Abstract

Air pollution and physical inactivity are leading contributors to the global burden of chronic disease and premature mortality. While exercise is a well-established stimulus for physiological adaptations and disease prevention, it also transiently increases reactive oxygen species (ROS) production, which function as essential signals for metabolic remodeling and cellular resilience. In contrast, exposure to air pollution, specifically fine particulate matter (PM2.5), leads to sustained and uncontrolled ROS production, promoting oxidative damage, inflammation, and cardiometabolic dysfunction.This review examines a critical and under-investigated question: How does exercising in polluted environments affect the redox signaling pathways that mediate the health benefits of exercise? We summarize current knowledge at the intersection of exercise physiology, redox biology, and environmental toxicology, with a particular focus on the roles of ROS sources, the scavenger system, and downstream physiological responses. By integrating findings from human and animal studies, we identify factors such as air pollution sources and level of exposure, exercise intensity, and age that shape redox outcomes. We also identify key knowledge gaps to clarify how context-specific redox responses determine whether exercise promotes adaptation or exacerbates pollution-related harm, providing essential insights for future mechanistic research and evidence-based public policies. © 2025 Elsevier Inc. All rights are reserved, including those for text and data mining, AI training, and similar technologies.