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.

We have studied outward currents of neurons acutely isolated from superficial layers of the entorhinal cortex with whole-cell patch-clamp recordings. If cells were held more negative than -50 mV, depolarizing voltage commands activated a transient A-type current together with a sustained outward current. Both currents were sensitive to 4-aminopyridine, while only the sustained current was blocked by tetraethylammonium. The sustained outward current showed a considerable rundown in amplitude over prolonged recording periods. At the same time its half-maximal inactivation shifted from -74 to -114 mV. Nystatin perforated patch recordings were used to minimize these perfusion effects. Under such conditions the amplitude and the steady-state inactivation properties of the sustained outward current remained stable for more than 1 h. Pharmacological investigations revealed that only a small part of the sustained outward current could be attributed to a calcium-activated potassium current. Therefore most of the rundown has to be due to changes in the delayed rectifier outward current. These results may suggest that the delayed rectifier current is under considerable metabolic control.

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In comparison with other industries, the internal PAH exposure at workplaces in a fireproof stone producing plant is high. This is probably caused by dermal PAH-absorption. Therefore, biological monitoring must be performed in the health surveillance of fireproof stone producing workers. The urinary PAH metabolites should be determined: 3-hydroxybenz(a)anthracene could probably be used as a biomarker representing the group of carcinogenic PAH.

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