**8. Conclusion**

All discussed studies indicate, that DNA adducts, Comet assay and DNA fragmentation in sperm are sensitive biomarkers of exposure to c-PAHs in polluted air, chromosomal aberra‐ tions by FISH and micronuclei as biomarkers of effect, and 8-oxodG and 15-F2t-IsoP as biomarkers of oxidative damage.

It seems that when using these biomarkers the dose-effect is seen only in a certain range, probably up to 10 ng B[a]P/m3 .

It is important to identify simultaneously the gene susceptibility, especially the genetic polymorphisms of metabolic genes and genes encoding DNA repair enzymes. DNA damage may be further affected by life style as smoking, ETS, diet – intake of vitamins A, C, E, folic acid, oxidative metabolism by lipid metabolism (triglycerides, cholesterol, HDL, LDL) – it is therefore pertinent to analyze all these endpoints in the biological material in the course of molecular epidemiology studies.

New perspectives may be seen in using the microarray methods, e.g. studying the gene expression of genes coding DNA repair enzymes.

Summing up, molecular epidemiology studies on the environmental exposure to c-PAHs in ambient air should be very complex: determining personal exposure, DNA and oxidative damage, gene susceptibility and life style factors. It will bring new results, which may specify new information important to evaluate properly c-PAHs human health risk.
