The association between elevated levels of cholesterol and tryglicerides, low levels of HDL cholesterol and elevated risk of atherosclerosis has been widely demonstrated. The exaggerated elevation of tryglicerides after a meal (postprandial lipemia) is an alteration which has grown a great concern in the last years. Several factors have shown their ability to affect postprandial lipemia. Tobacco smoking is, however, one of the least studied factors. Our aim was to evaluate if could tobacco smoking alter characteristics of postprandial Iipemia, and search for a direct relationship between the tobacco exposition and the magnitude of sueh alterations. Methods We analyzed the variation of HDL cholesterol (HDLc) and tryglicerides (TG) in a sample of 26 young healthy individuals (13 men and 13 women) with tobacco expositions between 0,75 and 9 packs/year during the first 6 hours after a meal with a standardized lipid contento The behavior of these parameters was compared with that found in a group ofhealthy young nonsmokers from a study realized by the same investigation group. A relationship between the tobacco exposition and the characteristics of postprandiallipemia was intended to be established. Results AH meditions of TG were higher in the smokers group than in non-smokers, with an area under curve (AVC) 21% higher, although this difference did not reach statistical significance (p=0,08). The medium values of TG at 5 and 6 hours after meal were significatively higher in smokers than in non-smokers, with a value 43 and 45% higher, respectively. (p=0,02 for hour 5, p=0,03 for hour 6). In the highest cuartile of tobacco exposition the AVC for TG was 46,2% higher than in the lowest cuartile. No differences in HDLc were evident between smokers and non-smokers. Conclusions The people who smoke show from early ages alterations in postprandial TG depuration. Such alterations consist initially of the apparition of augmented TG values 5 to 6 hours after the intake of lipids respect to non-smokers. 6 hours after the fat intake, smokers appear to stay more separated from basal value than non-smokers do. The fact that we didn't find differences in the behavior of HDL cholesterol suggests that these alterations require a longer exposition to tobacco, according to the findings in older people in other studies.