Objective: Smoking is one of the most important cause of cardiovascular disease and known as a preventable risk factor. Lipoproteins especially LDL has an important role in cardiovascular disease. Normally high density lipoproteins protect LDL from oxidation; proinflammatory HDLs do not. The aim of this study was to determine whether the young smokers who smoke acute or chronically, have more proinflammatory HDL which may predispose them to cardiovascular disease compared to nonsmokers.

Materials and Methods: Forty young smokers, who have been smoking for 8-10 years and forty healthy nonsmokers were included in this study. Blood samples were collected after overnight fast with on absence of smoking and one hour after smoking a cigarette. The ability of the subjects HDLs to prevent oxidation of LDL-C was measured. Total-C, TG, HDL-C, LDL-C, Apo A, Apo B, hsCRP and Lp(a) levels were also determined using routine standard methods.

Results: Total-C, LDL-C, Lp(a) and hsCRP levels were not different between the smokers and control groups. The plasma level of HDL-C was significantly lower and those of TG, and Apo B levels were significantly higher in the smoking group than in the control group. The smokers had higher proinflammatory HDL compared to those of nonsmokers (80% vs 10%). Antiinflammatory HDL levels of smokers were decreased after smoking (48% and 68% respectively).

Conclusion: Chronic smoking impairs HDLs anti inflammatory functions and balance between lipoproteins and apolipoproteins. This result may indicate that proinflammatory HDL induced by smoking may have a role in atherosclerosis process.