Exposure to cigarette smoke produces a functional iron deficiency following complexation of host metal to reactive groups at the cigarette smoke particle (CSP) surface. Though a component of the tissue response is actually focused on reversing the metal deficiency by way of inflammation, it rapidly proceeds to include fibrosis, reveals a new study. 

The research conducted by a team of researchers from various universities in the US found that exposure to CSP produces a deficiency of iron which the cells try to reverse through inflammation, mucus production and fibrosis. The study, published in the International Journal of Chronic Obstructive Pulmonary Disease,  highlighted that the clinical manifestations of this response can present as respiratory bronchiolitis, desquamative interstitial pneumonitis, pulmonary Langerhans’ cell histiocytosis, asthma, pulmonary hypertension, chronic bronchitis, and pulmonary fibrosis, adding that with significant disruption of iron homeostasis and unresolved metal deficiency, there will be injury associated with cell death, which is not reversible.