Abstract

Smoking is a cause of nonalcoholic fatty liver disease (NAFLD), but the dose-response relationship between secondhand smoke exposure (SHS) and NAFLD is unclear. This study sought to determine the relationship between SHS and NAFLD risk among adult nonsmokers in the United States. Data from 7412 adult nonsmokers aged ≥20 years who participated in the National Health and Nutrition Examination Survey (NHANES) between 2007 and 2016 were used in this study. SHS was defined as a nonsmoker with a serum cotinine concentration of 0.05-10.00 ng/mL. NAFLD was identified using the U.S. fatty liver index (USFLI), hepatic steatosis index (HSI), and fatty liver index (FLI). Weighted multivariable logistic regression and restricted cubic spline models were applied to evaluate the relationship between SHS and NAFLD risk. The participants had a weighted mean age of 49.2 years, and 55.5% were female. SHS was associated with NAFLD (odds ratio [OR] 1.22; 95% confidence interval CI: 1.05 to 1.42), showing a linear dose-response relationship (natural log of cotinine level: OR 1.10, 95% CI: 1.05 to 1.17). Sensitivity analyses using different NAFLD definitions (HSI: OR 1.21, 95% CI: 1.01 to 1.46; FLI: OR 1.26, 95% CI: 1.06 to 1.49), excluding participants taking hepatotoxic drugs, and propensity score-adjusted analysis yielded similar results. The association between SHS and NAFLD was consistent in analyses stratified by age, sex, and race/ethnicity. Among this nationally representative sample of U.S. adults, SHS had a linear dose-response relationship with the risk of NAFLD, suggesting that measures to lower SHS might lower NAFLD risk. This study assessed the association between secondhand smoke exposure and the risk of nonalcoholic fatty liver disease (NAFLD) using data from 7412 adult nonsmokers aged 20 years or older who participated in the United States NHANES between 2007 and 2016. Secondhand smoke exposure was measured using serum cotinine levels. Three different noninvasive indexes were used to measure NAFLD. Secondhand smoke exposure was associated with an increased risk of NAFLD, with a linear dose-response relationship. The results of sensitivity analyses and subgroup analyses were consistent.

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