Among the essential metals with which lead interacts are calcium, iron, and zinc.The lead ion has a lone pair in its electronic structure, which can result in a distortion in the coordination of ligands, and in 2007 was hypothesized to be important in lead poisonings effects on enzymes (see Lone pair § Unusual lone pairs).One of the main causes for the pathology of lead is that it interferes with the activity of an essential enzyme called delta-aminolevulinic acid dehydratase, or ALAD (see image of the enzyme structure), which is important in the biosynthesis of heme, the cofactor found in hemoglobin. Lead also inhibits the enzyme ferrochelatase, another enzyme involved in the formation of heme. Ferrochelatase catalyzes the joining of protoporphyrin and Fe2+ to form heme. Leads interference with heme synthesis results in production of zinc protoporphyrin and the development of anemia. Another effect of leads interference with heme synthesis is the buildup of heme precursors, such as aminolevulinic acid, which may be directly or indirectly harmful to neurons. Elevation of aminolevulinic acid results in lead poisoning having symptoms similar to acute porphyria. Neurons
The brain is the organ most sensitive to lead exposure. Lead is able to pass through the endothelial cells at the blood brain barrier because it can substitute for calcium ions and be taken up by calcium-ATPase pumps. Lead poisoning interferes with the normal development of a childs brain and nervous system; therefore children are at greater risk of lead neurotoxicity than adults are.
Chemical abnormalities
Methemoglobinemia:
a condition caused by elevated levels of methemoglobin in the blood. Methaemoglobin is a form of Hb that contains the ferric [Fe3+] form of iron. The affinity for oxygen of ferric iron is impaired. The binding of oxygen to methaemoglobin results in an increased affinity for oxygen in the remaining heme sites that are in ferrous state within the same tetrameric haemoglobin unit. B)  Quantitative
Production abnormalities
Copy number variation (e.g., deletion, duplication, insertion) is also a common genetic cause of Hb disorders, and complex rearrangements and globin gene fusions can also occur. Thalassemias: Thalassemias are quantitative defects that lead to reduced levels of one type of globin chain, creating an imbalance in the ratio of alpha-like chains to beta-like chains. As noted above, this ratio is normally tightly regulated to prevent excess globin chains of one type from accumulating. The excess chains that fail to incorporate into Hb form non-functional aggregates that precipitate within the RBC. This can lead to premature RBC destruction in the bone marrow (beta thalassemia) and/or in the peripheral blood (alpha thalassemia). Types:
Alpha
Beta (Major)
Beta (Minor)

Hemoglobin variants
Haemoglobin variant are not necessarily pathological. For example, haemoglobin Valletta and haemoglobin Marseille are two haemoglobin variants which are non-pathological

HbS
HbC
HbE
Hb Barts
Hb D-Punjab
HbO (Hb O-Arab)
Hb G-Philadelphia
Hb H
Hb Constant Spring
Hb Hasharon
Hemoglobin Kenya
Hb Korle-Bu
Hb Lepore
Hb M
Hb Kansas
Hb J
Hb N-Baltimore
Hb Hope
Hb Pisa

Electrophoretic migration patterns
Hemoglobin variants can be detected by gel electrophoresis.