From the Department of Medicine, University of Helsinki, Finland.
Correspondence to Timo Kuusi, MD, PhD, Department of Medicine, Helsinki University Hospital, Haartmaninkatu 4, 00290 Helsinki 29, Finland.
Background—According to the American
Heart Association, passive smoking is an important risk factor for
coronary heart disease (CHD), but the mechanisms underlying
this association are not fully understood. We studied the acute effect
of passive smoking on the factors that influence the development of
CHD: the antioxidant defense of human serum, the extent of lipid
peroxidation, and the accumulation of LDL cholesterol in
cultured human macrophages, the precursors of foam cells in
atherosclerotic lesions.
Methods and Results—Blood samples were collected during 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-free area
(day 1) or in a room for smokers (day 2). Passive smoking caused an
acute decrease (1.5 hours after exposure) in serum ascorbic acid
(P<.001) and in serum antioxidant defense
(P<.001), a decreased capacity of LDL to resist
oxidation (P<.01), and the appearance of increased
amounts of lipid peroxidation end products in serum
(P<.01). Finally, LDL isolated from subjects after
passive smoking was taken up by cultured macrophages at an
increased rate (P<.05).
Conclusions—Exposure of nonsmoking subjects to secondhand smoke
breaks down the serum antioxidant defense, leading to accelerated lipid
peroxidation, LDL modification, and accumulation of LDL
cholesterol in human macrophages. These data
provide the pathophysiological background for the
recent epidemiological evidence about the increased CHD risk among
passive smokers.
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Passive Smoking Induces Atherogenic Changes in Low-Density Lipoprotein
Key Words: lipoproteins • coronary disease • smoking • atherosclerosis
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