Lung T1 is a potential MRI biomarker of chronic obstructive pulmonary disease (COPD)^1,2 which is commonly caused by tobacco smoking. Smoking might affect the evaluation of lung T1 due to the presence of paramagnetic substances trapped in the lung tissue³ or the subsequent lung damage. The aim for this study was to examine whether tobacco smoking, pack years (PY), influenced T1 of the lung parenchyma in individuals with no known lung disease, to separate the smoking effect from disease related factors.Informed consent was taken from 35 asymptomatic volunteers, 23 never smokers and 12 current smokers that underwent MRI scanning and spirometry and reported physiological data. A snapshot FLASH acquisition⁴ was carried out on a 1.5 T Philips Achieva system (Philips Medical Systems, Best, NL) during free breathing (TR=2.2 ms, TE=1.0 ms, FA=5°, FOV=445² mm², slice thickness=15 mm, matrix=64x256 (zero filled to 256x256), NA=10) and on a 1.5 T-Siemens Magnetom Avanto Fit (Siemens Healthcare, Erlangen, Germany) during a light inspiration breath hold over 3 seconds (TR=3 ms, TE=0.7 ms, FA=7°, FOV=450² mm², slice thickness=15 mm, matrix=128x64 (zero filled to 256x256)). No significant difference on T1 was found the between the systems among the never smokers (p=0.35). Median lung T1 values were calculated by fitting the Look-Locker equation⁵ pixel-by-pixel and large pulmonary vessels were excluded in the quantification. A backward linear model approach was used with FEV1, FVC, weight, height, age and PY as covariates to investigate the most important variables in determining the value of a response on T1. The final backward regression model included age and PY with negative slopes of -3.1 ms/year (95%CI [-5.5, -0.6], p=0.02) and -2.3 ms/PY (95%CI [-4.9, 0.3], p=0.08), respectively. The negative slope was -4.0 ms/year (95%CI [-6.3, -1.7], p=0.001) when only age was included in the model with r=-0.52, indicating that lung T1 shortens with ageing (Fig 1). Among the never smokers, the slope of T1 as a function of age was found to be -3.7 ms/year (95%CI [-6.0, -1.3], p=0.003). Lung T1 shortens with ageing and smoking did not reach significant correlation to T1 (p=0.08). Age is a significant confounding factor when T1 is used as a biomarker in lung MRI studies that must be taken into account to detect underlying patterns of disease. The observed indication with shortened T1 in the smokers (p=0.08) most likely reflects early signs of smoking-induced lung pathology, that is not picked up by the spirometric measurements, rather than paramagnetic substances. Structural lung changes has been found in asymptomatic smokers with He-3 imaging⁶ that correlated ADC values and PY in asymptomatic subjects with similar smoking histories as in the present study. Lung T1 as a biomarker needs to be validated in larger cohorts with improved regional analysis that would increase the possibility to find a T1 relationship to PY. Our results may be of utility to power future prospective studies and increase the knowledge of the lung T1 relationship to tobacco smoking.