Ad M. Knaapen

TL;DR: Since most of the proposed molecular mechanisms underlying particle‐related carcinogenesis have been derived from in vitro studies, there is a need for future studies that evaluate the implication of these mechanisms for in vivo lung cancer development and transgenic and gene knockout animal models may provide a useful tool.

TL;DR: Oxidative stress arising from PM(10) has been shown to activate a number of redox-responsive signaling pathways in lung target cells that play a role in responses relevant to inflammation and pathological change, including MAPKs, NF-kappaB, AP-1, and histone acetylation.

TL;DR: Poorly soluble particles such as TiO2, carbon black, and diesel exhaust particles have been evaluated for their genotoxity using both in vitro and in vivo assays, since inhalation of these compounds by rats at high concentrations has been found to lead to tumor formation.

TL;DR: Investigation of the capacity of the major neutrophilic oxidant hypochlorous acid (HOCl), which is formed by myeloperoxidase (MPO), to induce DNA damage and mutagenicity in lung cells indicates that MPO catalysed formation of HOCl during lung inflammation should be considered as a significant source of neutrophil-induced genotoxicity.

TL;DR: It is demonstrated that the water-soluble fraction of PM elicits DNA damage via transition metal-dependent •OH formation, implicating an important role of H2O2.