Cigarette Smoke Particle-Induced Lung Injury and Iron Homeostasis.

Journal Article (Journal Article;Review)

It is proposed that the mechanistic basis for non-neoplastic lung injury with cigarette smoking is a disruption of iron homeostasis in cells after exposure to cigarette smoke particle (CSP). Following the complexation and sequestration of intracellular iron by CSP, the host response (eg, inflammation, mucus production, and fibrosis) attempts to reverse a functional metal deficiency. 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. If the response is unsuccessful, the functional deficiency of iron progresses to irreversible cell death evident in emphysema and bronchiectasis. The subsequent clinical and pathological presentation is a continuum of lung injuries, which overlap and coexist with one another. Designating these non-neoplastic lung injuries after smoking as distinct disease processes fails to recognize shared relationships to each other and ultimately to CSP, as well as the common mechanistic pathway (ie, disruption of iron homeostasis).

Full Text

Duke Authors

Cited Authors

  • Ghio, AJ; Pavlisko, EN; Roggli, VL; Todd, NW; Sangani, RG

Published Date

  • 2022

Published In

Volume / Issue

  • 17 /

Start / End Page

  • 117 - 140

PubMed ID

  • 35046648

Pubmed Central ID

  • PMC8763205

Electronic International Standard Serial Number (EISSN)

  • 1178-2005

Digital Object Identifier (DOI)

  • 10.2147/COPD.S337354


  • eng

Conference Location

  • New Zealand