A final consideration is that the relationship between cigarette smoke and ILDs has not been completely revealed and will continue unfolded. There is strong evidence supporting a potential causal role for the development of some ILDs, such as RB-ILD, DIP, and PLCH. Nevertheless, cigarette smoking exhibits also a paradoxical effect on parenchymal lung inflammation and fibrosis. Actually, it may promote or inhibit these pathologic processes, influencing the incidence, severity, or natural history of a wide array of ILDs. For example, current and former smokers show an increased risk for acquiring idiopathic pulmonary fibrosis, though smokers seem to have a better survival rate than nonsmokers.29–
By contrast, cigarette smoking appears to have a protective effect on the development of a number of ILD including hypersensitivity pneumonitis, sarcoidosis, and radiation-induced pneumonitis.30–32
Therefore, the window between long-term cigarette smoking and ILDs remains open.