Qiying Song1, Dianjianyi Sun2, Tao Zhou3, Xiang Li3, Hao Ma3, Zhaoxia Liang4, Haijun Wang5, Marly Augusto Cardoso6, Yoriko Heianza3, Lu Qi7. 1. 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. 2. 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. 3. Department of Epidemiology, School of Public Health and Tropical Medicine, Tulane University, New Orleans, LA, USA. 4. Department of Epidemiology, School of Public Health and Tropical Medicine, Tulane University, New Orleans, LA, USA; Department of Obstetrical, Women's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang Province, China. 5. Department of Maternal and Child Health, School of Public Health, Peking University, Beijing, China. 6. Department of Nutrition, School of Public Health, University of Sao Paulo, Sao Paulo, Brazil. 7. Department of Epidemiology, School of Public Health and Tropical Medicine, Tulane University, New Orleans, LA, USA; Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. Electronic address: lqi1@tulane.edu.
Abstract
BACKGROUND AND AIMS: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
BACKGROUND AND AIMS: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
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