Since 10% selleck chemicals of the particulate matter had a diameter smaller than 57 μm (Fig. 1), some of them reached alveolar spaces, as illustrated in the photomicrograph under polarized light (Fig. 4). As depicted in Table 1, particulate matter showed a high concentration of the element aluminum. The second most frequently element, iron, has been described as the main culprit in triggering oxidative stress (Park et al., 2006) and producing reactive oxygen species (ROS) (Smith and Aust, 1997). Some authors suggest that other metals act as

coadjutants in the genesis of pulmonary injury (Prahalad et al., 2000 and Prahalad et al., 2001). The initial phase of the pulmonary reaction to particle exposure seems to be influenced by individual metals, whereas the persistence of the response would reflect the complexity of the interaction among different metals (Dreher et al., 1997 and Antonini et al., 2004). However, it is not possible to exclude the contribution of other non-determined

constituents of the particle composition. We measured elastic, resistive and viscoelastic parameters by the end-inflation occlusion method, allowing the identification of elastic, resistive, and viscoelastic and/or inhomogeneous lung mechanical components (Bates et al., 1985 and Bates et al., 1988). In line with previous results (Mazzoli-Rocha et al., 2010), viscoelastic pressure, static elastance and viscoelastic component of elastance were higher in CA than in CS (Fig. 3), which Stem Cell Compound Library supplier implies that lung parenchyma was compromised, whereas large airways were not. Additionally, an influx of polymorphonuclear cells and an increase in alveolar collapse were more important in group CA than in CS (Fig. 5 and Table 2). The cell influx into the alveolar walls, as well as the decreased lung function reported in this study was previously observed in hamsters (Drew et al., 1974), mice (Mazzoli-Rocha et al., 2010), and rats (Halatek et al., 2005) after aluminum

exposure. According to Donaldson et al. (2001), the coarse particles may be mostly restrained in the superior airways Etoposide and cause local irritation unchaining symptoms as cough. On the other hand, ultrafine particles can cause damage to the lung periphery. Although an increase in resistive pressure was not found (in accordance with previous results), decreased lung function and parenchymal inflammation could be observed by pulmonary mechanics and histology analyses. This phenomenon could be explained by the fact that in general coarse particles are comprised of up to 50% by mass of ultrafine particles (Donaldson and Stone, 2003) and these small aggregated particles may be the active component of the coarse ones (Anderson et al., 2001). Particulate inhalation from environmental (Liu et al., 2007) and occupational (Trupin et al., 2003) air pollutants has been identified as being among the primary causes and exacerbations of pulmonary diseases.