OBJECTIVE: Passive smoking has been associated with increased cardiovascular morbidity. The present study aimed to examine the long-term effects of childhood exposure to tobacco smoke on endothelium-dependent vasodilation in adults. METHODS AND RESULTS: The analyses were based on 2171 participants in the population-based Cardiovascular Risk in Young Finns (N=2067) and Childhood Determinants of Adult Health (N=104) studies who had measures of conventional risk factors (lipids, blood pressure, adiposity, socioeconomic status) and self-reported parental smoking status when aged 3 to 18 years at baseline. They were re-examined 19 to 27 years later when aged 28 to 45 years. Brachial artery flow-mediated dilatation was measured at follow-up with ultrasound. In analyses adjusting for age, sex, and childhood risk factors, flow-mediated dilatation was reduced among participants who had parents that smoked in youth compared to those whose parents did not smoke (Young Finns: 9.2 ± 0.1% (mean ± SEM) versus 8.6 ± 0.1%, P=0.001; Childhood Determinants of Adult Health: 7.4 ± 0.6% versus 4.9 ± 0.9%, P=0.04). These effects remained after adjustment for adult risk factors including own smoking status (Young Finns, P=0.003; Childhood Determinants of Adult Health, P=0.03). CONCLUSIONS: Parental smoking in youth is associated with reduced flow-mediated dilatation in young adulthood measured over 20 years later. These findings suggest that passive exposure to cigarette smoke among children might cause irreversible impairment in endothelium-dependent vasodilation.
OBJECTIVE: Passive smoking has been associated with increased cardiovascular morbidity. The present study aimed to examine the long-term effects of childhood exposure to tobacco smoke on endothelium-dependent vasodilation in adults. METHODS AND RESULTS: The analyses were based on 2171 participants in the population-based Cardiovascular Risk in Young Finns (N=2067) and Childhood Determinants of Adult Health (N=104) studies who had measures of conventional risk factors (lipids, blood pressure, adiposity, socioeconomic status) and self-reported parental smoking status when aged 3 to 18 years at baseline. They were re-examined 19 to 27 years later when aged 28 to 45 years. Brachial artery flow-mediated dilatation was measured at follow-up with ultrasound. In analyses adjusting for age, sex, and childhood risk factors, flow-mediated dilatation was reduced among participants who had parents that smoked in youth compared to those whose parents did not smoke (Young Finns: 9.2 ± 0.1% (mean ± SEM) versus 8.6 ± 0.1%, P=0.001; Childhood Determinants of Adult Health: 7.4 ± 0.6% versus 4.9 ± 0.9%, P=0.04). These effects remained after adjustment for adult risk factors including own smoking status (Young Finns, P=0.003; Childhood Determinants of Adult Health, P=0.03). CONCLUSIONS: Parental smoking in youth is associated with reduced flow-mediated dilatation in young adulthood measured over 20 years later. These findings suggest that passive exposure to cigarette smoke among children might cause irreversible impairment in endothelium-dependent vasodilation.
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