Exposure to particulate matter (PM) may alter lung homeostasis inducing changes in fluid balance and host defense. Bioavailability of soluble PM compounds like polycyclic aromatic hydrocarbons (PAHs), polychlorinated biphenyls (PCBs), and transition metals has been shown to play a key role in lung injury. We have previously characterized the size, shape, and chemical components of urban air particles from Buenos Aires (UAP-BA) and their biological impact on lungs. Herein, we evaluate the possible toxic effect of UAP-BA-soluble fraction (UAP-BAsf) on pulmonary cells obtained from young (1–2 months old) and aged (9–12 months old) Wistar rats using phagocytosis, oxidant–antioxidant generation, and apoptosis as endpoints. UAP-BA were collected in downtown BA and residual oil fly ash (ROFA), employed as a positive control, was collected from Boston Edison Co., Mystic Power Plant, Mystic, CT, USA. Both particle-soluble fractions (sf) were employed at concentrations ranging from 0 to 100μg/mL. UAP-BAsf and ROFAsf even at the lowest dose assayed (10μg/mL) showed in both lung cell populations the ability to stimulate phagocytosis and increase superoxide anion (O2−) generation. Both types of air particles caused a marked intracellular oxidant stress in aged pulmonary cells that may contribute to subsequent cell activation and production of proinflammatory mediators, leading to cell dysfunction. These data suggest that the impact of UAP-BAsf on phagocytosis, oxidant radical generation, and apoptosis is clearly dependent on the maturational state of the animal and might have different mechanisms of action.