Ozone exposure and ferroptosis: Mechanistic links and current evidence.

Ambient ozone (O3) is a highly reactive secondary air pollutant whose health relevance is increasingly recognized. Although epidemiological evidence has linked O3 exposure to multiple diseases, the biological mechanisms underlying the health effects remain incompletely understood. Ferroptosis, a form of regulated cell death characterized by iron-dependent lipid peroxidation, has been implicated in diverse diseases and is increasingly considered a potential mechanism underlying pollutant-induced health injury. Notably, the core biochemical features of ferroptosis closely align with multiple O3-induced molecular responses, including reactive oxygen species accumulation, excessive lipid peroxidation, and impaired antioxidant defenses, suggesting that ferroptosis may be a regulated cell death mechanism involved in O3-related toxicity. However, evidence linking O3 exposure to ferroptosis remains limited and fragmented. Therefore, this review synthesizes current mechanistic insights and available evidence connecting O3 exposure with ferroptosis. Relevant literature was retrieved from databases including PubMed, Web of Science, and Scopus, covering studies published up to May 2026, and included studies addressing O3 exposure in relation to ferroptosis, or to ferroptosis-relevant processes such as lipid peroxidation, antioxidant disruption, iron dyshomeostasis, or mitochondrial dysfunction. We further discuss current limitations and priorities for future research, with the aim of evaluating ferroptosis as a candidate mechanism underlying O3-associated health effects.