The way I've understood it, all sideroblastic anemias (Pb poisoning, ALA synthase deficiency, copper deficiency, etc) share the same profile. High ferritin, normal to low TIBC. You're constantly consuming Fe, and without a reliable way to dump Fe the only real way to manage it is to not take it up in the first place.
With all sideroblastic anemias the Fe is trapped in the mitochondria, leading to improper sensing of serum Fe levels, leading to improper overabsorption of Fe. You're now in a temporary state of high ferritin, low serum Fe. As you overload the cells they rupture, spilling Fe into the blood, raising serum Fe, keeping ferritin high, and lowering TIBC (given enough time). In short, I don't think Pb poisoning is different than the other sideroblastic anemias (in terms of iron studies).