Loading...

JOURNAL OF CHEST & PULMONARY MEDICINE (ISSN:2732-480X)

Pulmonary Idiopatic Fibrosis, Interstitial Diseases and Smoke

Aldo Pezzuto

Department of Cardiovascular-Respiratory Science, Sant’ Andrea Hospital-Sapienza University, Via di Grottarossa, Rome, Italy

CitationCitation COPIED

Pezzuto A. Pulmonary Idiopatic Fibrosis, Interstitial Diseases and Smoke. J Chest Pulm Med. 2020 May;1(1):104.

2020 Pezzuto A. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 international License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.

Summary

Cigarette smoking is a mixture of more than 4,000 recognized substances responsible of lung inflammation, COPD and cancer but it could also promote the idiopatic pulmonary fibrosis development [1]. The latter is a condition characterized by a progressive worsening of lung function and frequent exacerbations. Indeed the main symptoms are exertional dyspnea, non-productive cough, and often the pathognomonic sign is the presence of honeycombing observed by high resolution computed tomography (HRCT) and an usual interstitial pneumonia (UIP) histopathology pattern. Smoking cessation in turn reduces the progression of the disease slowing down the risk.

Interstitial lung diseases are caused by smoking compounds through several pathways, inflammation, oxidative stress, immune-dysregulation.

There is a strong link between smoking habit and idiopathic pulmonary fibrosis IPF with OR 2.3 in current smokers and 1.6 in former smokers. Notably patients with a packyear major than 20 are more susceptible to developing idiopathic pulmonary fibrosis (IPF).

IPF is the most common type of idiopathic interstitial pneumonias (IIP) of unknown etiology that more often affects male, elderly people and smokers.

Smoking has been hypothesized to affect the development of idiopatic pulmonary fibrosis through different mechanisms, and notably oxidative stress from smoking might contribute to its pathogenesis in both current and former smokers. The functional parameters are consistent with a restrictive lung disease with reduced vital capacity.

We can find in clinical studies that among patients affected by IPF never-smokers had better survival than former smokers . Eventually smokers develop earlier IPF than nonsmokers and the most associated comorbidity is cardiovascular disease.

Another interstitial disease called Langerhans cell histiocytosis [2] is associated with substantial tobacco consumption, and smoking habit brings about infiltrative pneumopathy with increased percentage of macrophages in bronchial alveolar lavage fluid.

Another interstitial common disease, respiratory bronchiolitis is frequently found in heavy smokers and in case of tobacco cessation a fully regression of clinical signs and symptoms is observed [3-13].

Cigarette smoking has been associated with a form of pulmonary fibrosis associated with bronchiolitis. In this condition a combined action of smoking and pollutants may favor the development of bronchiolitis-associated fibrosis.

References

  1. Henrot P, Prevel R, Berger P, Dupin I. Chemokines in COPD: From Implication toTherapeutic Use. Int J Mol Sci. 2019 Jun 6;20(11):E2785.
  2. Tazi A, De Margerie C, Naccache JM, Fry S, Dominique S, et al. The natural history of adultpulmonary Langerhans cell histiocytosis: a prospective multicentre study. Orphanet JRare Dis. 2015 Mar 14;10:30.
  3. Pezzuto A, Citarella F, Croghan I, Tonini G. The effects of cigarette smoking extracts oncell cycle and tumor spread: novel evidence. Future Sci OA. 2019 May 3;5(5):FSO394.
  4. Kishaba T, Nagano H, Nei Y, Yamashiro S. Clinical characteristics of idiopathic pulmonaryfibrosis patients according to their smoking status. J Thorac Dis. 2016 Jun;8(6):1112-1120.
  5. American Thoracic Society. Idiopathic pulmonary fibrosis: diagnosis and treatment.International consensus statement. American Thoracic Society (ATS), and the EuropeanRespiratory Society (ERS). Am J Respir Crit Care Med. 2000 Feb;161(2pt):646-664.
  6. Okamoto T, Ichiyasu H, Ichikado K, Muranaka H, Sato K, et al. Clinical analysis of the acute exacerbation in patients with idiopathic pulmonaryfibrosis. Nihon Kokyuki Gakkai Zasshi. 2006 May;44(5):359-367. 
  7. Martinez FJ, Safrin S, Weycker D, et al. The clinical course ofpatients with idiopathic pulmonary fibrosis. Ann Intern Med.2005 Jun;142:963-967.
  8. Behrooz L, Balekian DS, Faridi MK, Espinola JA, Townley LP, etal. Prenatal and postnatal tobacco smoke exposure and risk ofsevere bronchiolitis during infancy. Respir Med. 2018 Jul;140:21-26.
  9. Baumgartner KB, Samet JM, Stidley CA, Colby TV, Waldron JA.Cigarette smoking: a risk factor for idiopathic pulmonary fibrosis.Am J Respir Crit Care Med. 1997 Jan;155(1):242-248.
  10. Antoniou KM, Hansell DM, Rubens MB, Marten K, Desai SR.Idiopathic pulmonary fibrosis: outcome in relation to smokingstatus. Am J Respir Crit Care Med. 2008 Jan;177(2):190-194.
  11. MacNee W. Pulmonary and systemic oxidant/antioxidantimbalance in chronic obstructive pulmonary disease. Proc AmThorac Soc 2005;2(1):50-60.
  12. Steele MP, Speer MC, Loyd JE, Brown KK, Herron A, et al. Clinicaland pathologic features of familial interstitial pneumonia. Am JRespir Crit Care Med. 2005 Nov;172:1146–1152.
  13. Kärkkäinen M, Kettunen HP, Nurmi H, Selander T, Purokivi M.Effect of smoking and comorbidities on survival in idiopathicpulmonary fibrosis. Respir Res. 2017 Aug 22;18(1):160.