O3 exposure is associated with increased morbidity and mortality in human patients with cardiopulmonary disease (Katsouyanni et al., 1995; Levy et al., 2005); furthermore, it is now understood that TLR4 mediates the development of inflammation and airway hyperresponsiveness (AHR) after O3 exposure (Garantziotis et al., 2010). This evidence concerns the gene TLR4 and cor pulmonale.