Abstract: Epidemiologic studies have confirmed that air pollutants exposure could result in various adverse health outcomes, but the specific biological mechanism is still unclear. Oxidative stress (OS) induced by air pollution exposure has been confirmed as a classical regulatory mechanism that affects our health. In recent years, it has been found that the combined effect of lipid peroxidation induced by OS and iron accumulation can induce programmed cell death, which has been termed "ferroptosis". Thus, ferroptosis could be an important regulatory mechanism of adverse health outcomes induced by air pollutants exposure. To explore the mechanisms by which air pollution triggers ferroptosis, we reviewed and summarized the targets and regulatory mechanisms of ferroptosis in regulating adverse health outcomes caused by air pollution, based on existing research results. The result showed that fine particulate matter (PM_2.5), ozone (O₃) and cigarette smoke (CS) could induce ferroptosis by affecting key genes in iron metabolism and lipid peroxidation pathways. In a word, air pollutants could cause OS and reduce the antioxidant capacity, then reduce the resistance of ferroptosis. This review further supplemented the mechanism of air pollution-induced diseases, which could provide theoretical support for potential disease treatment strategies.