Chronic Obstructive Pulmonary Disease (COPD) is a complex, heterogeneous and prevalent disease with a high socio-economic burden whose underlying biological mechanisms are unknown. It is now well established that about half of the patients with COPD never achieved a normal lung function early in life, and there is increasing evidence that some COPD risks may derive from early life factors in this setting it is highly likely that respiratory diseases are the end result of a set of different dynamic environmental-gene interactions that can occur during the entire life span of an individual (time). Lung development and lung aging are often considered two independent phenomena, but they are tightly interrelated.

Here we propose that alterations during lung development influence age-related physiological deterioration and cause premature lung aging. We expect that the lung (lung tissue and bronchial biopsies), as affected organ in COPD, accumulates the highest burden of methylation changes, but that some of them, are reflected in the circulating blood. Subsequently we will explore if these changes are identifiable early in life. We sought to explore this hypothesis by comparing the epigenetic profile associated with FEV1