Increased oxidative stress in children exposed to passive smoking

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Abstract

Background

Atherogenic process is accelerated with cigarette smoke that contains many oxidants and prooxidants, capable of producing free radical and enhancing the oxidative stress. We investigated oxidative and antioxidative status of children who had been exposed to passive smoking and compared with those of not exposed group.

Methods

One hundred forty-three school children aged 9–13 years, 61 of whom had never been exposed to passive smoking, and 82 of whom had been exposed to passive smoking at least 10 cigarette per day for at least last 1 year in their house, were enrolled in this study. Total antioxidative response (TAR) was measured to determine antioxidative status of plasma, and total peroxide concentration was measured to determine oxidative status of plasma. The ratio of TAR to total peroxide was accepted as an indicator of oxidative stress.

Results

TAR of plasma was significantly lower in children exposed to passive smoking than in those of not exposed group (p=0.018). Mean (S.D.) values were 1.49 (0.07) and 1.52 (0.08) mmol Trolox Equiv./l, respectively. In contrary, the mean (S.D.) total peroxide level of plasma was significantly higher in children exposed to passive smoking [13.06 (2.34) μmol H2O2/l] than in not exposed group [12.24 (1.74) μmol H2O2/l] (p=0.015). The mean (S.D.) oxidative stress index (OSI) value was significantly higher in the children exposed to passive smoking [0.87 (0.15)] than in not exposed group [0.80 (0.10)] (p=0.001).

Conclusion

Children who are exposed to passive smoking are exposed to oxidative stress, which has been implicated in the etiopathogenesis of over 100 disorders including atherosclerosis.

Introduction

Reactive oxygen species (ROS) such as superoxide radical anion, hydroxyl radical and hydrogen peroxide are produced in metabolic and physiological processes and harmful oxidative reactions may occur in organisms. The oxidative effects of ROS are controlled by exogenous antioxidants such as vitamins E and C, and also by endogenous antioxidants such as scavenger enzymes (superoxide dismutase and glutathione peroxidase), bilirubin and uric acid. Under some conditions, increases in oxidants and decreases in antioxidants cannot be prevented, and the oxidative/antioxidative balance shifts towards the oxidative status. Consequently, oxidative stress, which has been implicated in over 100 disorders including atherosclerosis, develops [1].

Blood contains many antioxidant molecules that prevent and/or inhibit harmful free radical reactions [2]. Plasma concentrations of antioxidants can be measured separately in the laboratory, but these measurements are time-consuming, labour-intensive and costly. Since antioxidative effects of antioxidant components of plasma are additive, the measurement of total antioxidant response (TAR) reflects the antioxidative status of plasma. We evaluated the total antioxidative status of plasma using a more recently developed measurement method by Erel [3]. In the method, total antioxidant response of plasma against especially potent free radical reactions, which strongly lead to oxidative damage of biomolecules such as lipids, proteins and DNA, is measured.

Hydrogen peroxide and other derivatives of peroxides, producing physiologically and increasing in some conditions, diffuse into plasma. Here, antioxidant components of plasma overwhelm them, and they are simultaneously consumed [4]. We evaluated total oxidative status of plasma by measuring total peroxide level [5].

Atherosclerosis begins at childhood, but the degree of atherogenesis is related with numerous risk factors such as cigarette smoking, hypercholesterolemia and hypertension [6]. Researchers have demonstrated that one of the prominent risk factors for atherosclerosis development is cigarette smoke [7], [8], [9]. Atherogenic process is accelerated with the presence of some oxidants such as cigarette smoke. It contains numerous compounds, many of which are oxidants and prooxidants, capable of producing free radical and enhancing the oxidative stress in vivo [10]. Each puff of a cigarette contains 1015 oxidants in gas phase [11].

To the best of our knowledge, all of the published studies related to the oxidative and atherogenic effects of passive smoking are only about adults, but not children. In this study, we investigated oxidative and antioxidative status of children who had been exposed to passive smoking, and compared with those of not exposed group.

Section snippets

Subjects

Healthy primary schoolchildren, whose socioeconomic status and vegetable–fruit consumption were similar, were enrolled in this study. One hundred forty-three school children aged 9–13 years, 61 of whom (35 male, 26 female) had never been exposed to passive smoking, and 82 of whom (59 male, 23 female) had been exposed to passive smoking at least 10 cigarette per day for at least last 1 year in their homes.

Samples

Blood samples were withdrawn into heparinised tubes from a cubital vein after overnight

Results

Demographic characteristics of the subjects are shown in Table 1. There were no difference in age, sex and a number of siblings and family individuals between children exposed to passive smoking and no exposed group.

As seen in Table 2, plasma TAR levels of children exposed to passive smoking were found to be significantly lower than those of not exposed group (p=0.018). In contrary, plasma total peroxide levels were significantly higher in children exposed to passive smoking than in not exposed

Discussion

An increasing number of reports have documented the harmful effects of environmental tobacco smoke, and passive smoking has been identified as an important risk factor for atherosclerosis [9], [13], [14], [15], [16]. In 1992, the American Heart Association reported that the risk of death due to heart diseases had been increased by about 30% among those exposed to environmental tobacco smoke at home, but the mechanisms underlying this association were not fully understood [13]. However, it has

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