Consistent with previous reports demonstrating that ADMA potentiates ovalbumin- or cigarette smoke-induced lung injury [14, 31], we found that PM2.5 exposure increased lung ADMA levels and that Ddah1 deficiency or ADMA administration exacerbated PM2.5-induced lung fibrosis, vessel remodeling, inflammation and oxidative stress. This evidence concerns the gene DDAH1 and pulmonary fibrosis.