In a recent publication we hypothesized that increased bone metabolism induced by thyroid hormones should increase lead excretion even in lead unexposed subjects. To examine this hypothesis, 10 hypothyroid patients were investigated before and after substitution therapy with levothyroxine. After a mean of 9 wk after onset of therapy (patients were then in an euthyroid state), lead concentrations in urine (PbU) corrected by the individual creatinine in urine were increased (p = .007), while lead concentrations in blood (PbB) were slightly decreased (3.44 +/- 1.73 vs. 2.74 +/- 1.38, p = .008). Desoxypyridinoline cross-links (Pyr), a sensitive marker for bone degradation and excreted in urine, correlated with PbU (r = .64, p = .002) but not with PbB. Additionally PbU significantly correlated with serum concentrations of free circulating T3 (fT3) or free circulating T4 (fT4). Thus, we may suspect that increased lead excretion was induced by accelerated bone metabolism, since Pyr was increased after therapy (3.21 +/- 1.19 vs. 6. 10 +/- 1.81 nM/mM Cr, p < .001), too.