Several studies have shown that exposure to air particulate matter (PM) might trigger toxic effects over the cardiorespiratory system. PM vary in size from a few nanometers to 10 micron in diameter. Due to the ability to reach lower airways, nanoparticles (NP) present in PM exert worse adverse health effects than coarse particles. It is suggested that transition metals present in NP could play an important role in this scenario, via increased production of reactive O2 species and oxidative tissue damage, through Fenton-like chemical reactions. Our aim was to build metal coated-NP, with similar physicochemical properties than airborne NP, in order to use them as a model to study the effects of transition metals present in air pollution on  the cardiorespiratory system. NP characterization was analysed by SEM, TEM, and DLS. Results show that every constructed NP has similar characteristics that PM´s NP. Swiss mice (25 g) were intranasally instilled with a suspension of NP containing Ni (II), Cd (II), Fe (III), or Cr (VI); at 0.01, 0.05, 0.1, and 1.0 mg metal/kg body weight. Control mice were exposed to empty NP. Samples were collected 1 hour after exposure. Biodistribution studies performed by NP labeled with 99mTc show that NP mostly remain in the lung, compared to stomach. Tissue O2 consumption and TBARS content were evaluated in lung. No changes were observed after Cd- NP exposure in any experimental condition. On the contrary, Fe-NP showed a significant increase in lung O2 consumption by 48% and 52% at 0.1 and 1.0 mg Fe/kg (p<0.05). TBARS content was significantly increased by 57% and 56% at the same doses respectively (p<0.05). When Cr-NP were tested, lung O2 consumption was increased by 44% at 0.05 mg Cr/kg (p<0.001). TBARS content showed a significant increase by 27% and 43% at 0.05 and 0.1 mg Cr/kg, respectively (p<0.05). Regarding Ni-NP, every experimental group showed a significant increased by up to 76% (p<0.05). Likewise, TBARS levels in lung were also significantly increased up to 51% (p<0.05). Mechanistically, studies performed with the highest dose of Ni-NP showed an increase in mitochondrial H2O2 production rate (41%; p<0.05) and NADPH oxidase activity (41%; p˂0.001) in lung. Activation of circulating PMN leukocytes and increase in TBARS levels were found after Ni-NP exposure in blood. In heart, the Ni-NP group showed a decrease in O2 consumption
(37%; p˂0.001), while mitochondrial H2O2 production rate was increased (39%; p<0.05). Our data suggests that Ni, Fe, and Cr induce alterations in lung oxidative metabolism after NP exposure. A deeper analysis with Ni-NP results showed that alterations in lung O2 metabolism are probably due to changes in mitochondrial function and activation of NADPH oxidase activity. Moreover, it seems that the adverse health effects are not limited to the lung given that cardiac toxicity was also observed. These findings provide new insights to the understanding of toxicity triggered by metals present in NP.