Exposure to polycyclic aromatic hydrocarbons and risk of abnormal liver function: The mediating role of C-reactive protein

Polycyclic aromatic hydrocarbons (PAHs) exposure has been suggested to be linked to abnormal liver function (ALF). However, the conclusions are inconsistent, and the underlying mechanism is still unclear. In this study, a cross-sectional design including 4935 adults from the National Health and Nutrition Examination Survey (NHANES) between 2003 and 2010 was conducted to quantify the PAHs-ALF associations, and to investigate the possible mediation role of systemic inflammation. Capillary gas chromatography coupled with tandem mass spectrometry (GC-MS/MS) was utilized to detect nine urinary levels of PAH metabolites (OH-PAHs). Plasma levels of systemic inflammation biomarker, C-reactive protein (CRP), were measured by enhanced turbidimetry. ALF was diagnosed on the basis of any abnormities in albumin (ALB), aspartate aminotransferase (AST), γ-glutamyl transpeptidase (GGT), and alanine aminotransferase (ALT). Logistic regression model and the least absolute shrinkage and selection operator (LASSO) regression models indicated positive associations between urinary 1-hydroxypyrene (1-OH-PYR), 2-hydroxyphenanthrene (2-OH-PHE), and ALF risk. Significant synergistic effect of 1-OH-PYR and 2-OH-PHE on ALF was observed via additive interaction analysis. The weighted quantile sum (WQS) analysis and the quantile-based g computation (qgcomp) were employed to investigate the mixed effect of PAHs but no significant results were found. However, these two analyses consistently showed that 2-OH-PHE and 1-OH-PYR had top dominant weights in the positive association with ALF. Furthermore, mediation analysis indicated that plasma CRP mediated 13.4 % of the association between 1-OH-PYR and ALF risk. These results enhanced our comprehension of the health effects of PAHs exposure on liver function as well as the underlying mechanism.