This study was designed to investigate whether topical solutions, as they are used in the treatment of selected cases of rhinosinusitis, influence nasal mucociliary clearance. The objective of this study was to evaluate the effects of the following topical solutions on the ciliary beat frequency (CBF) of nasal respiratory cells: ofloxacin as an antibiotic; Betadine and hydrogen peroxide (H2O2) as antiseptic; and amphotericin B, itraconazole, and clotrimazole as antifungal solutions. Differences are described between effects of each of these substances and we clarify whether ciliotoxic effects are dose dependent and if they can be reduced or eliminated by diluting the concentration of the applied solution. In a prospective study, nasal respiratory cells were harvested from healthy individuals and CBF was measured while cells were perfused with cell culture medium and the respective topical solution, using a Dvorak/Stotler exposure chamber. Controls were perfused with cell culture medium only. Video interference contrast microscopy was used to monitor CBF. A decrease of CBF occurred after application of all topical solutions used in this study. Except for clotrimazole, all solutions showed significantly stronger effects at high concentrations compared with diluted solutions. Our results indicate that topical application of antifungal, antibiotic, and antiseptic solutions may cause a marked impairment of mucociliary clearance. The strong dose dependence of these ciliotoxic effects indicates the need for a careful selection of the adequate concentration when using topical treatment in the nose.

Background: The aim of this study was to identify inflammatory changes as well as genotoxic effects in cultivated human respiratory epithelial cells after in vitro exposure to benzene. Methods: Primary cell cultures of nasal respiratory mucosa were exposed to synthetic air enriched with 5,000 µg/m³ of benzene at an air/liquid interface over 8 h and then to synthetic air only over the following 24 h. Controls were continuously exposed to synthetic air over 32 h. To detect inflammatory reactions, release of prostaglandin E₂ was quantified using a competitive enzyme immunoassay. The Comet Assay was used to quantify the ratio of apoptotic cells with benzene-induced DNA fragmentation. Results: Prostaglandin release as well as DNA fragmentation increased after 8 h of exposure and remained elevated throughout the following 24 h but did not increase in controls. Conclusions: High concentrations of benzene induce an inflammatory response and possibly fragmentation of DNA in respiratory epithelial cells. These findings have to be discussed with respect to possible mutagenic or carcinogenic effects of benzene in nasal respiratory cells.