Abstract • Workers in a Swedish factory making boats from plastics reinforced with glass fibre are exposed to a variety of chemicals, including styrene which is mutagenic after metabolic activation. • The concentrations of styrene in the air was measured in the breathing zones of workers occupied with various processes in boat making. Samples of air were taken 6 times during the years 1973–1978. The total exposure to styrene for the workers during this period was calculated and expressed as the averaged concentratin in mg per m 3 air during an 8-h workshift multipled by the number of years of employment. A low-dose group ( x = 137 mg × m −3) and a highdose group ( x = 1204 mg × m −3) were identified. • Blood samples were taken in 1978 from workers belonging to the exposed groups and from a matched control group of employees in the same factory not exposed to styrene. Lymphocytes were cultured and examined workers had a aberrations and sister-chromatid exchanges. Exposed workers for chromosal significantly p < 0.001) higher number of chromosomal aberrations (36 persons, x = 7.9 aberrations/100 cells ) compared with employees in the control group 37 persons, x = 3.2 aberrations/100 cells) . There was no significant difference between the mean values of the number of chromosomal aberrations between the highly exposed and the less exposed groups. But in the less exposed group there was an increase in the frequency of chromosomal aberrations with increasing exposure to styrene ( r = 0.576). In the highly exposed group this dose response was not observed ( r = -0.231). • For the frequency of sister-chromatid exchanges (SCE) a slight ( p < 0.05) relevant for the estimation of the risk for long-term deleterious effects such as cancer or inherited diseases, it can be concluded that exposure even to considerably lower concentrations of styrene than the Swedisch TLV should be avoided. • In the study of styrene-exposed workers in Finland, no clear dose response was found (Meretoja et al., 1978). Nor were clastogenic effects of dependent on dose according to epidemiological investigations of workers exposed to vinyl chloride (Ducatman et al., 1975; Funes-Cravioto et al., 1975; Heath et al., 1977; Kučerova et al., 1979). In all these studies the measurement of dose different from that in this investigation, and number of persons studied in a single investigation was usually too low to permit a dose-effect study. This is true, too, for our data on SCE. • There were numerous other chemicals in use in the boat-making department of the factory in our study and nothing is known about their clastogenic effects. E.g. methyl-ketone-peroxide, added to the polymer as an accelerator was measured in concentrations up to 100 mg/m 3. • Despite the possibility that other chemicals in the complex environment of the boat-making department contributed to the clastogenic effect, we propose that it is the exposure to styren that has caused the increase of chromosomal damage recorded in our study. This conclusion is supported by the positive dose response found in the less exposed group and the highly significant difference between styrene-exposed and unexposed men. Support is also given by the results from other epidemiological studies and experiments in vitro with styrene and its metabolite styrene-7,8-oxide.