Risk assessment of carcinogenicity and fibrogenicity in respiratory systems induced by fibrous and particulate materials

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Inhalation exposure to fibrous and particlate materials induces chronic inflammation in respiratory systems, leading to carcinogenesis and fibrosis. We have demonstrated that inflammation-mediated oxidative/nitrative DNA damage is closely associated with asbestos exposure in animal and human lung tissues. Carbon nanomaterials induced nitrative DNA damage in human lung epithelial cells through cellular internalization. In addition, we demonstrated that molecules involved in tissue fibrosis participate in inflammation-related carcinogenesis using experimental animals and human plasma.