Thalassemia is an autosome linked recessive blood disorder and it is:

The correct answer is Option (4) → Quantitative problem of synthesizing few globin molecules

Thalassemia is an autosome-linked recessive blood disease. A mutation or deletion lowers the rate at which one of the globin chains (α or β) is made. Too few globin chains give abnormal haemoglobin and anaemia.

(1) Qualitative problem of synthesizing incorrectly functioning globin — Incorrect. This describes sickle-cell anaemia, where one amino acid in the β chain is changed so that the globin works wrongly.

(2) Controlled by genes present on chromosome 11 and 12 — Incorrect. α thalassemia is controlled by the genes HBA1 and HBA2 on chromosome 16. β thalassemia is controlled by the HBB gene on chromosome 11. Chromosome 12 is not involved.

(3) Caused by duplication of genes that form haemoglobin — Incorrect. The defect comes from a mutation or deletion of the genes, not from duplication.

(4) Quantitative problem of synthesizing few globin molecules — Correct. Too few globin molecules are made, so this is a problem of quantity.

NCERT Extract:
Mendelian Disorders – “… Thalassemia : This is also an autosome-linked recessive blood disease transmitted from parents to the offspring when both the partners are unaffected carrier for the gene (or heterozygous). The defect could be due to either mutation or deletion which ultimately results in reduced rate of synthesis of one of the globin chains (α and β chains) that make up haemoglobin. This causes the formation of abnormal haemoglobin molecules resulting into anaemia which is characteristic of the disease. Thalassemia can be classified according to which chain of the haemoglobin molecule is affected. In α Thalassemia, production of α globin chain is affected while in β Thalassemia, production of β globin chain is affected. α Thalassemia is controlled by two closely linked genes HBA1 and HBA2 on chromosome 16 of each parent and it is observed due to mutation or deletion of one or more of the four genes. The more genes affected, the less alpha globin molecules produced. While β Thalassemia is controlled by a single gene HBB on chromosome 11 of each parent and occurs due to mutation of one or both the genes. Thalassemia differs from sickle-cell anaemia in that the former is a quantitative problem of synthesising too few globin molecules while the latter is a qualitative problem of synthesising an incorrectly functioning globin.”