Pulmonary Idiopatic Fibrosis, Interstitial Diseases and Smoke

Aldo Pezzuto

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

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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.


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.


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