Chronic obstructive pulmonary disease (COPD) is one of the major causes of morbidity and mortality globally. Inhalation of particulate matter (PM) air pollution has been studied to closely associate with COPD. However, the pathogenesis mechanisms underlying PM2.5-induced lung injury is largely unknown, leading to the poor stratification and treatment of the disease. Thus, we aim to explore the underlying molecular mechanisms associated with PM-mediated lung injury by quantitative proteomics analysis of lung tissues from ageing and young rat models with whole body exposure to traffic-related PM pollutants and compared it with that in rat models exposed to high-efficiency particulate air-filtered gaseous pollutants. Our data showed that before lung function decline the 0.5-yr rats had exhibited differential dysregulation of proteins involved in oxidative stress, cellular metabolism, calcium signalling, inflammatory responses, and actin dynamics under exposures to PM and gaseous pollutants. On the contrary, more significant and consistent molecular effects were observed in 1.5-yr rats exposed to PM and gaseous pollutants, of which the malignancy-related ERB signalling pathways were activated additionally in PM-exposed ageing rats. Based on our data, we proposed a detailed pathogenic mechanism to depict temporal and dynamic molecular regulations associated with PM- and gaseous pollutants-induced lung injury. We expect that our findings would provide valuable information towards progression of air pollution-caused lung injury and serve as a repository to search for potential draggable targets.