The effect of pretreatment and simultaneous treatment with thiamine on therapeutic efficacy of calcium disodium edetate (CaNa2EDTA) in lead intoxication was investigated in rats. The animals exposed to Pb as Pb (CH3COO)2·3 H2O through drinking water (0.1%) for 8 wk were treated with either saline, thiamine-HCl (sc), CaNa2EDTA (ip), or thiamine-HCl plus CaNa2EDTA, for 3 d or thiamine-HCl for 3 d followed by thiamine, then HCl plus CaNa2EDTA for a further 3 d. The Pb exposure caused significant accumulation of Pb in liver, kideny, and brain, inhibition in the activity of blood δ-amino-levulinic acid dehydratase (δ-ALAD), and increase in levels of urinary δ-aminolevulinic acid, homovanillic acid (HVA), vanillyl mandelic acid (VMA), brain HVA and VMA. The brain δ-ALAD and lipomide dehydrogenase remained unaffected by Pb. Thiamine significantly enhanced the urinary excretion of Pb by CaNa2EDTA, but only marginally influenced the efficacy of CaNa2EDTA to either mobilize tissue Pb or reverse the biochemical alterations.