Inflammation mediation of the association between brominated flame retardants and psoriasis among U.S. adults.

Background: Brominated flame retardants (BFRs), widely applied in fire prevention, are persistent environmental pollutants. Accumulating evidence indicates that BFRs can trigger inflammatory responses in humans, potentially contributing to various diseases. Given the central role of inflammation in psoriasis pathogenesis, investigating the association between BFR exposure and psoriasis risk is of considerable importance. Methods: We analyzed data from the 2005-2006 and 2009-2014 cycles of the National Health and Nutrition Examination Survey (NHANES). concentrations of BFRs were natural logarithmic transformed and categorized into quartiles. The association between BFR exposure and psoriasis was evaluated using multivariable regression models, restricted cubic spline analysis, mediation analysis, and interaction testing to assess both individual and combined effects. Results: Among 4,251 adult participants, 123 (2.9%) reported having psoriasis. After adjusting for covariates, individuals in the highest quartile of polybrominated diphenyl ether 153 (PBDE153) exposure (Q4) exhibited a significantly increased risk of psoriasis compared to those in the lowest quartile (Q1) (OR = 2.89, 95% CI: 1.26-6.61, p = 0.013). Restricted cubic spline analysis indicated a positive dose-response relationship between PBDE153 levels and psoriasis risk (P-overall = 0.012, P-nonlinear = 0.881), with a significant linear trend (p < 0.001). Weighted Quantile Sum (WQS) analysis revealed a statistically significant positive association between the BFR mixture and psoriasis risk (OR = 1.709, 95% CI: 1.241-2.370, p = 0.001). PBDE153 was identified as the primary contributor, with a weight of 0.691. In contrast, Quantile G-computation (Qgcomp) analysis showed a positive but non-significant association (psi1 = 0.273, 95% CI: -0.043 to 0.589, p = 0.090). Notably, individuals with higher poverty income ratios exhibited increased susceptibility to psoriasis risk associated with PBDE153 (p = 0.016). Inflammation accounted for 4.35% of the relationship between PBDE153 and psoriasis (p < 0.05). Conclusion: This study suggests a positive association between PBDE153 exposure and psoriasis risk, with inflammatory pathways playing a partial mediating role. However, the cross-sectional design precludes causal inference. Therefore, longitudinal studies and experimental research are needed to establish such causal relationships.