Objective: During the Iran-Iraq war, the Iraqi regime frequently used Sulfur Mustard as chemical weapon. Infected more than 100,000 people with chemical pollutants during these wars have been reported. Sulfur mustard can damage many different organs like the skin, respiratory system and eye. Most of these patients are suffering from chronic obstructive respiratory disease (COPD). TGF-βs as a cytokine with diverse actions including inhibition of cell growth and suppression of inflammation and adjustment processes play an important role in lung inflammation plays so that anti-inflammatory role of this molecule and its receptor Airway structural changes (Airway remodeling) and common diseases have been seen. In this study tried to express two isoforms of TGF-β receptor in the bronchial wall with chemically injured samples compared to healthy individuals volunteered to be. Materials and Methods: : 15 Veterans mustard gas exposure, 12 controls were enrolled. First total mRNA was extracted from airway wall biopsy and then cDNA was synthesized. To assess gene expression of TGF-βR1-2 semi-quantitative RT-PCR technique was used and finally densiometry technique was used for quantitative evaluation. Results::Findings showed that levels of TGF-BR1 and TGF-BR2 significantly in patients who had contact with the chemical gas was increased. (p<0.5) based on molecules found TGF-βR1 and TGF-βR2 in a group of chemical contact with the gas had caused the secretion of macrophage efferocytosis is in the process. Conclusion: Transient growth factor receptor beta (TGF-βR1-2) play a significant role in chronic airway remodeling caused by mustard gas.