The decreased AhR nuclear translocation in alveolar type II cells after CD exposure may well be a general response of alveolar type II cells to inflammation associated with lung-deposited particles, since CYP1A1 induction and its dependent activity (EROD) were inhibited by exposure to another type of occupational dust, crystalline silica, which does not contain PAH [23]. This evidence concerns the gene AHR and pulmonary arterial hypertension.