Because apoptosis is believed to play an essential role in the inflammation associated with one pneumoconiosis, acute silicosis, and because inflammation increased as CYP1A1 activity decreased in the rat model of coal workers’ pneumoconiosis (Ghanem et al. 2004), we investigated the hypothesis that apoptosis plays a critical role in lung injury and down-regulation of CYP1A1 induction in mixed exposures to CD and the model PAH β-naphthoflavone (BNF). This evidence concerns the gene CYP1A1 and pneumoconiosis.