The purpose of this study was to investigate the inhalation risks on the workers (operator and administrator) exposure to airborne particulate matter-bound arsenic (PMAs) in semiconductor manufacturing facilities. We reanalyzed published empirical data of the personal exposure levels and size distributions of airborne PMAs and linked a human respiratory tract model to calculate the concentrations deposited in target lung regions. We used a physiologically based pharmacokinetic model with a dose-response relationship based on an empirical three-parameter Hill equation model to simulate the exposure time-dependent arsenic dose profiles in human tissues and to estimate quantitatively the inhalation exposure risks. Results show that the threshold level of As(ill) for lipid peroxidation response (LPO) on human lung epithelial cells was estimated to be 11.89 (95% Cl: 8.09-15.69) mu M, whereas 16.39 (95% CI: 12.56-20.22) mu M for oxidative DNA damage on human dermal cells. Risk analysis shows that the LPO responses were estimated to be 3.79 (95% Cl: 2.44-5.33) for operator and 0.03 (95% CI: 0.01-0.10) for administrator at a risk of 0.5. The 10% probability (risk = 0.1) of human dermal cells affected by oxidative DNA damage responses is approximately 27.21% (95% Cl: 12.71-67.02%) for operator and 0.03% (95% Cl: 0.01-0.07%) for administrator. This study suggests that a potential link between inhalation exposure risk of operator to airborne PMAs in semiconductor manufacturing workplace. (C) 2009 Elsevier B.V. All rights reserved.