Chronic obstructive pulmonary disease (COPD) is a disease state characterized by airflow limitation that is not fully reversible, leading to respiratory insufficiency. Flow limitation is secondary to the remodeling of the pulmonary parenchyma (called also emphysema) related to an imbalance between the expression and/or the activity of matrix metalloproteases (MMPs) and their inhibitors (TIMPs). Cigarette smoke is the main risk factor to develop COPD, via its oxidative properties. Urban particulate pollution aggravates COPD. However, the mechanism(s) involved in this effect are not very well known. The hypothesis of this study is that particulate pollution could amplify lung remodeling induced by cigarette smoke. This effect of particles could be related to their oxidative properties. Therefore, we evaluated the effects of diesel particles, a main component of urban particulate pollution, alone or associated with cigarette smoke condensate, on MMPs/TIMP balance in alveolar epithelial cells (type II pneumocytes). The mechanism(s) involved in these effects were examined by studying the role of oxidative stress. The main results of this study are that diesel particles amplify the effects of cigarette smoke on cellular oxidative stress and decrease the expression of two antiproteases : TIMP-2 and a1-antitrypsin, whereas cigarette smoke increases the expression of MMP-1. Pre-induction of the antioxidant protein heme oxygenase 1 before cigarette smoke and diesel particles exposure protects cells against oxidative stress and proteases/antiproteases imbalance. We conclude that diesel particles could aggravate COPD by amplifying oxidative stress and proteases/antiproteases imbalance induced by cigarette smoke.