Air pollution and muscle-fat imbalance: How PM2.5 components and ozone drive sarcopenic obesity through inflammation

The combined impact of specific PM 2.5 components and ozone (O₃) on sarcopenic obesity (SO) remains unclear. This study examined the effects of PM 2.5 constituents and O₃ on SO risk and explored inflammation as a potential mediator. We analyzed data from the China Health and Retirement Longitudinal Study (CHARLS, 2011–2015). SO was defined as the co-occurrence of obesity (body mass index [BMI] ≥ 28 kg/m²) and sarcopenia, the latter characterized by low muscle mass plus either low muscle strength or impaired physical performance. Air pollution data (PM 2.5 , its components, and O₃) were derived from the Tracking Air Pollution in China database. Systemic inflammation was operationalized as a composite z-score from C-reactive protein and white blood cell count. We employed Cox regression and quantile-based g-computation to evaluate the air pollution-SO relationship, and performed causal mediation analysis to quantify the mediating role of inflammatory pathways. Long-term exposure to a mixture of PM 2.5 constituents was significantly associated with an increased risk of SO ( HR = 1.10, 95% CI : 1.06–1.14). Ammonium contributed most substantially to this effect (71%), followed by black carbon (22%) and organic matter (7%). In contrast, O₃ exhibited no independent association with SO risk. A significant positive synergistic interaction was observed between the PM 2.5 constituents and O₃, indicating a compounded adverse effect. Mediation analysis revealed that systemic inflammation accounted for 14–26% of the effect of PM 2.5 exposure on SO development. These associations were more pronounced among older adults, men, and urban residents. This study provides novel insights into environmental triggers of SO, highlighting the need for integrated air quality policies targeting specific PM 2.5 components and personalized prevention strategies addressing inflammatory pathways in at-risk populations.