Shared mechanisms linking PM2.5 exposure, obstructive sleep apnea and obesity.

Obesity and obstructive sleep apnea (OSA) are highly prevalent and interconnected conditions that contribute to the global burden of chronic non-communicable diseases. Fine particulate matter (PM2.5), a major component of air pollution, has emerged as a relevant factor linked to metabolic dysfunction and sleep disturbances. Chronic exposure to PM2.5 has been related to higher body mass index (BMI), central fat deposition, metabolic syndrome, and increased OSA risk and severity. Obesity remains the main modifiable risk factor for OSA, whereas intermittent hypoxia and sleep fragmentation can aggravate hormonal, inflammatory, and metabolic disturbances involved in weight gain. PM2.5 exposure and OSA overlap through pathways involving systemic inflammation, oxidative stress, neuroendocrine dysregulation, and gut microbiota alterations. These converging mechanisms highlight the potential role of environmental pollution and sleep disruption in obesity pathophysiology, particularly in urban populations chronically exposed to adverse environmental conditions. This review synthesizes current epidemiological and mechanistic evidence, identifies important knowledge gaps, and proposes shared biological pathways that may inform future research on the interplay among PM2.5 exposure, OSA, and obesity.