This study aims to examine the association between urinary cadmium (U-Cd) exposure and metabolic syndrome (MetS) in U. S. adults and evaluate whether thyroid function (TSH/T4) mediates this relationship. We analyzed National Health and Nutrition Examination Survey 2007–2012 data (n = 4869; age ≥18) to assess the relationship between U-Cd and MetS. U-Cd was measured by ICP-MS, adjusted for creatinine, and log-transformed. We employed weighted logistic regression, restricted cubic splines for nonlinearity, and multivariable models for U-Cd–TSH/T4 relations, with causal mediation analysis for indirect effects, considering demographics and lifestyle factors. Higher U-Cd was associated with greater MetS risk in a dose–response fashion: versus Q1, OR (95% CI) for Q2, Q3, Q4 were 1. 84 (1. 49–2. 26), 2. 36 (1. 92–2. 89), and 2. 49 (2. 04–3. 06) ; P -trend <. 0001. Restricted cubic splines showed a significant overall and nonlinear association (P ₒverall =. 006; P ₙonlinear =. 036), with relatively flat risk at low exposure and steeper increases beyond a turning point. U-Cd correlated positively with T4 (fully adjusted β ≈ 0. 26 ng/dL per unit increase; P <. 001) and inversely with TSH. Mediation indicated a small but significant indirect effect via T4 (indirect effect ≈ 0. 003; 95% CI, 0. 001–0. 005; proportion mediated ≈ 8. 3%), while TSH and TSH/T4 showed negligible or negative indirect effects; the direct path from U-Cd to MetS predominated. Findings were generally stronger in women, younger adults (<40 years), and those with higher physical activity, and were robust across chronic-disease strata. In a nationally representative sample, U-Cd exposure is positively – and nonlinearly – associated with MetS; this relationship is driven mainly by a direct effect with a modest mediating role of T4, underscoring the metabolic implications of environmental cadmium and the relevance of thyroid pathways.
Peng et al. (Fri,) studied this question.