Concerns of a tumorigenic risk of styrene (ST) originate from the findings that styrene (ST) is metabolized to the genotoxic, intermediate styrene-7,8-oxide (SO). Therefore, it was hypothesized that results of animal long-term studies with ST and SO together with the SO tissue burden are sufficient for conducting a 'worst case' estimate of the tumorigenic risk of ST. On this basis we predicted the excess human lifetime risk for lung tumors (p(HPS)) and the highest possible risk for other systemic tumors (p(HPS)) resulting from daily intake of ST via food and ambient air. As measures for p(EXL) the mean lifetime concentration of SO in the transitional zone of the lung and for p(HPS) the mean lifetime concentration of SO in blood were calculated using a physiological toxicokinetic model. For a daily oral intake of 12 mug ST, p(EXL) was obtained to be between 5 x 10(-9) and 2 x 10(-8) and p(HPS) to be between 7 x 10(-9) and 2 x 10(-8). Lifetime risks calculated for continuous exposure to 3 mug/m(3) ST in ambient air were between 8 x 10(-7) and 3 x 10(-6). (P-EXL) and between 2 x 10(-8) and 4 x 10(-8) (p(HPS)). Although these values indicate very low risks, the actual risks are expected to be even by far smaller. This is discussed in detail for lung tumorigenesis.