Significance Exposure to high levels of particulate matter (PM) poses a major threat to human health. Cigarette smoke is the most common irritant that causes chronic obstructive pulmonary disease (COPD); however, at least one-fourth of patients with COPD are nonsmokers, and their disease is largely attributed to air pollution. The occurrence of pollution episodes in China has raised an emergent question of how PM leads to the pathogenesis of COPD. In this paper, we show that deregulation of mitochondrial NADH dehydrogenase gene expression levels plays a key role in the aggravation of COPD during air pollutant exposure, which can be rescued by taurine and 3-MA treatments in both mammalian cells and animals.