PASSIVE SMOKING INDUCES ATHEROGENIC CHANGES IN LOW-DENSITY-LIPOPROTEIN

Background-According to the American Heart Association, passive smokin g is an important risk factor for coronary heart disease (CHD), but th e mechanisms underlying this association are not fully understood. We studied the acute effect of passive smoking on the factors that influe nce the development of CHD: the antioxidant defense of human serum, th e extent of lipid peroxidation, and the accumulation of LDL cholestero l in cultured human macrophages, the precursors of foam cells in ather osclerotic lesions. Methods and Results-Blood samples were collected d uring 2 ordinary working days from healthy, nonsmoking subjects (n=10) before and after (up to 5.5 hours) spending half an hour in a smoke-f ree area (day 1) or in a room for smokers (day 2). Passive smoking cau sed an acute decrease (1.5 hours after exposure) in serum ascorbic aci d (P<.001) and in serum antioxidant defense (P<.001), a decreased capa city of LDL to resist oxidation (P<.01), and the appearance of increas ed amounts of lipid peroxidation end products in serum (P<.01). Finall y, LDL isolated from subjects after passive smoking was taken up by cu ltured macrophages at an increased rate (P<.05). Conclusions-Exposure of nonsmoking subjects to secondhand smoke breaks down the serum antio xidant defense, leading to accelerated lipid peroxidation, LDL modific ation, and accumulation of LDL cholesterol in human macrophages. These data provide the pathophysiological background for the recent epidemi ological evidence about the increased CHD risk among passive smokers.