Kallio Katariina, Jokinen Eero, Raitakari Olli T, Hämäläinen Mauri, Siltala Marja, Volanen Iina, Kaitosaari Tuuli, Viikari Jorma, Rönnemaa Tapani, Simell Olli
Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, Kiinamyllynkatu 10, FIN-20520 Turku, Finland.
Circulation. 2007 Jun 26;115(25):3205-12. doi: 10.1161/CIRCULATIONAHA.106.674804. Epub 2007 Jun 4.
Passive smoking is associated with early arterial damage in adults, but its effect on endothelial function in children is unknown.
Serum cotinine concentration was measured annually in children between 8 and 11 years of age who had participated since infancy in a randomized, prospective atherosclerosis prevention trial (Special Turku Coronary Risk Factor Intervention Project for children [STRIP]). At age 11, endothelium-dependent flow-mediated vasodilatory responses of the brachial artery were examined with high-resolution ultrasound in 402 children. These children were divided into 3 groups according to serum cotinine concentrations: the noncotinine group (nondetectable cotinine, n=229), the low cotinine group (cotinine between 0.2 and 1.6 ng/mL, n=134), and the top decile cotinine group (cotinine > or = 1.7 ng/mL, n=39). Longitudinal cotinine data in children aged 8 to 11 years and ultrasound studies were available in 327 children. At age 11, the increase in cotinine concentration was associated with attenuated peak flow-mediated dilation response (mean+/-SD: the noncotinine group 9.10+/-3.88%, the low-cotinine group 8.57+/-3.78%, and the top-decile cotinine group 7.73+/-3.85%; P=0.03 for trend). Similarly, total dilation response (the area under the dilation response versus time curve between 40 and 180 seconds after hyperemia) was affected by the cotinine level (P=0.02 for trend). These trends were not explained by traditional atherosclerosis risk factors. Arterial measures and passive smoking showed even stronger associations when longitudinal cotinine data were used (peak flow-mediated dilation, P=0.01 for trend; total dilation response, P=0.008 for trend).
Exposure to environmental tobacco smoke confirmed by serum cotinine concentrations impairs endothelial function in a dose-dependent manner in 11-year-old children.
被动吸烟与成人早期动脉损伤相关，但其对儿童内皮功能的影响尚不清楚。
对自婴儿期起就参与一项随机、前瞻性动脉粥样硬化预防试验（儿童特殊图尔库冠状动脉危险因素干预项目[STRIP]）的8至11岁儿童每年测量血清可替宁浓度。11岁时，用高分辨率超声检查了402名儿童肱动脉的内皮依赖性血流介导的血管舒张反应。根据血清可替宁浓度将这些儿童分为3组：不可替宁组（可替宁检测不到，n = 229）、低可替宁组（可替宁在0.2至1.6 ng/mL之间；n = 134）和最高十分位数可替宁组（可替宁≥1.7 ng/mL，n = 39）。327名儿童有8至11岁儿童的纵向可替宁数据及超声研究资料。11岁时，可替宁浓度的升高与血流介导的峰值扩张反应减弱相关（均值±标准差：不可替宁组9.10±3.88%，低可替宁组8.57±3.78%，最高十分位数可替宁组7.73±3.85%；趋势P = 0.03）。同样，总扩张反应（充血后40至180秒之间扩张反应与时间曲线下的面积）受可替宁水平影响（趋势P = 0.02）。这些趋势无法用传统动脉粥样硬化危险因素解释。当使用纵向可替宁数据时，动脉测量指标与被动吸烟之间的关联更强（血流介导的峰值扩张，趋势P = 0.01；总扩张反应，趋势P = 0.008）。
血清可替宁浓度证实的环境烟草烟雾暴露以剂量依赖方式损害11岁儿童的内皮功能。
