Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals · 2026
Volatile gas exposure correlates with self-reported liver condition: insights from NHANES 2009-2018 and Mendelian randomization studies.
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Jia Yuyun, Cao Yanping, Yin Qin, Li Xueqian, Wen Xiu
Аннотация
INTRODUCTION: Volatile gas exposure and self-reported liver conditions share pathophysiologic risk factors, but their exact association remains unclear.
METHODS: We used a weighted multivariable-adjusted logistic regression model, using data from the National Health and Nutrition Examination Survey (NHANES) 2009-2018. Integrative analyses of Non-alcoholic fatty liver disease (NAFLD), liver fibrosis, liver cirrhosis GWAS summaries and blood expression quantitative trait loci (eQTLs) were conducted via summary data-based MR (SMR) and colocalization analysis to prioritize putative blood smoking-related genes and their associations with each liver condition risk. Finally, we further verified these gene-disease causal links through MR and colocalization analysis.
RESULTS: 12,099 NHANES participants were included. Male sex, 46-75 years, and smoke exposure correlated positively with LC; age and smoke exposure remained positively associated with LC incidence after adjustment, while non-Hispanic Black was a LC protective factor. SMR identified three blood-derived candidate genes: RGPD8 (Beta = -0.207), COX6B2 (Beta = -0.567), DNAJC27 (Beta = 0.859). MR and colocalization confirmed their associations with cirrhosis, fibrosis, and NAFLD, respectively.
CONCLUSION: This study confirms a causal link between smoke exposure and increased LC risk, identifies novel gene-disease associations, and provides cross-disciplinary insights for targeted LC prevention and personalized research.
METHODS: We used a weighted multivariable-adjusted logistic regression model, using data from the National Health and Nutrition Examination Survey (NHANES) 2009-2018. Integrative analyses of Non-alcoholic fatty liver disease (NAFLD), liver fibrosis, liver cirrhosis GWAS summaries and blood expression quantitative trait loci (eQTLs) were conducted via summary data-based MR (SMR) and colocalization analysis to prioritize putative blood smoking-related genes and their associations with each liver condition risk. Finally, we further verified these gene-disease causal links through MR and colocalization analysis.
RESULTS: 12,099 NHANES participants were included. Male sex, 46-75 years, and smoke exposure correlated positively with LC; age and smoke exposure remained positively associated with LC incidence after adjustment, while non-Hispanic Black was a LC protective factor. SMR identified three blood-derived candidate genes: RGPD8 (Beta = -0.207), COX6B2 (Beta = -0.567), DNAJC27 (Beta = 0.859). MR and colocalization confirmed their associations with cirrhosis, fibrosis, and NAFLD, respectively.
CONCLUSION: This study confirms a causal link between smoke exposure and increased LC risk, identifies novel gene-disease associations, and provides cross-disciplinary insights for targeted LC prevention and personalized research.