The mechanism responsible for the atherogenic effects of passive smoking was studied. Four weeks and 12 weeks of exposure of rats to tobacco sidestream smoke resulted in an increase in lipid peroxide contents, expressed as thiobarbituric-acid reactive substances, in low-density lipoprotein (LDL) and in aortic tissue. The LDL isolated from plasma exhibited elevations of 136, 155, and 170% over the control values for TBA, cholesterol, esterified cholesterol, respectively, whereas the corresponding increases in the aorta were 118, 148, and 254%, respectively. Electrophoretic examinations of LDL revealed a typical denatured LDL. Among esterified cholesterol-metabolizing enzymes in the aorta, lysosomal acid cholesteryl ester hydrolase, microsomal neutral cholesteryl ester hydrolase, and acyl coenzyme A: cholesterol acyltransferase were significantly suppressed by the 4 weeks' exposure; and further suppression of the acid cholesteryl ester hydrolase activity along with increases in the neutral cholesteryl ester hydrolase and acyl coenzyme A: cholesterol acyltransferase activities was observed after 12 weeks' exposure. A possible mechanism of the observed lipid accumulation in the aorta was discussed in connection with the effect of lipid peroxides in oxidatively modified-LDL on esterified cholesterol-metabolizing enzymes.