Chronic obstructive pulmonary disease (COPD) is primarily a lung condition characterised by the presence of persistent airflow limitation resulting from inflammation, remodelling of small airways, and emphysema. It is well-recognised that the impacts of COPD extend beyond the lung with many patients suffering systemic manifestations such as cardiovascular diseases that affect morbidity and mortality [1]. "Accelerated ageing" has been proposed as a mechanism that underlies many of the pulmonary and extrapulmonary consequences of COPD [2,3]. It is thought that a decline in organ function is a feature of ageing in response to the accumulation of cell and molecular damage, and in the case of COPD, noxious inhalants such as tobacco smoke increase this damage, thus accelerating the ageing process, leading to the development of COPD. With the exception of lung function decline, however, evidence indicating that tobacco smoking or COPD accelerates age-associated deterioration remains scarce.The degradation of elastin, a key protein component of connective tissues that critically provides the characteristics of elasticity, resilience and deformability, is an important feature in normal ageing and in COPD. Elastin has a long half-life (∼74 years [4]) in contrast to minutes to days for most intracellular proteins [5]. This longevity increases its susceptibility to oxidative and chemical damage, which are believed to drive age-related elastic fibre turnover associated with low-grade chronic inflammation. This turnover can be measured by the levels of circulating desmosine and isodesmosine (DES/IDES), two crosslinking moieties that specifically exist in mature elastin [6]. We and others have shown increased circulating DES/IDES levels in COPD patients in comparison with healthy smokers and never-smokers [7][8][9][10]. Recently, we further demonstrated that this increase was associated with higher mortality and cardiovascular morbidity in a large cohort study [10]. Interestingly, among all of the demographic variables analysed, circulating DES/IDES levels display the strongest consistent correlation with chronological age in three independent cohorts of COPD patients [10,11]. This marker also showed a stronger association with age than inflammatory markers (e.g. fibrinogen, club cell secretary protein 18 and high sensitivity C-reactive peptide) [10]. These observations raise the possibility that systemic elastin turnover is an age-dependent process, and that COPD and smoking can alter the rate of this process.