Induction of sister chromatid exchanges (SCE) in human tracheal epithelial cells by the fractions PM-10 and PM-2.5 of airborne particulates

Abstract

Recent epidemiological studies in the United States and in Europe indicate, that the coarse fraction (PM-10) of airborne particulates, smaller than 10 μm and particularly the fine fraction (PM-2.5) smaller than 2.5 μm are responsible for adverse health effects, causing an increasing morbidity and mortality. Furthermore, an association was reported between air pollution, especially the levels of the fine respirable particles and death from lung cancer. The epithelium of the respiratory tract is the major target of airborne particulates and the location of the most common cancer in man, bronchogenic carcinoma. The genotoxic activity of the coarse (PM-10) and the fine fraction (PM-2.5) of airborne particulates leading to mutation and cancer can be analyzed using in vitro models of human bronchoepithelial cells. In our study collection of the coarse (PM-10) and the fine fraction (PM-2.5) of airborne particulates was conducted in the winter of 1996 in the highly industrialized Rhine-Ruhr region (Germany). For collection we selected an urban area (Düsseldorf), an industrialized area Duisburg and a rural area (Borken). Airborne particulates were collected with a Low Volume M-10 dichotomous sampler (Graseby-Andersen) equipped with glass fiber filters. Chemical substances were extracted from filters with di-chloromethane and quantitatively transferred to dimethylsulfoxide (DMSO). As target cells for testing the genotoxic activity we used cultures of the human bronchioepithelial cell line (BEAS-2B). As a sensitive cytogenetic endpoint for evaluation of the genotoxic activity of extracts of airborne particulates we utilized the induction of ‘sister chromatid exchanges’ (SCE). The coarse fraction PM-10 and especially the fine fraction PM-2.5 of airborne particulates from all three locations caused a strong dose-related induction of ‘sister chromatid exchanges’. The fine fractions PM-2.5 from the three locations exerted a stronger genotoxic activity than the corresponding coarse fractions PM-10. While airborne particulates from Düsseldorf and Duisburg revealed a comparable genotoxic activity, the samples from Borken disclosed a lower genotoxicity. It is important that especially the fine fraction PM-2.5, exerted a strong genotoxicity equivalent to substances of airborne particulates from less than 0.5 m 3 of air. Results of this study and earlier reports demonstrate that the human tracheobronchial epithelial cell line (BEAS-2B) in vitro offer a reliable and sensitive in vitro model for genotoxicity testing of airborne particulates, especially of the coarse (PM-10) and fine fraction (PM-2.5).