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Obesity as a mediator in the association between urinary polycyclic aromatic hydrocarbon exposure and liver fibrosis risk in US adults
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DOI：10.1039/d5em00050e.png)
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Abstract
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Polycyclic aromatic hydrocarbon (PAH) exposure may be associated with obesity-mediated liver injury. However, there is a lack of evidence on the role of obesity in associations of PAH exposure with liver fibrosis among population-based studies. Participant data were sourced from the National Health and Nutrition Survey 2001-2016. Urinary metabolites of PAHs were analyzed using gas chromatography-mass spectrometry. Liver fibrosis was classified as low and high risk. The weight-adjusted waist index (WWI) was calculated by waist circumference divided by the square of the weight. Logistic regression models and WQS regression were used to explore associations between exposure to six types of PAHs and the risk of liver fibrosis in adults and the mediating effects of obesity on the above-mentioned associations were further analyzed. Multiple urinary PAH metabolites were associated with increased risk of liver fibrosis. Positive association between a mixture of 6 PAHs and liver fibrosis (OR: 1.41, 95% CI: 1.10-1.80) was found and 2-naphthol, 1-pyrene, 1-naphthol, and 2-fluorene were the primary contributors to this association. Furthermore, the proportion mediation of obesity on associations of individual and the mixture of PAHs with liver fibrosis ranged from 4.6% to 38.3%. The results of this study showed that exposure to the mixture of PAHs was associated with increased liver fibrosis and these associations were partially mediated by obesity.
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