The skin is one of the main organs exposed to airborne particulate matter (PM), which may contain various pollutants linked to a wide range of adverse health endpoints. In the present work, we analyzed the proinflammatory and oxidative effects of some PM components leading to inflammatory responses, cell proliferation or cell death. We investigated four redox-active chemicals, such as Cu (II) metal and quinones generated from polycyclic aromatic hydrocarbons (PAHs), i.e., 9,10 phenanthrenequinone and isomers 1,2 and 1,4 naphthoquinone. We performed in vitro biological tests on human keratinocyte (HaCaT) cells and also acellular assays based on the oxidation of dithiothreitol and ascorbic acid, antioxidants to assess the oxidative potential (OP). We found that treated keratinocytes showed increased activation of the redox-sensitive transcription factor NFκB and increased transcript levels of the NFκB-dependent gene IL8. Moreover, the treatment with Cu(II) and quinones increased the activities and the expression of genes involved in the redox response, SOD1 and GPX, suggesting that PM components induced cellular damage due to redox imbalances. Finally, we found alteration of the mitochondrial ultrastructure and increased apoptosis after 24 h of treatment. The results presented suggest that all of the analyzed pollutant components are able to modulate similar signal transduction pathways, resulting in activation of inflammatory processes in the skin, followed by oxidative damage. Altogether these observations indicate that exposure of skin to air pollutants modifies the redox equilibrium of keratinocytes, which could explain the increased skin damage observed in populations that live in high-pollution cities.