Air pollution and muscle-fat imbalance: How PM2.5 components and ozone drive sarcopenic obesity through inflammation
大気汚染と筋肉-脂肪の不均衡：PM2.5成分とオゾンが炎症を介してサルコペニア肥満を引き起こす仕組み (AI 翻訳)
Xianzhi Li, Yajie Li, Li Yin, Qian Zhu, Shunjin Liu, Xiangyi Xing, Zong-Lei Zhou
🤖 gxceed AI 要約
日本語
本研究は、PM2.5成分とオゾンがサルコペニア肥満（SO）リスクに与える影響を中国のデータで分析。PM2.5混合物への長期曝露はSOリスクを有意に増加させ、アンモニウムが最大の寄与因子であった。炎症がその効果の14-26%を媒介し、高齢者・男性・都市住民で関連が強かった。特定のPM2.5成分を標的とした大気質政策の重要性を示唆。
English
This study examines the impact of PM2.5 components and ozone on sarcopenic obesity (SO) using Chinese cohort data. Long-term exposure to PM2.5 mixture significantly increased SO risk, with ammonium contributing most. Inflammation mediated 14-26% of the effect, with stronger associations in older adults, men, and urban residents. It highlights the need for targeted air quality policies.
Unofficial AI-generated summary based on the public title and abstract. Not an official translation.
📝 gxceed 編集解説 — Why this matters
日本のGX文脈において
日本でもPM2.5対策は重要だが、特定成分（アンモニウム、ブラックカーボン）の影響を考慮した政策は限られる。本知見は日本の大気環境基準の再検討や、高齢者の健康保護策に示唆を与える可能性がある。
In the global GX context
Globally, air pollution policies often target total PM2.5 mass. This study underscores the importance of regulating specific components (ammonium, black carbon) for public health, which could inform more effective emission reduction strategies beyond climate goals.
👥 読者別の含意
🔬研究者:Provides novel evidence on specific PM2.5 components as risk factors for sarcopenic obesity, with mediation by inflammation.
🏢実務担当者:May inform public health interventions targeting air pollution reduction in vulnerable populations.
🏛政策担当者:Suggests that air quality regulations should consider component-specific effects, potentially strengthening ties between health and climate policy.
📄 Abstract（原文）
Background The combined impact of specific PM2.5 components and ozone (O₃) on sarcopenic obesity (SO) remains unclear. This study examined the effects of PM2.5 constituents and O₃ on SO risk and explored inflammation as a potential mediator. Methods 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 (PM2.5, 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. Results Long-term exposure to a mixture of PM2.5 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 PM2.5 constituents and O₃, indicating a compounded adverse effect. Mediation analysis revealed that systemic inflammation accounted for 14–26% of the effect of PM2.5 exposure on SO development. These associations were more pronounced among older adults, men, and urban residents. Conclusions This study provides novel insights into environmental triggers of SO, highlighting the need for integrated air quality policies targeting specific PM2.5 components and personalized prevention strategies addressing inflammatory pathways in at-risk populations.
🔗 Provenance — このレコードを発見したソース
- semanticscholar https://doi.org/10.1016/j.jnha.2026.100779first seen 2026-07-02 06:24:49
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