Ageing is a complex phenotype responsive to a plethora of ENVIRONmental inputs (ENVIRONAGE). Age related conditions in adults often find their origin in risk factors operative in early life. The molecular mechanisms behind these phenomena remain largely unknown. Mitochondria are involved in a variety of critical cell functions, including oxidative energy production and programmed cell death. Recently, I established in a study of 175 newborns, a strong association between mitochondrial DNA content and in utero exposure to particulate air pollution. Telomere length is highly heritable and erosion leads to an increasingly vulnerable structural integrity of the chromosomes. It is considered a marker of overall biological age compared with chronological age. In this regard, I demonstrated the heritability of telomere length and the influence of smoking on telomere erosion. These results support the ENVIRONAGE hypothesis, i.e. that environmental inputs influence biomolecular markers of ageing including mitochondrial function, telomere length along with DNA repair and epigenetics as the ‘core axis of ageing’. The aim is to establish prospective epidemiological evidence for molecular mechanisms or early biomarkers, which may underlie the origins or reflect the risk of age-related diseases and to understand its association with other processes and the influence of environmental factors. To this end, I will establish a birth cohort and a cohort in middle-aged and elderly. I measure environmental pollutants, in interaction with parameters that I consider to have an important role in the ageing process (mitochondrial function, telomere length, epigenetics and DNA repair capacity). ENVIRONAGE integrates environmental influences and molecular mechanisms on ageing. The common molecular epidemiological strategies in newborns, middle-aged and elderly to unravel the environmental influence on ageing are groundbreaking.