From Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia (H.W.W., S.L.G., C.G.M.); Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, and Division of Medicine and Department of Clinical Physiology and Nuclear Medicine, Turku University Hospital, Finland (M.J., J.S.A.V., O.T.R., C.G.M.); Department of Clinical Physiology, University of Tampere and Tampere University Hospital, Finland (M.K.); Department of Clinical Physiology, University of Kuopio, Finland (T.L.); and Department of Pediatrics, Vaasa Central Hospital, Finland (L.T.).
Circulation. 2015 Apr 7;131(14):1239-46. doi: 10.1161/CIRCULATIONAHA.114.013485. Epub 2015 Mar 23.
The association between passive smoking exposure in childhood and adverse cardiovascular health in adulthood is not well understood. Using a 26-year follow-up study, we examined whether childhood exposure to passive smoking was associated with carotid atherosclerotic plaque in young adults.
Participants were from the Cardiovascular Risk in Young Finns Study (n=2448). Information on childhood exposure to parental smoking was collected in 1980 and 1983. Carotid ultrasound data were collected in adulthood in 2001 or 2007. Childhood serum cotinine levels from 1980 were measured from frozen samples in 2014 (n=1578). The proportion of children with nondetectable cotinine levels was highest among households in which neither parent smoked (84%), was decreased in households in which 1 parent smoked (62%), and was lowest among households in which both parents smoked (43%). Regardless of adjustment for potential confounding and mediating variables, the relative risk of developing carotid plaque in adulthood increased among those children with 1 or both parents who smoked (relative risk, 1.7; 95% confidence interval, 1.0-2.8; P=0.04). Although children whose parents exercised good "smoking hygiene" (smoking parents whose children had nondetectable cotinine levels) had increased risk of carotid plaque compared with children with nonsmoking parents (relative risk, 1.6; 95% confidence interval, 0.6-4.0; P=0.34), children of smoking parents with poor smoking hygiene (smoking parents whose children had detectable serum cotinine levels) had substantially increased risk of plaque as adults (relative risk, 4.0; 95% confidence interval, 1.7-9.8; P=0.002).
Children of parents who smoke have increased risk of developing carotid atherosclerotic plaque in adulthood. However, parents who exercise good smoking hygiene can lessen their child's risk of developing plaque.
儿童时期被动吸烟暴露与成年后心血管健康不良之间的关联尚未得到充分理解。本研究采用一项 26 年的随访研究,旨在探讨儿童时期被动吸烟暴露是否与年轻人颈动脉粥样硬化斑块有关。
参与者来自心血管风险在芬兰年轻人研究(n=2448)。1980 年和 1983 年收集了父母吸烟的儿童时期暴露信息。2001 年或 2007 年在成年期采集颈动脉超声数据。2014 年从冷冻样本中测量了 1980 年的儿童血清可替宁水平(n=1578)。在双亲均不吸烟的家庭中,儿童的血清可替宁水平检测不出的比例最高(84%),双亲中只有 1 人吸烟的家庭中比例降低(62%),双亲均吸烟的家庭中比例最低(43%)。无论是否调整潜在的混杂和中介变量,与双亲均不吸烟的儿童相比,双亲中至少有 1 人吸烟的儿童(相对风险,1.7;95%置信区间,1.0-2.8;P=0.04)发生颈动脉斑块的相对风险增加。尽管父母采取良好的“吸烟卫生”(吸烟的父母其子女的血清可替宁水平检测不出)的儿童与非吸烟父母的子女相比,颈动脉斑块的风险增加(相对风险,1.6;95%置信区间,0.6-4.0;P=0.34),但父母吸烟卫生不佳(吸烟的父母其子女的血清可替宁水平检测出)的儿童成年后患斑块的风险大大增加(相对风险,4.0;95%置信区间,1.7-9.8;P=0.002)。
父母吸烟的儿童在成年后患颈动脉粥样硬化斑块的风险增加。然而,父母采取良好的吸烟卫生可以降低其子女发生斑块的风险。