomarker of polycyclic aromatic hydrocarbons (PAHs): urinary 1-hydroxyprene glucuronide in relation to smoking and low ambient levels of exposure.

The study was conducted in a Chinese population with occupational or environmental exposures to polycyclic aromatic hydrocarbons (PAHs). A total of 106 subjects were recruited from coke-oven workers (workers), residents in a metropolitan area (residents) and suburban gardeners (gardeners). All subjects were monitored twice for their personal exposures to PAHs. The biological samples were collected for measurements of 1-hydroxypyrene (1-OHP) and cotinine in urine. The geometric means of personal exposure levels of pyrene, benz(a)anthracene (BaA) and benzo(a)pyrene (BaP) in workers were 1.470, 0.978 and 0.805 microg m-3, respectively. The corresponding levels in residents were 0.050, 0.034 and 0.025 microg m-3; and those in gardeners were 0.011, 0.020 and 0.008 microg m-3, respectively. The conjugate of 1-OHP with glucuronide (1-OHP-G) is the predominant form of pyrene metabolite in urine and it showed strong associations with exposures not only to pyrene, but also to BaA, BaP and total PAHs. Most importantly, a significant difference in 1-OHP-G was even detected between the subgroups with exposures to BaP at < 0.010 and > 0.010 but < 0.020 microg m-3, suggesting that 1-OHP-G is a good marker that can be used for the risk assessment of BaP exposure at levels currently encountered in ambient air. Furthermore, multiple regression analyses of 1-OHP-G on PAHs exposure indicated that cigarette smoke was a major confounding factor and should be considered and adjusted for while using 1-OHP to estimate PAHs exposure.     

Environmental polycyclic aromatic hydrocarbon (PAH) exposure and DNA damage in Mexican children

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous pollutants presenting a public health risk, particularly to children, a vulnerable population. PAHs have genotoxic and carcinogenic properties, which depend on their metabolism. Many enzymes involved in PAH metabolism, including CYP1A1, CYP1B1, GSTM and GSTT are polymorphic, which may modulate the activation/deactivation of these compounds. We evaluated PAH exposure and DNA damage in children living in the vicinity of the main petrochemical complex located in the Gulf of Mexico, and explored the modulation by genetic polymorphisms of PAH excretion and related DNA damage. The participants (n=82) were children aged 6-10y attending schools near the industrial area. Urinary 1-hydroxypyrene (1-OHP; a biomarker of PAH exposure) was determined by reverse-phase-HPLC; DNA damage by the comet assay (Olive Tail Moment (OTM) parameter); CYP1A1*2C and CYP1B1*3 polymorphisms by real time-PCR; and GSTM1*0 and GSTT1*0 by multiplex PCR. The median value of 1-OHP was 0.37μmol/mol creatinine; 59% of children had higher 1-OHP concentrations than those reported in environmentally exposed adults (0.24μmol/mol creatinine). A stratified analysis showed increased DNA damage in children with 1-OHP concentrations greater than the median value. We observed higher 1-OHP concentrations in children with CYP1A1*2C or GSTM1*0 polymorphisms, and a positive influence of CYP1A1*2C on OTM values in children with the highest PAH exposure. The data indicate that children living in the surroundings of petrochemical industrial areas are exposed to high PAH levels, contributing to DNA damage and suggesting an increased health risk; furthermore, data suggest that polymorphisms affecting activation enzymes may modulate PAH metabolism and toxicity.     

Contamination,source identification,and risk assessment of polycyclic aromatic hydrocarbons in agricultural soils around a typical coking plant in Shandong,China

Coking is one of the most important emission sources of polycyclic aromatic hydrocarbons (PAHs) in China. Investigation of the contamination, distribution, and sources of PAHs in agricultural soils around Rong Xin coking plant, China, was conducted, and the potential human health risks were addressed. The total concentration of the 16 PAHs (∑₁₆PAHs) on the United States Environmental Protection Agency priority list had a range from 1774 to 4621 µg/kg (mean 3016 µg/kg). Meanwhile, seven carcinogenic PAHs (∑PAH_7c) owned the total concentrations of 684–2105 µg/kg, and they had the benzo[a]pyrene equivalent (BaP_eq) concentrations at 139.616–1672.850 µg/kg. All soil samples were dominated by PAHs with two to four rings. Data analyses for the potential sources of PAHs showed that the PAHs in soils were principally from pyrogenic sources. Ecological risk assessment of soil PAHs showed that the BaP_eq concentrations of ∑PAH_7c accounted for 99% of the total ∑₁₆PAHs, being a major carcinogenic contributors of ∑₁₆PAHs. Higher levels of PAHs and higher total BaP_eq concentrations in this study indicate a potential carcinogenic risk for humans. Therefore, long-term exposure to coking plants may increase the PAH concentrations in the environment and further raise a potential risk to human health.     

High urine 1-hydroxypyrene glucuronide concentrations in Linxian, China, an area of high risk for squamous oesophageal cancer

Most squamous cell carcinomas of the oesophagus in low-risk populations are attributable to alcohol and tobacco consumption, but the aetiologic agents in many high-risk populations have yet to be definitively identified. Linxian, China has some of the highest oesophageal cancer rates in the world. Recent studies suggest that an association exists between high-level exposure to carcinogenic polycyclic aromatic hydrocarbons (PAHs), such as benzo[a]pyrene (B[a]P), and the development of oesophageal cancer. The inhabitants of this high-risk region extensively use coal and wood for cooking and heating in unvented stoves, and thus may be exposed to PAHs produced during the incomplete combustion of these fuel sources. High levels of B[a]P were recently detected in staple food samples from Linxian and histopathologic changes that may be associated with PAH exposure have also been identified in oesophagectomy specimens from the region. In an effort to determine whether this high-risk population is exposed to high levels of PAHs, voided urines from non-smokers (n = 22) without occupational exposure were collected and analysed using immunoaffinity chromatography and synchronous fluorescence spectroscopy for 1-hydroxypyrene glucuronide, a PAH metabolite and index biomarker for mixed PAH exposure. The median urine 1-hydroxypyrene glucuronide concentration (2.06 pmol ml^-1) was equivalent to concentrations detected in current smokers. To the authors' knowledge, this represents the first report of elevated urine 1-hydroxpyrene glucuronide concentrations in Linxian, and the first biologic confirmation that the inhabitants of this rural, non-industrial, high oesophageal cancer risk region are exposed to carcinogenic PAHs.     

High urine 1-hydroxypyrene glucuronide concentrations in Linxian,China, an area of high risk for squamous oesophageal cancer

Most squamous cell carcinomas of the oesophagus in low-risk populations are attributable to alcohol and tobacco consumption, but the aetiologic agents in many high-risk populations have yet to be definitively identified. Linxian, China has some of the highest oesophageal cancer rates in the world. Recent studies suggest that an association exists between high-level exposure to carcinogenic polycyclic aromatic hydrocarbons (PAHs), such as benzo[a]pyrene (B[a]P), and the development of oesophageal cancer. The inhabitants of this high-risk region extensively use coal and wood for cooking and heating in unvented stoves, and thus may be exposed to PAHs produced during the incomplete combustion of these fuel sources. High levels of B[a]P were recently detected in staple food samples from Linxian and histopathologic changes that may be associated with PAH exposure have also been identified in oesophagectomy specimens from the region. In an effort to determine whether this high-risk population is exposed to high levels of PAHs, voided urines from non-smokers (n = 22) without occupational exposure were collected and analysed using immunoaffinity chromatography and synchronous fluorescence spectroscopy for 1-hydroxypyrene glucuronide, a PAH metabolite and index biomarker for mixed PAH exposure. The median urine 1-hydroxypyrene glucuronide concentration (2.06 pmol ml^-1) was equivalent to concentrations detected in current smokers. To the authors' knowledge, this represents the first report of elevated urine 1-hydroxpyrene glucuronide concentrations in Linxian, and the first biologic confirmation that the inhabitants of this rural, non-industrial, high oesophageal cancer risk region are exposed to carcinogenic PAHs.     

Potential Health Risk of Reused Creosote-Treated Old Railway Ties at Recreational Sites in Korea

Old creosote-treated railway ties reused at recreational sites in Korea are potential hazards, due to the presence of harmful substances in creosote, such as polycyclic aromatic hydrocarbons (PAHs). In such sites, PAHs in ties can be leached or emitted, and human exposure might then occur. In this study, the concentrations of 16 PAHs in soil, air, and tie surfaces in old creosote-treated railway ties reused in recreational sites were investigated, and the potential health risk of the ties was evaluated through two exposure scenarios: a recreational scenario (ingestion of and dermal contact with soil and inhalation of soil particles) and a playground scenario (ingestion after contact and dermal contact with ties). For the recreational scenario, the health risks of PAHs were safe; however, for the playground scenario, the carcinogenic risk of ingestion after contact, and dermal contact with benz(a)anthracene and benzo(a)pyrene on the tie surfaces, exceeded the acceptable risk level (10^–6). For the carcinogenic risks of ingestion after contact with ties, the probabilities of cancer development were 8 and 5 in one million people for benz(a)anthracene and benzo(a)pyrene, respectively. The carcinogenic risks for dermal contact with ties were 2.4 × 10^–6 and 1.4 × 10^–6 for benz(a)anthracene and benzo(a)pyrene, respectively.     

Assessment of occupational exposure to PAHs in an Estonian coke oven plant- correlation of total external exposure to internal dose measured as 1-hydroxypyrene concentration

The exposure of cokery workers to polynuclear aromatic hydrocarbons at an Estonian oil shale processing plant was assessed by using occupational hygiene and biomonitoring measurements which were carried out twice, in midwinter and in the autumn. To assess the external dose of polynuclear aromatic hydrocarbons, pyrene and benzo[a]pyrene concentrations were measured from the breathing zone of workers during a workshift. Skin contamination with pyrene and benzo[a]pyrene was assessed by skin wipe sampling before and after the workshift. As a biomarker of overall exposure to polynuclear aromatic hydrocarbons, and as an integral of all absorption routes of pyrene, 1-hydroxypyrene concentration was measured from post shift urine samples. Of the personal air samples, 18% exceeded the Finnish threshold limit value of benzo[a]pyrene (10 μg m^-3). Mean value (two separate measurements together) for benzo[a]pyrene was 5.7 μg m^-3 and for pyrene, 8.1 μg m^-3. Based on skin wipe sample analyses, the skin contamination was also obvious. The mean value of benzo[a]pyrene in the samples collected after the shift was 1.2 ng cm^-2. Benzo[a]pyrene was not found in control samples. The mean value of urinary 1-hydroxypyrene concentration was 6.0 μmol mol^-1 creatinine for the exposed workers and 0.5 μmol mol^-1 creatinine for the controls. This study undoubtedly shows the usefulness of 1-hydroxypyrene as an indicator of internal dose of polynuclear aromatic hydrocarbons. It can be concluded that the cokery workers at the Kohtla-Järve plant are exposed to high concentrations of polynuclear aromatic compounds, and the exposure level is considerably higher during the winter measurements.     

Levels,Sources, and Toxic Potential of Polycyclic Aromatic Hydrocarbons in Urban Soil of Delhi,India

This study was done to determine the concentration of PAHs in urban soil of Delhi (India). Surface top soil (up to 10 cm depth) samples were collected from four different sampling sites including industrial, roadside, residential, and agricultural areas of Delhi and 16 USEPA priority polycyclic aromatic hydrocarbons (PAHs) were evaluated. Total PAH concentrations at industrial, roadside, residential, and agricultural sites were 11.46 ± 8.39, 6.96 ± 4.82, 2.12 ± 1.12, and 1.55 ± 1.07 mg/kg (dry weight), respectively, with 3–7 times greater concentrations in industrial and roadside soils than that in residential and agricultural soils. The PAH pattern was dominated by 4- and 5-ring PAHs (contributing >50% to the total PAHs) at industrial and roadside sites with greater concentration of fluoranthene, chrysene, benzo[b]fluoranthene, benzo[k]fluoranthene, benzo[a]anthracene, benzo[ghi]perylene, and pyrene, whereas, residential and agricultural sites showed a predominance of low molecular weight 2- and 3-ring PAHs (fluoranthene, acenaphthene, naphthalene, chrysene, and anthracene). Isomeric pair ratios suggested biomass combustion and fossil fuel emissions as the main sources of PAHs. The toxic equivalency factors (TEFs) showed that carcinogenic potency (benzo[a]pyrene-equivalent concentration (B[a]P_eq) of PAH load in industrial and roadside soils was ～10 and ～6 times greater than the agricultural soil.     

Estimation of Toxicity Equivalency and Probabilistic Health Risk on Lifetime Daily Intake of Polycyclic Aromatic Hydrocarbons from Urban Residential Soils

In this study, toxicity equivalents and health risks, based on concentration of 16 priority polycyclic aromatic hydrocarbons (PAHs) in urban residential soils were estimated for the human population in Gwalior, India. Benzo(a)pyrene total potency equivalents (BaP TPE) were estimated for assessment of human health risk from direct contact with PAH-contaminated soil. Potential risk to contaminated groundwater from leaching of carcinogenic PAHs was assessed by estimating the index of additive cancer risk (IACR). On the basis of lifetime average daily intake of 16 PAHs through ingestion of PAH-contaminated soils, lifetime cancer risk to human adults and children was estimated. The concentration of probable human carcinogenic PAHs in soils accounted for 38% of ∑16PAHs. BaP TPE and index of additive cancer risk (IACR) were lower than guideline values of 0.6 mg kg^?1 and <1, respectively. Estimated lifetime average daily intakes of PAHs via soil ingestion were lower than recommended dose. However, the ILCR for human adults was within acceptable limits recommended by regulatory agencies, but may need action for children in Gwalior, India.     

Protein biomarkers in the plasma of workers occupationally exposed to polycyclic aromatic hydrocarbons

Polycyclic aromatic hydrocarbons (PAHs) form a chemical family containing several hundred compounds, including benzo[a]pyrene and pyrene. They are usually produced by the incomplete burning of coal, oil, gas, garbage, or other organic substances like tobacco or charbroiled meat. Exposure to PAH causes tumors, primarily in the lung, the bladder, and the skin. To investigate the differentially expressed proteins resultant from PAH exposure, the protein expression in human plasma was analyzed using two-dimensional electrophoresis (2-DE). The plasma exposed to PAH was obtained from 48 waste gas pollution measurers working at an automobile emission inspection center. The 1-hydroxypryene (1-OHP) level, which is the urinary PAH metabolite used for evaluation of PAH exposure, was 0.28 micromol/mol creatinine in PAH exposure groups, and 0.078 micromol/mol creatinine in unexposed groups (control, n = 33). A protein upregulated by PAH (putative capacitative calcium entry channel) and five overexpressed proteins (two fibrinogen gamma-A chain precursors, a hemopexin precursor, an albumin precursor, and T-cell receptor beta chain C region) were identified with matrix assisted laser desorption/ionization-time of flight-mass spectrometry (MALDI-TOF-MS) and confirmed with tandem MS (MS/MS) and Western blotting. The putative capacitative calcium entry channel was partially validated with a laboratory made antibody of a representative peptide fragment in PAH-exposed human plasma samples.     

Concentrations,Source and Risk Assessment of Polycyclic Aromatic Hydrocarbons in Soils from Midway Atoll,North Pacific Ocean

This study was designed to determine concentrations of polycyclic aromatic hydrocarbons (PAHs) in soil samples collected from Midway Atoll and evaluate their potential risks to human health. The total concentrations of 16 PAHs ranged from 3.55 to 3200 µg kg⁻¹ with a mean concentration of 198 µg kg⁻¹. Higher molecular weight PAHs (4–6 ring PAHs) dominated the PAH profiles, accounting for 83.3% of total PAH mass. PAH diagnostic ratio analysis indicated that primary sources of PAHs in Midway Atoll could be combustion. The benzo[a]pyrene equivalent concentration (BaP_eq) in most of the study area (86.5%) was less than 40 µg kg⁻¹ BaP_eq and total incremental lifetime cancer risks of PAHs ranged from 1.00×10⁻¹⁰ to 9.20×10⁻⁶ with a median value of 1.24×10⁻⁷, indicating a minor carcinogenic risk of PAHs in Midway Atoll.     

Polynuclear Aromatic Hydrocarbons (PAHs) in fish from the Red Sea Coast of Yemen

A detailed analytical study using combined normal phase high pressure liquid chromatography (HPLC), gas chromatography (GC) and gas chromatography/mass spectrometry (GC/MS) of Polynuclear Aromatic Hydrocarbons (PAHs) in fish from the Red Sea was undertaken. This investigation involves a preliminary assessment of the sixteen parent compounds issued by the U.S. Environmental Protection Agency(EPA). The study revealed measurable levels of Σ PAHs (the sum of three to five or six ring parent compounds) (49.2 ng g⁻¹ dry weight) and total PAHs (all PAH detected) (422.1 ng g⁻¹ dry weight) in edible muscle of fishes collected from the Red Sea. These concentrations are within the range of values reported for other comparable regions of the world. Mean concentrations for individual parent PAH in fish muscles were; naphthalene 19.5, biphenyl 4.6, acenaphthylene 1.0, acenaphthene 1.2, fluorene 5.5, phenanthrene 14.0, anthracene 0.8, fluoranthene 1.5, pyrene 1.8, benz(a)anthracene 0.4, chrysene 1.9, benzo(b)fluoranthene 0.5, benzo(k)fluoranthene 0.5, benzo(e)pyrene 0.9, benzo(a)pyrene 0.5, perylene 0.2, and indeno(1,2,3-cd)pyrene 0.1 ng g⁻¹ dry weight respectively. The Red Sea fish extracts exhibit the low molecular weight aromatics as well as the discernible alkyl-substituted species of naphthalene, fluorene, phenanthrene and dibenzothiophene. Thus, it was suggested that the most probable source of PAHs is oil contamination originating from spillages and/or heavy ship traffic. It was concluded that the presence of PAHs in the fish muscles is not responsible for the reported fish kill phenomenon. However, the high concentrations of carcinogenic chrysene encountered in these fishes should be considered seriously as it is hazardous to human health. Based on fish consumption by Yemeni‘s population it was calculated that the daily intake of total carcinogens were 0.15 μg/person/day. This revised version was published online in August 2006 with corrections to the Cover Date.     

Distribution,Levels, and Risk Assessment of Polycyclic Aromatic Hydrocarbons (PAHs) in Singed Cattle Hide

Human beings are exposed to polycyclic aromatic hydrocarbons (PAHs) from various occupational, environmental, and dietary sources. The study was carried out in the Cape Coast Metropolis of Ghana to assess the levels of PAHs in treated and untreated cattle hide and the associated health risks thereof. Treated cattle hide (wele) is one of the most well-patronized meat products in Ghana. A total of 90, treated (n = 36), untreated (n = 36), and control (n = 18) cattle hide samples were treated and analyzed using a gas chromatography flame ionization detection (GC/FID) technique. The total PAH concentration in the treated cattle hide ranged from 5.9 μg/kg naphthalene to 719.9 μg/kg benzo[b]fluoranthene. The total PAHs in untreated hide ranged from 57.6 μg/kg naphthalene to 19840.9 μg/kg benzo[b]fluoranthene. The amount of PAHs in the control hide, however, ranged from non-detectable for many of the PAHs to 0.5 μg/kg for fluorene. The carcinogenic risk value associated with the consumption of treated hide in children ranged between 1.0 × 10^?3 and 9.4 × 10^?3 whereas that of adults ranged between 1.9 × 10^?4 and 2.1 × 10^?5. This implies that the continuous consumption of heavily burnt cattle hide may not exempt the consumers from all the possible health cases associated with PAHs.     

Polycyclic aromatic hydrocarbons in the diet.

Polycyclic aromatic hydrocarbons (PAHs), of which benzo[a]pyrene is the most commonly studied and measured, are formed by the incomplete combustion of organic matter. They are widely distributed in the environment and human exposure to them is unavoidable. A number of them, such as benzo[a]pyrene, are carcinogenic and mutagenic, and they are widely believed to make a substantial contribution to the overall burden of cancer in humans. Their presence in the environment is reflected in their presence at detectable levels in many types of uncooked food. In addition, cooking processes can generate PAHs in food. PAHs can also be formed during the curing and processing of raw food prior to cooking. Several studies have been carried out to determine the levels of exposure to PAHs from representative human diets, and the proportion of the overall burden of environmental exposure to PAHs that is attributable to the diet. In most cases, it is concluded that diet is the major source of human exposure to PAHs. The major dietary sources of PAHs are cereals and vegetables, rather than meat, except where there is high consumption of meat cooked over an open flame. More recently, biomonitoring procedures have been developed to assess human exposure to PAHs and these have also indicated that diet is a major source of exposure. Exposure to nitro-PAHs through food consumption appears to be very low.     

Aryl hydrocarbon receptor-mediated activity of mutagenic polycyclic aromatic hydrocarbons determined using in vitro reporter gene assay

Activation of aryl hydrocarbon receptor (AhR) by 30 polycyclic aromatic hydrocarbons (PAHs) was determined in the chemical-activated luciferase expression (CALUX) assay, using two exposure times (6 and 24h), in order to reflect the metabolization of PAHs. AhR-inducing potencies of PAHs were expressed as induction equivalency factors (IEFs) relative to benzo[a]pyrene and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). In 24h exposure assay, the highest IEFs were found for benzo[k]fluoranthene, dibenzo[a,h]anthracene and dibenzo[a,k]fluoranthene (approximately three orders of magnitude lower than TCDD) followed by dibenzo[a,j]anthracene, benzo[j]fluoranthene, indeno[1,2,3-cd]pyrene, and naphtho[2,3-a]pyrene. The 6h exposure to PAHs led to a significantly higher AhR-mediated activity than the 24h exposure (generally by two orders of magnitude), probably due to the high rate of PAH metabolism. The strongest AhR inducers showed IEFs approaching that of TCDD. Several PAHs, including some strong mutagens, such as dibenzo[a,l]pyrene, cyclopenta[cd]pyrene, and benzo[a]perylene, elicited only partial agonist activity. Calculation of IEFs based on EC25 values and/or 6h exposure data is suggested as an alternative approach to estimation of toxic potencies of PAHs with high metabolic rates and/or the weak AhR agonists. The IEFs, together with the recently reported relative mutagenic potencies of PAHs [Mutat. Res. 371 (1996) 123; Mutat. Res. 446 (1999) 1] were combined with data on concentrations of PAHs in extracts of model environmental samples (river sediments) to calculate AhR-mediated induction equivalents and mutagenic equivalents. The highest AhR-mediated induction equivalents were found for benzo[k]fluoranthene and benzo[j]fluoranthene, followed by indeno[1,2,3-cd]pyrene, dibenzo[a,h]anthracene, benzo[a]pyrene, dibenzo[a,j]anthracene, chrysene, and benzo[b]fluoranthene. High mutagenic equivalents in the river sediments were found for benzo[a]pyrene, dibenzo[a,e]pyrene, and naphtho[2,3-a]pyrene and to a lesser extent also for benzo[a]anthracene, benzo[b]fluoranthene, indeno[1,2,3-cd]pyrene, benzo[j]fluoranthene, dibenzo[a,e]fluoranthene and dibenzo[a,i]pyrene. These data illustrate that AhR-mediated activity of PAHs, including the highly mutagenic compounds, occurring in the environment but not routinely monitored, could significantly contribute to their adverse effects.     

Identification of the highest potential human health and environmental hazard in contaminated sediment near the point sources in the northwest Persian Gulf

Abstract

The overall goal of this work was to determine the concentration levels and the potential ecological risks of 30 polycyclic aromatic hydrocarbons in the Persian Gulf sediments, Iran. The study also predicted the bioaccumulation of PAHs using the Monte Carlo simulation. For these goals, 68 surface sediment samples were collected from the Persian Gulf in January 2017. Then, the experiments were performed with Soxhlet system, chromatographic column and GC-MS instrument. According to the Canadian Sediment Quality Guidelines, 35.29% of sampling sites exhibited high potential adverse biological effects and 79.41% of samples have a low probability of toxicity. The mean bioaccumulated concentrations of carcinogenic PAHs in the Persian Gulf were predicted as 207.78?±?262.23, 116.06?±?146.47 and 69.26?±?87.41?ng g^–1 for mollusks, shrimps and crabs, respectively. The mean Toxic Equivalency and Mutagenic Equivalent Quotient for sediments was 702.06?±?1012.37 and 500.37?±?665.71?ng g^?1, respectively. The 95th percentile carcinogenic and non-carcinogenic risks calculated for children and adults were lower than the threshold values of 10^?6 and 1.0, respectively, revealing no potential health risk. The highest potential risks for toxicity were observed at sampling sites close to the Nowruz oil field and Mahshahr petrochemical economic zone based on the highest TEQcarc and MEQcarc values in this area.     

Distribution patterns of selected PAHs in bulk peat and corresponding humic acids from a Swiss ombrotrophic bog profile

An ombrotrophic peat core was collected in 2005 from Etang de la Gruère, Jura Mountains, Switzerland. The concentrations of nine among the U.S. Environmental Protection Agency priority polycyclic aromatic hydrocarbons (PAHs) (i.e., acenaphthene, phenanthrene, fluorene, pyrene, fluoranthene, benzo[jbk]fluoranthene, benzo[a]pyrene, benzo[ghi]perylene, and indeno[1,2,3-cd]pyrene) were determined in both bulk peat and corresponding humic acids (HA) samples by gas chromatography equipped with a mass spectrometry detector (GC-MS). The maximum PAHs concentrations in peat (around 1,250 μg Σ PAHs kg^?1 dry matter) were found at 28–30 cm of depth, which correspond to ca. 1920–1930, when coal inputs to Switzerland reached their maximum level. Amongst the nine PAHs analyzed in the peat samples, pyrene (Pyr) was the predominant species, accounting for ca. 20–100% of the total PAHs throughout the profile. In the HA fraction, that represents 24.7% (average value) of the bulk peat, only phenanthrene (Phe), and sporadically Pyr and fluoranthene (Fth), were detected. In particular, HA showed Phe concentrations that were ten–150 times higher than corresponding bulk peat samples, thus suggesting its preservation against biodegradation due to the incorporation into HA molecules.     

Optimization of high-molecular-weight polycyclic aromatic hydrocarbons' degradation in a two-liquid-phase bioreactor

A microbial consortium degrading the high-molecular-weight polycyclic aromatic hydrocarbons (HMW PAHs) pyrene, chrysene, benzo[a]pyrene and perylene in a two-liquid-phase reactor was studied. The highest PAH-degrading activity was observed with silicone oil as the water-immiscible phase; 2,2,4,4,6,8, 8-heptamethylnonane, paraffin oil, hexadecane and corn oil were much less, or not efficient in improving PAH degradation by the consortium. Addition of surfactants (Triton X-100, Witconol SN70, Brij 35 and rhamnolipids) or Inipol EAP22 did not promote PAH biodegradation. Rhamnolipids had an inhibitory effect. Addition of salicylate, benzoate, 1-hydroxy-2-naphtoic acid or catechol did not increase the PAH-degrading activity of the consortium, but the addition of low-molecular-weight (LMW) PAHs such as naphthalene and phenanthrene did. In these conditions, the degradation rates were 27 mg l-1 d-1 for pyrene, 8.9 mg l-1 d-1 for chrysene, 1.8 mg l-1 d-1 for benzo[a]pyrene and 0.37 mg l-1 d-1 for perylene. Micro-organisms from the interface were slightly more effective in degrading PAHs than those from the aqueous phase.     

Widespread environmental contamination in agricultural soils and human health risk at the vicinity of an oil refinery site

In this research, carcinogenic and non-carcinogenic human health risks due to polycyclic aromatic hydrocarbons (PAHs) were investigated via three exposure pathways: accidental ingestion of soil, dermal contact of soils, and contaminated vegetable ingestion. To determine the contaminant concentrations in soil, samples were collected from areas adjacent to the Tehran oil refinery, located in Shahr-e-Ray city, Iran. Analyses of the samples indicated that the average of PAHs concentration in the soil samples were greater than clean-up level guidelines. Cancer risk of contaminants due to ingestion of cultivated vegetables that are sold in Tehran markets was significant in comparison with other exposure pathways. Moreover, the total cancer risk for 5th percentile, 95 upper confidence limit, and 95th percentile concentration of contaminants were 5.69E-04, 8.78E-02, and 2.13E-01, classifying the site as having a significant cancer risk potential. Furthermore, non-carcinogenic health risk analyses for the contaminants demonstrated hazard index of less than 1. Remediation of the soils is highly recommended to eliminate the potential cancer risks and prevent the contamination of the food chain for approximately 10 million Tehran residents.