Association of Exposure to Brominated Flame Retardants with Hyperuricemia: A Mediation Analysis of Inflammatory...

There is increasing evidence that environmental factors play an important role in the pathogenesis of hyperuricemia. However, the relationship between Brominated Flame Retardants (BFRs) and serum uric acid and hyperuricemia remains unclear.

This study used data from 7996 National Health and Nutrition Examination Survey (NHANES) participants from 2005 to 2016. Ten BFRs, including PBB153 and PBDE28, were included in the analysis. Multivariate logistic regression, subgroup analysis, Spearman correlation analysis, Weighted Quantile Sum (WQS), and Bayesian Kernel Machine Regression (BKMR) were used to assess the association between BFRs and hyperuricemia. We also evaluated the mediating role of the Systemic Immunoinflammatory Index (SII) in the relationship between BFRs and hyperuricemia.

Results show that, after adjusting for all covariates, PBDE47, PBDE99, PBDE100, and PBDE154 were significantly associated with hyperuricemia risk. The results of the WQS regression and BKMR model showed a significant positive correlation between exposure to mixed BFRs and hyperuricemia risk. PBDE183 (weight: 38%) was found to have the highest weight in the mixture. Further mediating analysis showed that the relationship between PBDE28 and PBDE183 exposure and hyperuricemia risk was mediated by SII.

Exposure to BFRs increases the risk of hyperuricemia, which may be mediated by inflammation. Therefore, future research should further explore the potential mechanisms underlying the association between BFR exposure and hyperuricemia risk.

Exposure to BFRs may increase the risk of hyperuricemia. Large-scale prospective cohort studies and experimental research are needed to confirm the relationship between BFRs and hyperuricemia.