The article examines the association between cigarette smoking and serum lipid and lipoprotein concentrations in adults, analyzing 54 published studies. Smokers had significantly higher serum concentrations of cholesterol (3-0%), triglycerides (9-1%), very low density lipoprotein cholesterol (10-4%), and low density lipoprotein cholesterol (1-7%), and lower concentrations of high density lipoprotein cholesterol (−5-7%) and apolipoprotein AI (−4-2%) compared to non-smokers. A dose-response effect was observed, with higher smoking intensity correlating with greater changes in lipid and lipoprotein levels. These findings suggest a potential causal link between cigarette smoke exposure and changes in serum lipid and lipoprotein concentrations, possibly through physiological or dietary changes induced by smoking. The study estimates that the increased serum cholesterol concentration in smokers may account for at least 9% of the excess risk of coronary artery disease, with a gradient of increased absolute risk between light and heavy smokers. The study also discusses the mechanisms by which smoking may affect lipid levels, including the release of adrenaline, stimulation of hepatic secretion of lipoproteins, and changes in lipid metabolism. The findings are supported by a range of studies, including those on the effects of smoking on lipid metabolism, the relationship between smoking and coronary artery disease, and the impact of smoking cessation on lipid levels. The study concludes that smoking is associated with significantly higher serum lipid concentrations and lower high density lipoprotein cholesterol and apolipoprotein AI levels, with a dose-dependent relationship. The results suggest that smoking may contribute to the increased risk of coronary artery disease, and further research is needed to better understand the relationship between lipid changes and coronary artery disease risk.The article examines the association between cigarette smoking and serum lipid and lipoprotein concentrations in adults, analyzing 54 published studies. Smokers had significantly higher serum concentrations of cholesterol (3-0%), triglycerides (9-1%), very low density lipoprotein cholesterol (10-4%), and low density lipoprotein cholesterol (1-7%), and lower concentrations of high density lipoprotein cholesterol (−5-7%) and apolipoprotein AI (−4-2%) compared to non-smokers. A dose-response effect was observed, with higher smoking intensity correlating with greater changes in lipid and lipoprotein levels. These findings suggest a potential causal link between cigarette smoke exposure and changes in serum lipid and lipoprotein concentrations, possibly through physiological or dietary changes induced by smoking. The study estimates that the increased serum cholesterol concentration in smokers may account for at least 9% of the excess risk of coronary artery disease, with a gradient of increased absolute risk between light and heavy smokers. The study also discusses the mechanisms by which smoking may affect lipid levels, including the release of adrenaline, stimulation of hepatic secretion of lipoproteins, and changes in lipid metabolism. The findings are supported by a range of studies, including those on the effects of smoking on lipid metabolism, the relationship between smoking and coronary artery disease, and the impact of smoking cessation on lipid levels. The study concludes that smoking is associated with significantly higher serum lipid concentrations and lower high density lipoprotein cholesterol and apolipoprotein AI levels, with a dose-dependent relationship. The results suggest that smoking may contribute to the increased risk of coronary artery disease, and further research is needed to better understand the relationship between lipid changes and coronary artery disease risk.