**1. Introduction**

It is becoming evident that both environmental and genetic factors may influence the development of many diseases [1–7]. It is therefore important to consider gene-environment interactions when studying diseases related to exposure to different hazards and lifestyle factors.

Environmental and lifestyle factors have been investigated in many epidemiological studies using self-reported information obtained by questionnaires, interviews, records or measurements of exposure. However, very few epidemiological studies included the information on genetic risk factors. Similarly, many studies investigating genetic factors obtained little information on environmental factors and lifestyle. Genetic predisposition can be presumed from family history, from phenotypic characteristics (e.g. metabolic capacity) or, most importantly, from an analysis of deoxyribonucleic acid (DNA) sequence [8].

The research into gene-environment interactions requires the information on both environmental/lifestyle and genetic factors [7, 8]. Primary candidates for gene-environment interaction studies have been mostly genes coding for xenobiotic-metabolising enzymes [3]. Genetic variability in these genes may lead to interindividual differences in the capacity for xenobiotic metabolism, thus modifying an individual's susceptibility to the development of disease [3].

The approach to the analysis of gene-environment interactions is presented using the example of our study into asbestosis, which is one of the most frequent asbestos-related diseases. According to the model of causation, asbestos exposure, genetic factors and possibly also unknown causes have a crucial role in the occurrence of asbestosis [9]. Although asbestosrelated diseases are among the most extensively studied occupational diseases, and the causal relationship between asbestos exposure and asbestosis has been well proved [10–14], relatively little has been known about the genetic factors that might modify an individual's susceptibility to the development of this disease [6, 15–17].
