Epidemiological and experimental studies have suggested the enhancement of asbestos-induced disease processes by simultaneous exposure to kerosene, its soot, and cigarette smoke in asbestos-exposed animals as well as in humans. To determine the influence of these factors on the genotoxic potential of asbestos, a micronucleus test was performed in Syrian hamster embryo fibroblasts (SHE) and human ... [Show full abstract] lymphocytes. To observe the specific chromosomal damages, multicolor fluorescence in situ hybridization (FISH) was done in the lymphocytes from smokers and nonsmokers exposed in vitro to asbestos. Significantly higher numbers of micronuclei were observed in SHE cells after combined treatment with chrysotile and kerosene soot (111 micronuclei/1000 cells) in comparison to chrysotile and kerosene soot separately. Kinetochore staining revealed mainly clastogenic effects in all the cases. In human lymphocytes exposed in cultures to chrysotile and crocidolite the numbers of micronuclei were found higher in smokers than nonsmokers. Multicolor FISH assay suggested that asbestos fibers inflict high damage within 1q12 and in the region between 1cen and 1q12 of chromosome 1. In the exposed population of an asbestos cement factory, the highest genetic damage was found in the blood lymphocytes of exposed smokers. The study suggests that smokers occupationally exposed to asbestos and domestically to kerosene soot are at higher risk for the early development of asbestos-induced diseases.