<p>A model is developed of disease initiation and progression for asbestos related plaque deposition and mesothelioma based on prior models of wound healing and asbestos transport. The model includes short term processes such as macrophage polarization and immune system response, extending the time frame to that of detectable disease. Model results were in a biologically reasonable range. Cancer development and plaque deposition are shown to be dependent on total exposure (intensity * duration). Plaque deposition was sensitive to many systemic parameters, suggesting that assays could be developed to identify individuals with higher risk. Tumor development was sensitive only to a few parameters describing exposure and T-cell levels, indicating potential for immune system intervention.</p>