Non-carcinogenic Polycyclic Aromatic Hydrocarbons Research Articles

Benzo[a]pyrene and total polycyclic aromatic hydrocarbons (PAHs) levels in vegetable oils and fats do not reflect the occurrence of the eight genotoxic PAHs

Concentrations of polycyclic aromatic hydrocarbons (PAHs) were determined in 115 samples of olive oil (extra virgin olive oil, virgin olive oil, olive oil, pomace olive oil and blended olive oil), cooking oil (corn oil, sunflower oil, sesame oil, palm olein oil, soya oil, canola oil, mustard oil, peanut oil and mixed vegetable oil) and fat (butter and table margarine) collected from retail stores in Kuwait. Carcinogenic benzo[a]pyrene (BaP) was detected in 43% of the samples analyzed. Benz[a]anthracene and chrysene were detected in 37 and 45% of the samples, respectively, that did not contain BaP. Of the individual non-carcinogenic PAHs, naphthalene showed the highest mean concentration (14 µg kg−1), while for the carcinogenic PAHs, BaP (0.92 µg kg−1) and chrysene (0.87 µg kg−1) showed the highest mean values. Approximately 20% of the samples within the olive oil and cooking oil sub-categories exceeded the EU maximum tolerable limit for BaP, with the highest level of 6.77 and 11.1 µg kg−1, respectively. For the fat sub-category, 9% of the samples exceeded the tolerance limit, with the highest level of 3.67 µg kg−1. The Kuwaiti general population's dietary exposure to the genotoxic PAHs (PAH8: benz[a]anthracene, chrysene, benzo[b]fluoranthene, benzo[k]fluoranthene, benzo[a]pyrene, indeno[1,2,3-cd]pyrene, dibenz[a,h]anthracene and benzo[ghi]perylene) was estimated to be 196 ng day−1 (3.3 ng kg−1 bw day−1, assuming an average adult body weight of 60 kg). Results indicated that PAH8 and BaPeq (total sum benzo[a]pyrene equivalents) are more reliable measures of the concentrations of other carcinogenic PAHs in oil and fat samples, while BaP and PAHs alone are not good indicators of the occurrence or degree of contamination by carcinogenic PAHs in these food products.

Polychlorinated biphenyls, organochlorine pesticides, and polycyclic aromatic hydrocarbons in wild, farmed, and frozen marine seafood marketed in Campania, Italy.

Polychlorinated biphenyls (PCBs), organochlorine pesticides, and polycyclic aromatic hydrocarbons (PAHs) were detected in fresh-catch, farmed, and frozen marine fish marketed in Campania, Italy. Additionally, polychlorobiphenyl congeners were found: six were non-dioxin-like (NDL-PCB) (IUPAC no. 28, 52, 101, 138, 153, and 180), and one was dioxin-like (DL-PCB) (IUPAC no. 118). In all, 93% of fresh-catch, 100% of aquaculture, and 74% of the frozen specimens contained PCBs at concentrations varying from 0.12 to 35.11 ng/g, wet weight; NDL-PCBs ranged between 0.12 and 32.44 ng/g. Penta-, hexa-, and heptachlorobiphenyls were predominant. Regarding organochlorine pesticides, hexachlorobenzene was detected in 35% of fresh catch, 36% of farmed, and 46% of the frozen fish specimens, in a range between < 0.01 and 3.29 ng/g. Contents of the dichlorodiphenyltrichloroethane isomer amounted to 0.12 to 11.00 ng/g. Finally, PAHs were detected in 100% of the specimens. Benzo[a]pyrene was detected in 66% of the aquaculture, 35% of the fresh catch, and 24% of the frozen species, at concentrations varying from 0.03 to 9.18 ng/g. On the basis of annual fish consumption, an average daily intake of NDL-PCBs of 6.02 ng/kg of body weight was estimated. Calculated daily hexachlorobenzene and total dichlorodiphenyltrichloroethane intakes were, respectively, 0.11 and 0.90 ng/kg of body weight per day. The contribution of fish to the daily consumption of the noncarcinogenic PAHs can be considered low; for benzo[a]pyrene, the estimated daily intake is considerably lower than the doses considered carcinogenic for experimental animals by the European Union Scientific Committee on Food.

Risk Assessment as a Decision-Making Tool for Treatment of Emissions at a New Aluminum Smelter in Iceland: 2. Human Health Risk Assessment

ABSTRACT Alcoa recently constructed the Fjarðaál aluminum smelter in Reyðarfjörður, East Iceland. The smelter is designed to produce a maximum of 346,000 metric tons per year of aluminum. A risk assessment was conducted to evaluate the differential human health risk related to estimated potential air emissions from the planned Fjarðaál smelter with and without seawater scrubbers. Air-dispersion modeling results provided for particulate matter (PM10), sulfur dioxide (SO2), hydrogen fluoride (HF), and polycyclic aromatic hydrocarbons (PAHs) were compared to ambient air standards or air quality guidelines from Norway, Iceland, or European directives and from the U.S. Environmental Protection Agency. Risk estimates were calculated for PAHs. Modeled air estimates were mapped geospatially, to identify potential receptors, including onsite outdoor worker, seagoing worker, hypothetical fence-line resident, future hypothetical resident, closest current resident, residents in neighboring villages, closest farmer, and a visitor to the nearby Holmanes Nature Reserve. Both with and without seawater scrubbers, the predicted exceedances of standards per year for SO2 were well below the maximum number allowed. Use of seawater scrubbers was predicted to decrease average SO2 air concentration estimates in the short term; however, annual estimates were lower without seawater scrubbers. Risk estimates for carcinogenic and non-carcinogenic PAHs, and modeled air concentrations of HF and PM10, were well within acceptable levels.

A metabolomics based approach to assessing the toxicity of the polyaromatic hydrocarbon pyrene to the earthworm Lumbricus rubellus

The biochemical response of the earthworm Lumbricus rubellus to pyrene exposure was assessed using 1H nuclear magnetic resonance (NMR) spectroscopy, gas chromatography mass spectrometry (GC–MS) and pattern recognition techniques. Both analytical methods enabled the establishment of reproducible metabolic profiles. NMR analysis identified a total of 32 metabolites while GC–MS identified 51. The results demonstrate that not only is pyrene toxic to L. rubellus, but that alterations in its normal metabolic profile could be observed even when individuals were exposed to concentrations of 40 mg kg −1: a pollution level that is both below the concentration previously found to significantly reduce reproduction and within the range of polycyclic aromatic hydrocarbons (PAHs) found on some contaminated sites. Pyrene was found to cause a dose dependant decrease in lactate and the concentrations of the saturated fatty acids tetradecanoic, hexadecanoic and octadecanoic acid and an increase in production of the amino acids alanine, leucine, valine, isoleucine, lysine, tyrosine and methionine. It is proposed that this indicates impaired glucose metabolism, with an associated increase in fatty acid metabolism and changes in TCA cycle intermediates. This study demonstrates the versatility of metabolomics as a tool to monitor toxicity in the environment as opposed to utilising model species studied in a laboratory setting. Since it is a non-carcinogenic PAH, we propose that the metabolic changes observed in worms may reflect the non-specific toxic effects of pyrene as a typical, non-polar organic compound.

Blood Levels of Polycyclic Aromatic Hydrocarbons in Children of Lucknow, India

Polycyclic aromatic hydrocarbons (PAHs) are compounds with two or more fused benzene rings produced by incomplete combustion of organic substances involved in natural and anthropogenic processes. Children are exposed to these compounds through inhalation, dietary ingestion, and, also, soil at the playground. It has been well established that PAHs have carcinogenic, mutagenic, and teratogenic effects. Considering possible health risks due to PAHs exposure among children, the present study was carried out in collaboration with the Pediatrics Department, King George's Medical University (KGMU), Lucknow, to determine its exposure in children by estimating blood PAHs levels. Due to the variable composition of PAHs mixtures emitted from different environmental sources, any single compound or metabolite may not be representative of all exposure conditions. For these reasons, the measurement of blood PAHs levels as a possible biomarker, especially of the EPA (Environmental Protection Agency, USA) priority list, has been proposed. Acenaphthylene, anthracene, phenanthrene, fluoranthene, naphthalene, pyrene, benzo(b)fluoranthene, benzo(k)fluoranthene, and benzo(a)pyrene were determined by HPLC-FD/UV. On the basis of the individual compound, the median (50th percentile) of naphthalene (19 ppb) was highest, however, benzo(a)pyrene (4.0 ppb) level was found to be lowest among all detected PAHs. The median level of total noncarcinogenic PAHs (113.55 ppb) was higher than the total carcinogenic PAHs (32.35 ppb) in blood samples of children. A significant correlation was found between period of time spent in the surrounding breathing zone of the cooking place and total noncarcinogenic PAHs (p < 0.05), while the blood carcinogenic PAHs level in children was found to be associated with lower status of their families (p < 0.05). It is speculated that there may be chances of health hazards through exposure to PAHs, those not yet declared hazardous and present at higher concentrations in the Indian environment. Further study with a larger sample size and accompanying environmental data is desired to validate the findings of this pilot study and strengthen the database of PAHs exposure in India.

Bitumen products alter bax, bcl‐2 and cytokeratin expression: An in vivo study of chronically exposed road pavers

The skin of road pavers is chronically exposed to bitumen fumes, a mixture of volatile compounds and particles, containing several carcinogenic and non-carcinogenic polycyclic aromatic hydrocarbons. Bitumen fumes can alter cutaneous barrier integrity in various ways and induce skin diseases. The present study was devised to investigate the expression of apoptosis proteins (bax and bcl-2) and the cytokeratin pattern in skin specimens from road paving workers exposed to bitumen fumes using immunohistochemical techniques. Skin forearm punch biopsies from 16 occupationally exposed workers and an unexposed control group were processed for immunohistochemistry using a broad-spectrum anti-cytokeratin antibody and monoclonal antibodies for bax and bcl-2 immunostaining. Urinary 1-hydroxypyrene (1-OHP) was also determined. Morphological specimen evaluation showed epidermal thinning of exposed skin and flattened dermal papillae. In sections from exposed subjects, grade 3 bax overexpression and cytokeratin immunoreaction was detected in all layers, while bcl-2 expression was downregulated (grade 1) and confined to the basal layer. There was a significant difference in 1-OHP values between road pavers and the control group (p < 0.05). Overexpression of the cytokeratin pattern and bax and underexpression of bcl-2 in chronically bitumen-exposed skin suggest that bitumen fumes induce activation of apoptosis as a defense mechanism.

Genotoxic effects of bitumen fumes in Big Blue ® transgenic rat lung

Road paving workers are exposed to bitumen fumes (CAS No. 8052-42-4), a complex mixture of volatile compounds and particles containing carcinogenic and non-carcinogenic polycyclic aromatic hydrocarbons. However, epidemiological and experimental animal studies failed to draw unambiguous conclusions concerning their toxicity. In order to gain better insights on their genotoxic potential, we used an experimental design able to generate bitumen fumes at road paving temperature (temperature: 170 °C, total particulate matter: 100 mg/m 3) and perform a nose-only exposure of Big Blue ® transgenic rodents 6 h/day for five consecutive days. The mutagenic properties of bitumen fumes were determined by analyzing the mutation frequency and spectrum of the neutral reporter gene cII inserted into the rodent genome. We previously observed in mouse lung, that bitumen fumes did not induce an increase of cII mutants, a modification of the mutation spectrum, nor the formation of DNA adducts. Since DNA adducts were found in the lungs of rats exposed to asphalt fumes in similar conditions, we decided to carry out an analogous experiment with Big Blue ® rats. A DNA adduct was detected 3 and 30 days after the end of treatment suggesting that these genetic alterations were quite steady. Thirty days after exposure, the cII mutant frequency was similar in control and exposed rats. In addition, a slight but not significant modification of the mutation spectrum associated with an increase of G:C to T:A and A:T to C:G transversions was noticeable in the treated animals. Then, these data failed to demonstrate a pulmonary mutagenic potential for bitumen fumes generated at road paving temperature in our experimental conditions despite the presence of a DNA adduct. These results may provide information concerning the pulmonary mechanism of action of this aerosol and may contribute to the occupational health hazard assessment.

Effect of some carcinogenic and non-carcinogenic polycyclic aromatic hydrocarbons on gap junction intercellular communication in hepatoma cell cultures

One of the systems that regulate tissue homeostasis is gap junction intercellular communication (GJIC). It is accepted that the down-regulation of GJIC is linked to the tumor-promoting properties of carcinogens. In this study, the effect of some carcinogenic and non-carcinogenic polycyclic aromatic hydrocarbons (PAH) on GJIC was investigated. It was found that in hepatoma cell culture (Hep G2) carcinogenic PAH inhibited GJIC after 24 h exposure by 75–100% depending on the PAH structure. The inhibition effect on GJIC is reversible because removing the PAH by changing of culture medium restores the GJIC. The non-carcinogenic PAH do not significantly influence GJIC. α-Naphthoflavone, an inhibitor of PAH metabolism, has no effect on inhibition of GJIC by carcinogenic PAH. 2,3,7,8-Tetrachloro- p-dibenzodioxin, an aryl hydrocarbon (Ah) receptor ligand, inhibits GJIC by about 50% only after 48 h exposure. To clarify the role of formation of PAH metabolites and interaction with Ah receptor on inhibition of GJIC, we determined the effect of benzo/a/pyrene on hepatoma G27 cells in which neither mRNA of CYP1A1 nor Ah receptor was determined. As in Hep G2 cells, benzo/a/pyrene, unlike non-carcinogenic benzo/e/pyrene, inhibits GJIC. We conclude that in the studied hepatoma cells carcinogenic PAH inhibit GJIC directly (that is, not via their metabolites) and this effect is not associated with Ah receptor interaction.

Occupational exposure profiles of polycyclic aromatic hydrocarbons in coke oven workers

To study the characteristics of occupational exposure of polycyclic aromatic hydrocarbons (PAHs) in coke oven workers. Samples were collected individually and PAHs concentration in the ambient air were assayed by high performance liquid chromatography (HPLC) and toxic equivalency factors (TEFs) were introduced to assess the carcinogenic potency. The levels of PAHs occupational exposure in oven workers at topside was higher than at side oven and bottom oven (P < 0.05). Non-carcinogenic PAHs were more than 70% of total PAHs and benzo[a]pyrene accounted for 65.5% approximately 72.4% of total benzo[a]pyrene equivalents. Total occupational exposure level of PAHs in coke oven workers was positively related to the content of benzo[a]pyrene and pyrene, respectively (r(2) = 0.84, r(2) = 0.94, P < 0.05). Coke oven workers were exposed to a high level of PAHs which possessed some extent of carcinogenic potency, and benzo[a]pyrene is the chief carcinogenic substance.

Toxicological and biochemical responses of the earthworm Lumbricus rubellus to pyrene, a non-carcinogenic polycyclic aromatic hydrocarbon

The effects of the polycyclic aromatic hydrocarbon (PAH) pyrene on earthworms were investigated in contact and soil tests. In addition to measuring toxic effects on survival and reproduction, Ethoxyresorufin- o-deethylase (EROD) activity and catalase activity were also studied as possible biomarkers of toxic stress. The survival data indicated that LC 50 values were 0.0068 mg/ml for the contact test, and 283 mg/kg in the soil test. Cocoon production rate was significantly reduced compared to controls at 160, 640 and 2560 mg/kg in the soil test. No EROD activity could be detected in preliminary studies using control and exposed animals from the contact test, so this assay was not used to the soil test. Catalase activity was shown to be significantly lower at 640 mg/kg in the soil test compared to all other treatments and the control. When compared to toxicological data for other soil invertebrates, Lumbricus rubellus has an intermediate sensitivity in respects of survival and a lower sensitivity for reproductive effects, although the soil used in this study had a higher organic content than previous studies, meaning that the sensitivity of this species may be underestimated in comparison to previous published data for other soil invertebrates.

Inhibition of gap junction intercellular communications in cell culture by polycyclic aromatic hydrocarbons (PAH) in the absence of PAH metabolism.

We have studied the effect of polycyclic aromatic hydrocarbons (PAH) on gap junction intercellular communications (GJIC) in culture of hepatoma cells Hep G2 and G27. Carcinogenic PAH inhibited GJIC in both cultures in contrast to non-carcinogenic PAH. We showed that both constitutive and inducible expressions of mRNAs of Ah receptor and cytochrome P4501A1 (the main isoform involved in PAH metabolism) were absent in hepatoma G27 cells. We concluded that the initial, non-metabolized molecules of carcinogenic PAH are responsible for changes in GJIC through interaction with an unknown factor in the cellular membrane.

Naphthalene--an environmental and occupational toxicant.

For many years naphthalene had been considered as a non-carcinogenic polycyclic aromatic hydrocarbon (PAH). Airborne naphthalene concentrations have always been observed to be below the limit values of various national committees, such as the threshold limit value (TLV) of the American Conference of Governmental Industrial Hygienists (ACGIH) and the MAK of the Deutsche Forschungsgemeinschaft (DFG) (10 ppm). Since 2000, when the US National Toxicology Program revealed clear evidence of the carcinogenic activity of naphthalene in rats, international agencies [the International Agency for Research on Cancer (IARC), the US Environmental Protection Agency (US EPA), DFG] have reclassified naphthalene as a potential human carcinogen, and the European Union (EU) is currently preparing a new risk assessment report. It is presently unknown how to protect humans from health risks resulting from occupational and environmental naphthalene exposure. Knowledge about the external and internal exposure of humans serves as the key determinant in a comprehensive risk assessment. We review here ambient monitoring studies concerning the external naphthalene exposure that results from ubiquitous environmental sources (indoor and outdoor air, water, soil, food) and from a variety of critical workplaces (coking plants, creosote impregnation, distillation of coal tar and naphthalene, manufacture of refractories, graphite electrodes, aluminium and mothballs). Based on results of ambient monitoring studies published so far, a new hygiene-based exposure limit of 1.5 mg naphthalene per cubic metre of air (0.3 ppm) is proposed. Furthermore, results from biological monitoring studies are summarised in this article. The internal burden was almost exclusively determined by means of the urinary metabolites 1-naphthol and 2-naphthol, but it is currently not possible for one to evaluate a biological tolerance level (BAT) or a biological exposure index (BEI). Based on the toxicokinetics and metabolism of naphthalene, the central question on its carcinogenicity is briefly sketched. Naphthoquinones play an important role in this context. Their adducts with macromolecules may be the parameters of choice for the estimation of effects to human health.

A QSAR Model of PAHs Carcinogenesis Based on Thermodynamic Stabilities of Biactive Sites.

Polycyclic aromatic hydrocarbons (PAHs) have been adopted to study the carcinogenesis of chemicals experimentally and theoretically. A model of carcinogenic activity of 48 PAHs was obtained based on the calculated relative thermodynamic stabilities of epoxide and carbonium intermediates of the PAHs. Using both epoxyl-energy and cationized-energy of two active sites, the model reasonably predicts the carcinogenic activity of these PAHs and shows a good ability to distinguish between carcinogenic and noncarcinogenic PAHs. Furthermore, the model suggests that double active sites and their distance characteristics are important factors in the chemical carcinogenesis of PAHs. The physical meaning of the energies corresponding addition reactions with DNA is also discussed.

A QSAR model of PAHs carcinogenesis based on thermodynamic stabilities of biactive sites.

Polycyclic aromatic hydrocarbons (PAHs) have been adopted to study the carcinogenesis of chemicals experimentally and theoretically. A model of carcinogenic activity of 48 PAHs was obtained based on the calculated relative thermodynamic stabilities of epoxide and carbonium intermediates of the PAHs. Using both epoxyl-energy and cationized-energy of two active sites, the model reasonably predicts the carcinogenic activity of these PAHs and shows a good ability to distinguish between carcinogenic and noncarcinogenic PAHs. Furthermore, the model suggests that double active sites and their distance characteristics are important factors in the chemical carcinogenesis of PAHs. The physical meaning of the energies corresponding addition reactions with DNA is also discussed.

Selective clonal expansion and microenvironmental permissiveness in tobacco carcinogenesis.

Historically our knowledge about the direct carcinogenic activity of cigarette smoke and its constituents grew from painting experiments on the skin of mice to produce papillomas and carcinomas. The neutral fraction of cigarette smoke condensate had most of the carcinogenic activity in this test and was rich in carcinogenic polycyclic aromatic hydrocarbons (PAHs), the most abundant by far being BP. However, the concentration of BP in the condensate was only about 2% the amount of pure BP required to cause skin tumors. In other fractions there were non-carcinogenic constituents that promoted tumor formation when applied repeatedly to mouse skin that had been initiated by a single subcarcinogenic application of BP. There were also constituents of cigarette smoke that acted as co-carcinogens when applied simultaneously with repeated applications of BP. BP was effective as an initiator at lower concentrations than as a complete carcinogen, and some non-carcinogenic PAHs in the condensate were also active initiators. It was concluded from these studies that cigarette smoke condensate is primarily a tumor-promoting and co-carcinogenic agent with weak activity as a complete carcinogen. A major effect of promoters, and possibly of co-carcinogens, is a diffuse hyperplasia which includes selective expansion of clones carrying endogenous mutations and/or mutations induced by PAHs and other carcinogens such as NNK. The induced mutations as well as damaged cells would occur throughout the exposed region and, along with the hyperplasia, increase the permissiveness of the cellular microenvironment for neoplastic expression of any potential tumor cell in its midst. Since neither the promoters nor co-carcinogens in tobacco smoke are known to interact directly with DNA, their effects can be considered epigenetic processes that act upon genetically altered cells. Examples are cited from studies of experimental skin carcinogenesis, smoking-induced histopathological changes in human lung and spontaneous transformation in cell culture to illustrate the genetic and epigenetic interactions of neoplastic development in general and their significance for smoking-induced lung cancer in particular. Certain dietary modifications that appear to be effective in moderating the promotional phase of animal and human carcinogenesis are suggested for trial in managing lung cancer.

Indoor Air Pollution in a Zone of Extreme Poverty of Metropolitan Santiago, Chile

Few studies have been done on indoor air pollution in areas of extreme poverty in developing countries. In such countries, for economic reasons, people use solid fuel for cooking and heating fuels which by incomplete combustion generate high levels of toxic pollutants. These represent an important risk factor for human health. We have investigated the levels of carbon monoxide (CO), sulphur dioxide (SO₂), respirable particulate matter (PM₁₀ ), polycyclic aromatic hydrocarbons (PAHs) and mutagenicity in the PM₅ fraction, as well as temperature and humidity, in the interior of 24 houses in La Pintana, Santiago. In addition, we have conducted a survey about symptoms, signs and respiratory diseases possibly associated with socio-economic factors in the area. The survey showed that in children younger than 2 years, most respiratory diseases occur during winter (75%), the most frequent complaint being bronchitis (62%) and obstructive bronchitis (50%). The higher pollutant concentrations were observed during heating hours, in houses that used coal (mean PM₁₀ 250 µg·m^–3, CO 42 ppm, SO₂ 192 ppb) or firewood (mean PM₁₀ 489 µg·m^–3, CO 57 ppm, SO₂ 295 ppb). PAHs were detected in all houses and we concluded that they came from inside the house and not from outdoor infiltration. Coal, firewood and cigarette smoke were important sources of mutagenic and carcinogenic PAHs, whereas kerosene and gas contributed mainly to the non-carcinogenic PAH fraction. In the houses studied, the population was exposed to levels of toxic pollutants that are much higher than those found outdoors in the highly polluted city of Santiago. In addition, overcrowding, excessive indoor humidity, very low indoor temperatures when the heating system was turned off, the presence of domestic animals, cats and dogs indoors and general lack of hygiene (with attendant bacteria and fungi) are risk factors to explain the high incidence of respiratory diseases in children.

DNA adducts as a biomarker of polycyclic aromatic hydrocarbon exposure in aquatic organisms: relationship to carcinogenicity

The use of DNA adduct measurement as a biomarker of exposure to polycyclic aromatic hydrocarbons (PAHs) is now well established in ecotoxicology. In particular, DNA adduct levels in aquatic organisms has been found to produce a better correlation with PAH exposure than PAH concentrations in organisms. DNA adducts levels are most commonly determined using the 32P-postlabelling assay which measures total aromatic adducts. The relationship between relative DNA adduct formation and carcinogenicity has been investigated for a number of carcinogenic and non-carcinogenic PAHs using an in vitro system. Our results demonstrate that relatively high levels of DNA adducts can be produced by some non-carcinogenic PAHs, while other non-carcinogenic compounds do not produce detectable adducts. In addition, it has been shown that all carcinogenic PAHs investigated produce DNAadducts and that a relationship exists between relative adduct formation and carcinogenic potency. An investigation of adduct levels in fish liver and crustacean hepatopancreas in Oxley Ck, Brisbane has shown that higher than expected DNA adduct levels were correlated with the presence of carcinogenic and non-carcinogenic PAHs with high relative adduct forming potential.

Extraction Method for Analysis of PAHs in Coal-Tar-Contaminated Soils

A direct solvent-extraction method was evaluated to assess its application for the extraction and analysis of PAHs (polycyclic aromatic hydrocarbons) in coal-tar-contaminated soils. Eight individual solvents and two combined solvents were used in a screening test to determine the suitability of different solvents for the direct solvent-extraction method. Based on the extracted concentrations of the Total PAH, noncarcinogenic PAH (N-PAH), and carcinogenic PAH (C-PAH), three different solvents—acetone, ethanol, and methylene chloride—were selected for further investigation by testing these solvents on four coal-tar-contaminated soils and a certified PAH-contaminated soil. The extraction results for the Total PAH and N-PAH concentrations showed that there were no statistical differences for the three solvents at a confidence interval of 95%. However, ethanol gave lower concentrations of C-PAH than acetone and methylene chloride. Fifteen coal-tar-contaminated soil samples from a land farming treatment unit were used to compare the direct solvent-extraction method using acetone as the extraction solvent with the conventional Soxhlet extraction method (EPA Method 3540) and ultrasonic extraction method (EPA Method 3550). The results showed that the direct solvent-extraction method gave higher mean PAH concentrations than the Soxhlet and ultrasonic extraction method and that the direct extraction method was equivalent to the Soxhlet method at a confidence interval of 99%. Because of its simplicity of use and its equivalent extraction capability with the Soxhlet extraction method, the direct solvent-extraction method may be used as a technique for the extraction and analysis of PAHs in contaminated soil.

Carcinogenic polycyclic aromatic hydrocarbons increase intracellular Ca2+ and cell proliferation in primary human mammary epithelial cells.

Previous studies have shown that polycyclic aromatic hydrocarbons (PAHs) mobilize intracellular Ca2+ in human T cells by inositol trisphosphate-dependent mechanisms resulting from activation of phospholipase C-gamma by SRC-related protein tyrosine kinases, thereby mimicking antigen-receptor activation. Ca2+ appears to play an important second messenger role in growth factor control of cell proliferation in human mammary epithelial cells (HMEC), such as the epidermal growth factor receptor pathway. The purpose of the present studies was to determine if PAHs are able to increase intracellular Ca2+ in primary cultures of HMEC and increase cell proliferation. Two carcinogenic and two non-carcinogenic PAHs were tested for their ability to increase intracellular Ca2+ in HMEC. The carcinogenic PAHs dimethylbenz[a]anthracene (DMBA) and benzo[a] pyrene (BaP) were able to cause Ca2+ elevation in HMEC at early time points (2 h) and caused sustained alterations in Ca2+ homeostasis (18 h). DMBA showed maximal effects at early time points (2 h), while BaP showed maximal effects on sustained Ca2+ (18 h). 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a potent dioxin and tumor promoter, produced maximal Ca2+ elevation at 2 h, with a return to near baseline levels by 6 h. The non-carcinogenic PAHs benzo[e]pyrene and anthracene did not significantly alter intracellular Ca2+ at any time point. alpha-Naphthoflavone significantly reduced the Ca2+ response induced by BaP treatment, but not by DMBA or TCDD, suggesting that P450 1A or 1B metabolism of BaP may be important in the sustained Ca2+ elevating response. In evaluating the effects of BaP on HMEC proliferation, BaP was found to increase the number of cells recovered after 4 days in culture in the absence or presence of various concentrations of epidermal growth factor. These studies provide initial evidence that Ca2+ signaling may be associated with mitogenesis in HMEC, which may play a role in tumor promotion and progression produced by PAHs.

Determination of polycyclic aromatic hydrocarbons in smoked fishery products from different smoking kilns.

The levels of 13 polycyclic aromatic hydrocarbons (PAH) were determined by an HPLC method with fluorescence and UV detection and by a GC/MS technique in smoked fishery products from modern smoking kilns with external smoke generation and from traditional smoking kilns. The average benzo(a)pyrene (BaP) concentration of all 35 samples from commercial smoking kilns with external smoke generation was 0.1 microgram/kg (wet weight) and the sum of the carcinogenic compounds determined in the study, i.e. benz(a)anthracene, chrysene, benzo(b)fluoranthene, benzo(k)fluoranthene, benzo(a)pyrene, dibenz(a,h)anthracene and indeno(1,2,3-c,d)pyrene did not exceed 4.5 micrograms/kg (wet weight). The BaP levels of the 27 smoked fish samples from traditional kilns ranged from 0.2 microgram/kg to 4.1 micrograms/kg, with a mean value of 1.2 micrograms BaP/kg. The average concentration of the sum of the carcinogenic compounds was 9.0 micrograms/kg. Large variations were found in the content of the non-carcinogenic PAHs phenanthrene, anthracene, fluoranthene and pyrene in all samples from both types of smoking kilns.