Department of Epidemiology, School of Public Health and Tropical Medicine, Tulane University, New Orleans, LA, USA; Department of Maternal and Child Health, School of Public Health, Peking University, Beijing, China; Maternal-Fetal Medicine Institute, Shenzhen Baoan Women's and Children's Hospital, Jinan University, Shenzhen, China.
Department of Epidemiology, School of Public Health and Tropical Medicine, Tulane University, New Orleans, LA, USA; Department of Epidemiology and Biostatistics, School of Public Health, Peking University, Beijing, China.
Atherosclerosis. 2021 Jul;328:52-59. doi: 10.1016/j.atherosclerosis.2021.05.009. Epub 2021 May 26.
Little is known about the associations between perinatal exposure to maternal smoking and cardiovascular disease (CVD) incidence in offspring, and whether such associations are modified by adulthood and genetically determined smoking behaviors.
A total of 414,588 participants without CVD at baseline were included from the UK Biobank in 2006-2010 and followed up through 2018. Cox-proportional hazard models were used to examine the association of perinatal maternal smoking with CVD, and both multiplicative and additive interaction analyses were performed to investigate the modification effects of own smoking behaviors.
During a median follow-up of 8.93 years, we observed 10,860 incident CVD events, including 7006 myocardial infarction (MI) and 4147 stroke. We found that perinatal exposure to maternal smoking was associated with increased risks of CVD (HR: 1.10; 95% CI: 1.05-1.14), MI (1.10; 1.05-1.16) and stroke (1.10; 1.03-1.18). In addition, we observed significant interactions between perinatal exposure to maternal smoking and adulthood exposure to own smoking on CVD and MI on both the multiplicative and additive scales (all p < 0.05). The attributable proportions due to additive interaction between perinatal and adulthood exposure to smoking were 14% (9%-19%) for CVD and 16% (10%-22%) for MI, respectively. Perinatal exposure to maternal smoking also showed an interaction with genetically determined smoking on MI (p < 0.05), but no interactions were found on the total CVD and stroke.
Our results indicate that perinatal exposure to maternal smoking is associated with increased risks of CVD events, and such relations are modified by adulthood smoking behaviors.
围产期母亲吸烟与后代心血管疾病（CVD）发病之间的关联知之甚少，且这种关联是否受成年期和遗传决定的吸烟行为的影响也不清楚。
我们纳入了 2006 年至 2010 年间参加英国生物银行（UK Biobank）且基线时无 CVD 的 414588 名参与者，并随访至 2018 年。使用 Cox 比例风险模型来检验围产期母亲吸烟与 CVD 的关系，并进行了乘法和加法交互作用分析，以探讨自身吸烟行为的修饰作用。
在中位随访 8.93 年期间，我们观察到 10860 例 CVD 事件，包括 7006 例心肌梗死（MI）和 4147 例卒中。我们发现，围产期母亲吸烟暴露与 CVD（风险比 [HR]：1.10；95%置信区间 [CI]：1.05-1.14）、MI（1.10；1.05-1.16）和卒中（1.10；1.03-1.18）发病风险的增加相关。此外，我们还发现围产期母亲吸烟暴露与成年期自身吸烟暴露之间在 CVD 和 MI 上存在乘法和加法交互作用（均 P<0.05）。由于围产期和成年期吸烟暴露之间的相加交互作用，归因于 CVD 和 MI 的比例分别为 14%（9%-19%）和 16%（10%-22%）。围产期母亲吸烟暴露与 MI 上的遗传决定吸烟之间也存在交互作用（P<0.05），但在总 CVD 和卒中等其他终点上未发现交互作用。
我们的研究结果表明，围产期母亲吸烟暴露与 CVD 事件风险增加相关，这种关系受成年期吸烟行为的影响。
