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PubMed1998

Potency equivalency factors for some polycyclic aromatic hydrocarbons and polycyclic aromatic hydrocarbon derivatives.

Potency equivalency factors (PEFs) for cancer induction relative to benzo[a]pyrene have been derived for 21 polycyclic aromatic hydrocarbons (PAHs) and PAH derivatives based on a data preference scheme. PEFs have been derived only for PAHs with demonstrated carcinogenicity in bioassays. Cancer potency values and inhalation unit risks are presented for four additional carcinogenic PAHs based on expedited risk assessments conducted for California's Proposition 65. A much larger number of PAHs and PAH derivatives are considered mutagenic or genotoxic and may have limited evidence for carcinogenicity, but these compounds are not considered in this evaluation. New cancer bioassay data and possibly structure-activity analysis may indicate that additional PAHs are carcinogenic. Thus, additional PAHs may be identified as potential human carcinogens when such data become available. However, until that time the PEFs proposed for use in risk assessment were estimated only for PAHs currently classified as carcinogens.

Animals↗
PubMed2005

CYP1A1-mediated mechanism for atherosclerosis induced by polycyclic aromatic hydrocarbons.

Polycyclic aromatic hydrocarbons (PAHs) have been known to induce atherosclerosis. It has been reported that the metabolic activation of PAHs by cytochrome P450 (CYP) is an important step for PAH-induced atherosclerosis. We recently reported that PAHs down-regulated the liver X receptor (LXR) alpha-regulated genes via aryl hydrocarbon receptor (AHR) as one of the causes responsible for atherosclerosis induced by PAHs. Thus, the aim of this study was to clarify the role of CYP1A1 in the suppression of LXR-mediated signal transductions by 3-methlychoranthrene (MC), one of the PAHs. We found that LXR-mediated transactivation was inhibited by the PAH, but not by halogenated aromatic hydrocarbon, which is scarcely metabolized by CYP1A1. The repression of LXR-mediated signal transductions by MC was restored by co-treatment of HepG2 cells with a CYP1A1 inhibitor, alpha-naphthoflavone, and by the transfection of short interference RNA for CYP1A1. Based on these lines of evidence, we propose that the metabolic activation of PAHs by CYP1A1, but not the activation of AHR by PAHs, is a direct mechanism for atherosclerosis via the suppression of LXR-mediated signal transductions.

Animals↗
PubMed1995

An efficient route to N6 deoxyadenosine adducts of diol epoxides of carcinogenic polycyclic aromatic hydrocarbons.

Polycyclic aromatic hydrocarbons are metabolized to a wide variety of oxidized derivatives, including highly reactive diol epoxides which alkylate DNA. The reaction lacks regio- or stereospecificity but occurs primarily at the exocyclic amino groups of deoxyguanosine and deoxyadenosine. An efficient route to N6 adducts of deoxyadenosine is described using as examples those arising from trans opening of the anti-tetrahydrodiol epoxides of naphthalene, benzo[a]pyrene, and benzo[c]phenanthrene. The adducts were synthesized in 50-92% yields by reaction of 6-fluoropurine 2'-deoxyriboside with aminotriols formed by trans opening of racemic dihydrodiol epoxides using liquid NH3. The diastereomeric adducts were separated by HPLC and their absolute configurations were assigned by circular dichroism. 1H NMR studies revealed significant differences in conformation of the tetrahydroaromatic ring between the sterically unrestricted naphthalene derivative and the sterically congested derivatives of benzo[a]pyrene and benzo[c]phenanthrene. These differences may have a bearing on the higher carcinogenicity shown by the latter hydrocarbons. Undecadeoxyoligonucleotides bearing regio- and stereochemically defined adenine N6-anti-trans-benzo[a]pyrene adducts have been prepared.

Base Sequence↗
PubMed2005

A possible mechanism for atherosclerosis induced by polycyclic aromatic hydrocarbons.

Polycyclic aromatic hydrocarbons (PAHs), aryl hydrocarbon receptor (AHR) ligands, induce atherogenesis. Liver X receptor (LXR) alpha is known to be involved in the control of cholesterol homeostasis. Thus, the purpose of this study was to investigate the effects of 3-methlycholanthrene (MC), one of the PAHs, on LXRalpha-mediated signal transductions. We found that expression of mRNAs for ATP binding cassette A1, sterol regulatory element binding protein 1c (SREBP-1c), fatty acid synthase, and stearoyl-CoA desaturase was suppressed by treatment of HepG2 cells with MC. A luciferase reporter assay revealed that LXRalpha- and SREBP-1c-mediated transactivations were inhibited by MC via AHR. Based on these lines of evidence, we propose that down-regulation of the LXRalpha-regulated genes by PAHs is one of the causes responsible for atherosclerosis induced by PAHs.

Arteriosclerosis↗
PubMed2004

Bioavailability and risk assessment of orally ingested polycyclic aromatic hydrocarbons.

Polycyclic aromatic hydrocarbons (PAHs) are a family of toxicants that are ubiquitous in the environment. These contaminants generate considerable interest, because some of them are highly carcinogenic in laboratory animals and have been implicated in breast, lung, and colon cancers in humans. These chemicals commonly enter the human body through inhalation of cigarette smoke or consumption of contaminated food. Of these two pathways, dietary intake of PAHs constitutes a major source of exposure in humans. Although many reviews and books on PAHs have been published, factors affecting the accumulation of PAHs in the diet, their absorption following ingestion, and strategies to assess risk from exposure to these hydrocarbons following ingestion have received much less attention. This review, therefore, focuses on concentrations of PAHs in widely consumed dietary ingredients along with gastrointestinal absorption rates in humans. Metabolism and bioavailability of PAHs in animal models and the processes, which influence the disposition of these chemicals, are discussed. The utilitarian value of structure and metabolism in predicting PAH toxicity and carcinogenesis is also emphasized. Finally, based on intake, disposition, and tumorigenesis data, the exposure risk to PAHs from diet, and contaminated soil is presented. This information is expected to provide a framework for refinements in risk assessment of PAHs from a multimedia exposure perspective.

Administration, Oral↗
PubMed2005

Human CD34-positive hematopoietic stem cells constitute targets for carcinogenic polycyclic aromatic hydrocarbons.

Polycyclic aromatic hydrocarbons (PAHs) are major carcinogenic environmental contaminants known to exert bone marrow toxicity and to induce leukemias, suggesting that these chemicals target hematopoietic stem cells. To investigate this hypothesis, we studied the effects of PAHs on cell proliferation and differentiation in human hematopoietic CD34+ cell cultures. Benzo(a)pyrene (BP), a prototypical PAH, was shown to markedly impair CD34+ cell expansion and to inhibit CD34+ cell differentiation into various hematological cell lineages, including erythroid, granulomacrophagic, and megakaryocytic lineages. This was associated with the induction of a caspase- and mitochondrion-related apoptosis process. CD34+ progenitor cells were found to exhibit functional expression of the aryl hydrocarbon receptor (AhR), and the use of the pure AhR antagonist 3'-methoxy-4'-nitroflavone partially counteracted the deleterious effects of BP in CD34+ cell cultures, underlining the involvement of AhR in BP toxicity. Additional events such as CYP1A1/1B1-dependent PAH metabolism and adduct formation were also required since 1) 2,3,7,8-tetrachlorodibenzo-p-dioxin, a very potent ligand of the AhR that is poorly metabolized and therefore does not generate reactive metabolites in contrast to PAHs, failed to affect CD34+ cell expansion; 2) the CYP1A1/1B1 inhibitor alpha-naphthoflavone blocked both BP adduct formation and BP toxicity; and 3) benzo(a)pyrene-trans-7,8-dihydrodiol-9,10-epoxide, a highly reactive BP metabolite, exerted a marked toxicity toward CD34+ cell cultures. Overall, these data indicate that human hematopoietic CD34+ cells can bioactivate chemical carcinogens such as PAHs and, in this way, constitute targets for such carcinogenic environmental contaminants.

Antigens, CD34↗
PubMed2005

Parking lot sealcoat: an unrecognized source of urban polycyclic aromatic hydrocarbons.

Polycyclic aromatic hydrocarbons (PAHs) are a ubiquitous contaminant in urban environments. Although numerous sources of PAHs to urban runoff have been identified, their relative importance remains uncertain. We show that a previously unidentified source of urban PAHs, parking lot sealcoat, may dominate loading of PAHs to urban water bodies in the United States. Particles in runoff from parking lots with coal-tar emulsion sealcoat had mean concentrations of PAHs of 3500 mg/kg, 65 times higher than the mean concentration from unsealed asphalt and cement lots. Diagnostic ratios of individual PAHs indicating sources are similar for particles from coal-tar emulsion sealed lots and suspended sediment from four urban streams. Contaminant yields projected to the watershed scale for the four associated watersheds indicate that runoff from sealed parking lots could account for the majority of stream PAH loads.

Construction Materials↗
PubMed2002

Slurry-phase ozonation for remediation of sediments contaminated by polycyclic aromatic hydrocarbons.

Polycyclic aromatic hydrocarbons (PAHs) are a group of toxic, persistent, bioaccumulating organic compounds containing two or more fused aromatic rings. They are listed by the U.S. Environmental Protection Agency as priority pollutants because of their carcinogenicity and toxicity. Employing ozonation as a remediation technique, this work investigated the treatability of a sediment sample from a freshwater boat slip subjected to coal tar contamination over a long period. The contaminated sediment sample contained high levels of PAHs in the forms of naphthalene, phenanthrene, pyrene, and benzo[a]pyrene, among other byproducts present in the humic and solid phases of the sediment. The objectives of this work were to examine (1) the degradation of PAHs in the contaminated sediment as treated by ozonation in the slurry form, (2) the effects of ozonation upon the soil matrix and the biodegradability of the resultant PAH intermediates, and (3) the feasibility of a combined technique using O3 as a pretreatment followed by biological degradation. The sediment was made into 3% w/w soil slurries and ozonated in a 1.7-L semi-batch, well-stirred reactor equipped with pH control and a cold trap for the gaseous effluent. Samples were collected after different ozonation durations and tested for biochemical oxygen demand (BOD), chemical oxygen demand (COD), UV absorbance, and toxicity, along with quantitative and qualitative determinations of the parent and daughter intermediates using gas chromatography/flame ionization detection (GC/FID), GC/mass spectrometry (MS), and ion chromatography (IC) techniques. The GC/MS technique identified 16 compounds associated with the humic and solid phases of the sediment. Intermediates identified at different ozonation times suggested that the degradation of PAHs was initiated by an O3 attack resulting in ring cleavage, followed by the intermediates' oxidation reactions with O3 and the concomitant OH radical toward their mineralization. Results suggested that ozonation for 2 hr removed 50-100% of various PAHs in the solid and liquid phases (as well as the aqueous and gaseous media resulting from the treatment process) of the sediment sample and that organic and inorganic constituents of the sediment were also altered by ozonation. Measurements and comparisons of BOD, COD, UV absorbance, and toxicity of the samples further suggested that ozonation improved the bioavailability and biodegradability of the contaminants, despite the increased toxicity of the treatment effluent. An integrated chemical-biological system appeared to be feasible for treating recalcitrant compounds.

Environmental Pollution↗
PubMed2005

High time resolution and size-segregated analysis of aerosol bound polycyclic aromatic hydrocarbons.

Polycyclic aromatic hydrocarbons (PAHs) are an ubiquitous class of compounds in the environment, mostly generated by anthropogenic processes. High time resolution measurements are necessary to gain further knowledge on the fate and diurnal pattern of these often carcinogenic and mutagenic compounds in the atmosphere. It is expected to find a strong correlation of the PAH levels with the strength and proximity to sources, as well as with meteorological parameters. To determine the fate of particle-bound PAHs, they were sampled in this study at an urban background site in Zurich, Switzerland, during summer 2002 and winter 2003. Particle-bound PAHs were collected with a rotating drum impactor and subsequently analyzed with two-step laser mass spectrometry. Using this combination of sampling and measurement, size-segregated (10-1.1, 1.1-0.3, and 0.3-0.1 microm) and high time resolution (20 min) data were obtained. The pronounced diurnal cycle (with day/night ratios of 0.1) was only altered during intensive atmospheric mixing periods (resulting in day/night ratios of up to 8) by cleaner air from upper atmospheric layers which was mixed into the boundary layer. During summer, signal intensities due to particle-bound PAHs were about a factor of 2-10 lower than during winter.

Aerosols↗
PubMed2003

Comparison of synthetic surfactants and biosurfactants in enhancing biodegradation of polycyclic aromatic hydrocarbons.

Polycyclic aromatic hydrocarbon (PAH) contamination of the environment represents a serious threat to the health of humans and ecosystems. Given the human health effects of PAHs, effective and cost-competitive remediation technologies are required. Bioremediation has shown promise as a potentially effective and low-cost treatment option, but concerns about the slow process rate and bioavailability limitations have hampered more widespread use of this technology. An option to enhance the bioavailability of PAHs is to add surfactants directly to soil in situ or ex situ in bioreactors. Surfactants increase the apparent solubility and desorption rate of the PAH to the aqueous phase. However, the results with some synthetic surfactants have shown that surfactant addition can actually inhibit PAH biodegradation via toxic interactions, stimulation of surfactant degraders, or sequestration of PAHs into surfactant micelles. Biosurfactants have been shown to have many of the positive effects of synthetic surfactants but without the drawbacks. They are biodegradable and nontoxic, and many biosurfactants do not produce true micelles, thus facilitating direct transfer of the surfactant-associated PAH to bacteria. The results with biosurfactants to date are promising, but further research to elucidate surfactant-PAH interactions in aqueous environments is needed to lead to predictive, mechanistic models of biosurfactant-enhanced PAH bioavailability and thus better bioremediation design.

Biodegradation, Environmental↗
PubMedDate not supplied

Sidestream tobacco smoke as the main predictor of exposure to polycyclic aromatic hydrocarbons.

Polycyclic aromatic hydrocarbons (PAHs) were measured in mainstream and sidestream tobacco smoke from 14 commercial brands of cigarettes purchased in Italy during 2001-2002. The PAHs detected in smoke and analysed with HPLC and a fluorimetric detector were: fluoranthene, pyrene, benzo[a]anthracene, chrysene, benzo[a]pyrene, benzo[b] fluoranthene, benzo[k] fluoranthene, benzo[g,h,i]perylene and dibenzo[a,h]anthracene. The PAH levels in mainstream smoke from different cigarette brands obtained using an official smoking machine varied by about threefold (from 118 to 374 ng per cigarette for total PAHs and from 23.5 to 100 ng per cigarette for carcinogenic PAHs). Total PAH levels in mainstream smoke were correlated with tar content (r = 0.615, P < 0.05, n = 14). Total PAH content in sidestream smoke, measured by collection of all the smoke produced by a lit cigarette in a glass chamber, was about tenfold higher compared with mainstream smoke. The PAH content in sidestream smoke was relatively uniform (2.3-3.9 and 0.49-1.21 micro g per cigarette for total and carcinogenic PAHs, respectively) and was not correlated with tar content. These results indicate that cigarette manufacturing and filter characteristics influence the PAH composition of mainstream smoke, but have no effect on the PAH content in sidestream smoke, which is the main determinant of smokers' and non-smokers' exposure to PAHs in environmental tobacco smoke.

Chromatography, High Pressure Liquid↗
PubMed2002

Lipid analysis of the response of a sedimentary microbial community to polycyclic aromatic hydrocarbons.

Polycyclic aromatic hydrocarbons (PAH) are widespread environmental contaminants that can, under proper conditions, be degraded by microorganisms. The responses of a riverine sedimentary microbial community to PAH contamination were examined using an integrated biochemical assay that yielded data on PAH concentration, total microbial biomass, and microbial community structure and were interpreted using perturbation theory and the subsidy-stress gradient. Microbial mineralization of naphthalene, anthracene, fluorene, and phenanthrene was observed 24 h after their addition to all sediments sampled and ranged from 0.9 to 16.3% in ambient sediments and from 14.8 to 35.8% in contaminated sediments. Total microbial biomass, determined by phospholipid phosphate, increased in response to intermediate PAH concentration and decreased at sites with the highest PAH concentration (p < 0.05) during seven out of nine (78%) seasonal sampling periods. The two sampling periods that were not statistically different followed periods of high water and cold temperatures. Phospholipid fatty acid analysis of microbial community structure analysis indicated that increases in the relative abundance of gram-negative aerobes and heterotrophic eukaryotes were responsible, in part, for these observed increases in total microbial biomass. These findings (increased degradation rates, increased biomass at intermediate PAH concentrations, and altered community structure) indicate that a component of the microbial community responded to PAH as a usable input and are consistent with the predictions of perturbation theory and a subsidy-stress gradient.

Biomass↗
PubMed2004

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.

Biomarkers↗
PubMed2003

Evaluation of bacterial strategies to promote the bioavailability of polycyclic aromatic hydrocarbons.

Polycyclic aromatic hydrocarbon (PAHs)-degrading bacteria may enhance the bioavailability of PAHs by excreting biosurfactants, by production of extracellular polymeric substances, or by forming biofilms. We tested these hypotheses in pure cultures of PAHs-degrading bacterial strains. Most of the strains did not substantially reduce the surface tension when grown on PAHs in liquid shaken cultures. Thus, pseudo-solubilization of PAHs in biosurfactant micelles seems not to be a general strategy for these isolates to enhance PAHs-bioavailability. Three semi-colloid Sphingomonas polysaccharides all increased the solubility of PAHs (Gellan 1.3- to 5.4-fold, Welan 1.8- to 6.0-fold and Rhamsan 2.4- to 9.0-fold). The increases were most pronounced for the more hydrophobic PAHs. The polysaccharide-sorbed PAHs were bioavailable. Mineralization rates of 9-[14C]-phenanthrene and 3-[14C]-fluoranthene by Sphingobium EPA505, were similar with and without sphingans, indicating that mass-transfer rates from PAHs crystals to the bulk liquid were unaffected by the polysaccharides. Biofilm formation on PAHs crystals may favor the diffusive mass transfer of PAHs from crystals to the bacterial cells. A majority of the PAHs-degraders tested formed biofilms in microtiter wells coated with PAHs crystals. For strains capable of growing on different PAHs; the more soluble the PAHs, the lower the percentage of cells attached. Biofilm formation on PAHs-sources was the predominant mechanism among the tested bacteria to overcome mass transfer limitations when growing on poorly soluble PAHs.

Anthracenes↗
PubMed2006

Xenobiotic-metabolizing enzymes involved in activation and detoxification of carcinogenic polycyclic aromatic hydrocarbons.

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental carcinogens and metabolized by a variety of xenobiotic-metabolizing enzymes such as cytochrome P450 (P450 or CYP), epoxide hydrolase, glutathione transferase, UDP-glucuronosyltransferase, sulfotransferase, NAD(P)H quinone oxidoreductase 1, and aldo-keto reductase. These enzymes mainly participate in the conversion of PAHs to more polar and water-soluble metabolites, and the resultant metabolites are readily excreted from the body. However, during the course of metabolism, a variety of unstable and reactive intermediates of PAHs are formed, and these metabolites attack DNA, causing cell toxicity and transformation. P450s and epoxide hydrolase convert PAHs to proximate carcinogenic metabolites, PAH-diols, and these products are further metabolized by P450s to ultimate carcinogenic metabolites, PAH diol-epoxides, or by aldo-keto reductase to reactive PAH o-quinones. PAHs are also activated by P450 and peroxidases to reactive radical cations that bind covalently to DNA. The oxygenated and reactive metabolites of PAHs are usually converted to more polar and detoxified products by phase II enzymes. Inter-individual differences exist in levels of expression and catalytic activities of a variety of enzymes that activate and/or detoxify PAHs in various organs of humans and these phenomena are thought to be critical in understanding the basis of individual differences in response to PAHs. Factors affecting such variations include induction and inhibition of enzymes by diverse chemicals and, more importantly, genetic polymorphisms of enzymes in humans.

Carcinogens, Environmental↗
PubMed2006

New method for testing phototoxicity of polycyclic aromatic hydrocarbons.

Polycyclic aromatic hydrocarbons (PAHs), widespread environmental pollutants, were recently reported to show photomutagenesis. As contaminants in the environment are usually exposed to sunlight, a way to evaluate the phototoxic characteristics of pollutants is required. We have previously found that phosphorylation of histone H2AX (gamma-H2AX), which accompanied the induction of DNA double strand breaks (DSBs), was significantly induced by low concentrations of benzo[a]pyrene (10(-9)-10(-7) M) and UVA (0.6 J/cm2) in CHO-K1 cells. Higher concentrations have been required for the detection of DSBs. The aim of the present study is to investigate the applicability of gamma-H2AX in a new phototoxicity assay of PAHs. The human keratinocytes, HaCaT, were treated with four model PAHs (naphthalene, phenanthrene, pyrene, and benzo[a]pyrene, 10(-11)-10(-7) M) and/or UVA (5 J/cm2), and the induction of gamma-H2AX was assessed. Furthermore, DSBs were directly detected using a biased sinusoidal field gel electrophoresis, and the cell viability was examined as a general assay of phototoxicity. The induction of gamma-H2AX was detected in the presence of all the PAHs except naphthalene at concentrations of 10(-9)-10(-7) M, whereas neither DSBs nor cell death could be detected at those concentrations, and higher concentrations were required for the detection. Naphthalene showed no phototoxicity in any of the three different assays. These findings suggest that histone H2AX is a potential moleculartargetfor detecting the phototoxicity of PAHs more sensitively than the detection of cell viability and DSBs.

Animals↗
PubMed2006

Regressing gas/particle partitioning data for polycyclic aromatic hydrocarbons.

Polycyclic aromatic hydrocarbons (PAHs) were measured in the rural atmosphere of Southern Ontario, Canada from October 2001 to November 2002. Sixty seven pairs of gaseous and particle-bound concentrations of PAHs were determined concurrently in a forest and a clearing. The gas/particle partitioning behavior of the PAHs was investigated by fitting the original Junge-Pankow equation to the fraction in the particle phase phi for each set of measured data, either allowing the slope m to deviate from -1 (two-parameter model) or not (one-parameter model). This fitting procedure was judged more robust than linear logarithmic regressions involving the gas/particle partition coefficient, because the latter is sensitive to the applied blank correction, tends to ignore a significant amount of analytical information, and gives undue weight to more uncertain data points. The experimental data fit was good for both nonlinear models, and discrepancies between experimental data and models and between models are mostly related to sampling/experimental artifacts. In particular, samples taken close to the freezing point appear to suffer from blow-off artifacts. Applying slopes m different from -1 appears only justified if it can be assured that a second parameter indeed provides a better fit and that this better fit is not due to experimental, analytical, or statistical artifacts. The magnitude of the differences in the model fitting parameters between sampling events is consistent with the reported variability in the nature and concentration of atmospheric particles. Statistical tests on the regression results indicate that the gas/particle partitioning was not significantly different between the forest and the clearing.

Air Pollutants↗
PubMed1997

Biological monitoring and biochemical effect monitoring of exposure to polycyclic aromatic hydrocarbons.

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous carcinogenic substances to which man is exposed in the environment and at certain workplaces. Estimation of the resulting health risk is therefore of great occupational-medical and environmental-medical importance. Determination of the DNA and protein adducts of PAHs is the most suitable way of estimating this risk. The analytical methods used thus far, above all, 32P postlabeling, immunoassays, and synchronous fluorescence spectroscopy, are, however, too nonspecific; therefore, the results lack accuracy and are not comparable with one another. Only the use of very specific methods of instrumental analysis [above all, high-performance liquid chromatography (HPLC) and gas chromatography/ mass spectrometry (GC/MS)] can counteract this deficit. However, these methods can successfully be used mainly to determine the protein adducts of PAHs. Hemoglobin adducts, for example, do not have repair mechanisms like DNA adducts. They therefore occur in higher concentrations and can thus be analytically detected more easily. At present, mainly the monohydroxylated metabolites of PAHs are being determined in urine with great success. Using specific enrichment methods and HPLC with fluorescence detection it is even possible today to determine the internal PAH exposure of the general population. The detection limits lie in the lower nanogram-per-liter range. In view of the importance of this group of substances, determination of PAH adducts and the detection of their metabolites in urine will remain at the center of future occupational-medical and environmental-medical/toxicological research. In general, the lack of reference substances must be lamented.

Benzo(a)pyrene↗